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inos  (Elabscience Biotechnology)


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    Structured Review

    Elabscience Biotechnology inos
    Inos, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 43 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nitric+oxide/Rat+NOS2%2FiNOS+(Nitric+Oxide+Synthase+2/pm42826808-142-22-26
    Average 93 stars, based on 43 article reviews
    inos - by Bioz Stars, 2026-10
    93/100 stars

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    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Inhibiting cathepsin B alleviates acute lung injury caused by sepsis through suppression of pyroptosis in lung epithelial cells
    Article Snippet: They were then incubated with the TUNEL reaction mixture in a humid dark chamber at 37 °C for 1 h. Nuclear visualization was performed using 4′,6-diamidino-2-phenylindole (DAPI, Beyotime, Cat# C1002) as a counterstain, and images were captured using a fluorescence microscope (Olympus, Japan). .. The concentrations of IL-1β (Elabscience, China, Cat# E-EL-M0064) , TNF-α (Elabscience, China, Cat# E-EL-M0019c) , and nitric oxide (NO, Elabscience, China, Cat# E-BC-K035-M) in lung tissue and cell supernatants were quantified using ELISA kits according to the manufacturer’s instructions. ..

    Article Title: Inhibiting cathepsin B alleviates acute lung injury caused by sepsis through suppression of pyroptosis in lung epithelial cells.
    Article Snippet: They were then incubated with the TUNEL reaction mixture in a humid dark chamber at 37 °C for 1 h. Nuclear visualization was performed using 4′,6-diamidino2-phenylindole (DAPI, Beyotime, Cat# C1002) as a counterstain, and images were captured using a fluorescence microscope (Olympus, Japan). .. The concentrations of IL-1β (Elabscience, China, Cat# E-EL-M0064), TNF-α(Elabscience, China, Cat# E-ELM0019c), and nitric oxide (NO, Elabscience, China, Cat# E-BC-K035-M) in lung tissue and cell supernatants were quantified using ELISA kits according to the manufacturer’s instructions. ..

    Article Title: Aging aggravates cognitive dysfunction in spontaneously hypertensive rats by inducing cerebral microvascular endothelial dysfunction
    Article Snippet: .. Centrifuge the blood sample (5,000 rpm, 4°C, 30 min), take the supernatant and store at -80◦C.The concentrations of interleukin-6(IL-6)(E-UNEL-M0070,Elabscience), inter-cellular adhesion molecule-1 (ICAM-1)(E-EL-R2850,Elabscience), matrix metalloproteinase-9 (MMP-9)(E-EL-H1451km,Elabscience), total superoxide dismutase (T-SOD)(E-BC-K020-M,Elabscience), glutathione peroxidase (GSH-Px)(E-BC-K096-S,Elabscience), malondialdehyde (MDA)(E-BC-K025-S, Elabscience), nitric oxide (NO)(E-BC-K035-M,Elabscience), endothelin-1 (ET-1) (E-EL-H0064c, Elabscience) and CALB/SA(BES5633K, Bioesn) in serum and brain were determined by the ELISA Kit according to the manufacturer’s instructions. ..

    Article Title: Aging aggravates cognitive dysfunction in spontaneously hypertensive rats by inducing cerebral microvascular endothelial dysfunction.
    Article Snippet: .. Centrifuge the blood sample (5,000 rpm, 4°C, 30 min), take the supernatant and store at -80◦C.The concentrations of interleukin-6(IL-6)(E-UNEL-M0070,Elabscience), inter-cellular adhesion molecule-1 (ICAM-1)(E-EL-R2850,Elabscience), matrix metalloproteinase-9 (MMP-9)(E-EL-H1451km,Elabscience), total superoxide dismutase (T-SOD)(E-BC-K020-M, Elabscience), glutathione peroxidase (GSH-Px)(E-BC-K096-S,Elabscience), malondialdehyde (MDA)(E-BC-K025-S, Elabscience), nitric oxide (NO)(E-BC-K035-M,Elabscience), endothelin-1 (ET-1) (E-EL-H0064c, Elabscience) and CALB/SA(BES5633K, Bioesn) in serum and brain were determined by the ELISA Kit according to the manufacturer’s instructions. ..

    Multiple Displacement Amplification:

    Article Title: Exploring the effects of Citrus aurantifolia fruits peel essential oil, cultivated in Al-Hasa, in Methotrexate induced kidney and hepatic toxicities: Network Pharmacology, Molecular Docking, and in vivo Experiments.
    Article Snippet: Ethnopharmacological relevance: Ancient and medieval sources, particularly from Arabic and Mediterranean traditions, reported Citrus aurantifolia (Lime) as antidotes against poison, tonics for digestion, antibacterial and immunomodulatory effects.. Moreover, its traditional use as a diuretic and antitoxic agent supports its ethnomedicinal relevance in managing renal ailments such as urolithiasis and toxin-induced nephropathies.. Methotrexate (MTX) is consumed in several types of carcinomas.

    Article Title: In vivo and molecular docking investigation of the novel anti-inflammatory and mitochondrial mechanisms underlying the renoprotective effects of resmetirom and curcumin in gentamicin-induced renal toxicity in rats
    Article Snippet: .. Nitric oxide (Cat. no. E-BC-K035-M), GSH (Cat. no. E-BC-K030-S), and MDA (Cat. no. E-BC-K025-S) concentrations in kidney tissue homogenates were assessed spectrophotometrically using a commercially available kit from Elabscience in China [ ]. .. We used a rat-specific sandwich ELISA kit from Sunlong Biotechnology in Shanghai, Hangzhou, Zhejiang, China, to measure the levels of KIM-1 (Cat. no. E-EL-R3019) and NGAL (Cat. no. E-EL-R3055) in kidney tissue [ ].

    Article Title: In vivo and molecular docking investigation of the novel anti-inflammatory and mitochondrial mechanisms underlying the renoprotective effects of resmetirom and curcumin in gentamicin-induced renal toxicity in rats.
    Article Snippet: .. Nitric oxide (Cat. no. E-BC-K035-M), GSH (Cat. no. E-BC-K030-S), and MDA (Cat. no. E-BC-K025-S) concentrations in kidney tissue homogenates were assessed spectrophotometrically using a commercially available kit from Elabscience in China [32]. .. Kidney injury markers assessment We used a rat-specific sandwich ELISA kit from Sunlong Biotechnology in Shanghai, Hangzhou, Zhejiang, China, to measure the levels of KIM-1 (Cat. no. E-EL-R3019) and NGAL (Cat. no. E-EL-R3055) in kidney tissue [31].

    Article Title: Aging aggravates cognitive dysfunction in spontaneously hypertensive rats by inducing cerebral microvascular endothelial dysfunction
    Article Snippet: .. Centrifuge the blood sample (5,000 rpm, 4°C, 30 min), take the supernatant and store at -80◦C.The concentrations of interleukin-6(IL-6)(E-UNEL-M0070,Elabscience), inter-cellular adhesion molecule-1 (ICAM-1)(E-EL-R2850,Elabscience), matrix metalloproteinase-9 (MMP-9)(E-EL-H1451km,Elabscience), total superoxide dismutase (T-SOD)(E-BC-K020-M,Elabscience), glutathione peroxidase (GSH-Px)(E-BC-K096-S,Elabscience), malondialdehyde (MDA)(E-BC-K025-S, Elabscience), nitric oxide (NO)(E-BC-K035-M,Elabscience), endothelin-1 (ET-1) (E-EL-H0064c, Elabscience) and CALB/SA(BES5633K, Bioesn) in serum and brain were determined by the ELISA Kit according to the manufacturer’s instructions. ..

    Article Title: Aging aggravates cognitive dysfunction in spontaneously hypertensive rats by inducing cerebral microvascular endothelial dysfunction.
    Article Snippet: .. Centrifuge the blood sample (5,000 rpm, 4°C, 30 min), take the supernatant and store at -80◦C.The concentrations of interleukin-6(IL-6)(E-UNEL-M0070,Elabscience), inter-cellular adhesion molecule-1 (ICAM-1)(E-EL-R2850,Elabscience), matrix metalloproteinase-9 (MMP-9)(E-EL-H1451km,Elabscience), total superoxide dismutase (T-SOD)(E-BC-K020-M, Elabscience), glutathione peroxidase (GSH-Px)(E-BC-K096-S,Elabscience), malondialdehyde (MDA)(E-BC-K025-S, Elabscience), nitric oxide (NO)(E-BC-K035-M,Elabscience), endothelin-1 (ET-1) (E-EL-H0064c, Elabscience) and CALB/SA(BES5633K, Bioesn) in serum and brain were determined by the ELISA Kit according to the manufacturer’s instructions. ..



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    GA promotes M2 polarization via PRKCD to alleviate SI-ALI. (A) Immunohistochemistry analysis of PRKCD expression. (B) Hematoxylin and eosin staining of lung tissues. (C) Assessment of pulmonary edema by W/D ratio. (D) Immunofluorescence analysis <t>of</t> <t>iNOS</t> and Arg1 expression in lung tissues. (E) ELISA analysis of IL-1β and TNF-α levels in BALF. Data are presented as mean ± SD (n=6 mice per group). For multiple-group comparisons, one-way ANOVA followed by Tukey’s post hoc test was applied. *, P<0.05; ***, P<0.001; ****, P<0.0001. ANOVA, analysis of variance; BALF, bronchoalveolar lavage fluid; DAPI, 4',6-diamidino-2-phenylindole; ELISA, enzyme-linked immunosorbent assay; GA, glycyrrhizic acid; IL-1β, interleukin-1 beta; NC, negative control; PRKCD, protein kinase C delta; SD, standard deviation; SI-ALI, sepsis-induced acute lung injury; TNF-α, tumor necrosis factor-alpha; W/D, wet-to-dry weight.
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    Establishment of the APAP-induced liver injury in mice and cell models. (A) Paraffin-embedded liver sections underwent H&E staining as well as TNF-α, IL-6 and IL-1β immunostaining; scale bars, 100 μ m. (B) Serum ALT and AST levels were measured in APAP-induced mice (n=6). (C) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from APAP-induced mouse liver tissues. (D) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in liver extracts prepared from APAP-induced mouse liver tissues. (E) Representative western blots and densitometry analysis of <t>iNOS</t> and NOX4 expression in liver extracts prepared from APAP-induced mouse liver tissues. (F) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in APAP-induced AML-12 cells. (G) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in APAP-induced AML-12 cells. (H) Representative western blots and densitometry analysis of iNOS and NOX4 expression in APAP-induced AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, **** P<0.0001. APAP, acetaminophen; H&E, hematoxylin and eosin; IHC, immunohistochemistry; ALT, alanine aminotransferase; AST, aspartate aminotransferase; SREBP-1, sterol regulatory element-binding protein 1; PPAR-α, peroxisome proliferator-activated receptor α; Fasn, fatty acid <t>synthase;</t> iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.
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    Establishment of the APAP-induced liver injury in mice and cell models. (A) Paraffin-embedded liver sections underwent H&E staining as well as TNF-α, IL-6 and IL-1β immunostaining; scale bars, 100 μ m. (B) Serum ALT and AST levels were measured in APAP-induced mice (n=6). (C) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from APAP-induced mouse liver tissues. (D) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in liver extracts prepared from APAP-induced mouse liver tissues. (E) Representative western blots and densitometry analysis of <t>iNOS</t> and NOX4 expression in liver extracts prepared from APAP-induced mouse liver tissues. (F) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in APAP-induced AML-12 cells. (G) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in APAP-induced AML-12 cells. (H) Representative western blots and densitometry analysis of iNOS and NOX4 expression in APAP-induced AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, **** P<0.0001. APAP, acetaminophen; H&E, hematoxylin and eosin; IHC, immunohistochemistry; ALT, alanine aminotransferase; AST, aspartate aminotransferase; SREBP-1, sterol regulatory element-binding protein 1; PPAR-α, peroxisome proliferator-activated receptor α; Fasn, fatty acid <t>synthase;</t> iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.
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    Image Search Results


    GA promotes M2 polarization via PRKCD to alleviate SI-ALI. (A) Immunohistochemistry analysis of PRKCD expression. (B) Hematoxylin and eosin staining of lung tissues. (C) Assessment of pulmonary edema by W/D ratio. (D) Immunofluorescence analysis of iNOS and Arg1 expression in lung tissues. (E) ELISA analysis of IL-1β and TNF-α levels in BALF. Data are presented as mean ± SD (n=6 mice per group). For multiple-group comparisons, one-way ANOVA followed by Tukey’s post hoc test was applied. *, P<0.05; ***, P<0.001; ****, P<0.0001. ANOVA, analysis of variance; BALF, bronchoalveolar lavage fluid; DAPI, 4',6-diamidino-2-phenylindole; ELISA, enzyme-linked immunosorbent assay; GA, glycyrrhizic acid; IL-1β, interleukin-1 beta; NC, negative control; PRKCD, protein kinase C delta; SD, standard deviation; SI-ALI, sepsis-induced acute lung injury; TNF-α, tumor necrosis factor-alpha; W/D, wet-to-dry weight.

    Journal: Journal of Thoracic Disease

    Article Title: Glycyrrhizic acid attenuates sepsis-induced acute lung injury by regulating macrophage M2 polarization via PRKCD

    doi: 10.21037/jtd-2026-1327

    Figure Lengend Snippet: GA promotes M2 polarization via PRKCD to alleviate SI-ALI. (A) Immunohistochemistry analysis of PRKCD expression. (B) Hematoxylin and eosin staining of lung tissues. (C) Assessment of pulmonary edema by W/D ratio. (D) Immunofluorescence analysis of iNOS and Arg1 expression in lung tissues. (E) ELISA analysis of IL-1β and TNF-α levels in BALF. Data are presented as mean ± SD (n=6 mice per group). For multiple-group comparisons, one-way ANOVA followed by Tukey’s post hoc test was applied. *, P<0.05; ***, P<0.001; ****, P<0.0001. ANOVA, analysis of variance; BALF, bronchoalveolar lavage fluid; DAPI, 4',6-diamidino-2-phenylindole; ELISA, enzyme-linked immunosorbent assay; GA, glycyrrhizic acid; IL-1β, interleukin-1 beta; NC, negative control; PRKCD, protein kinase C delta; SD, standard deviation; SI-ALI, sepsis-induced acute lung injury; TNF-α, tumor necrosis factor-alpha; W/D, wet-to-dry weight.

    Article Snippet: Samples were incubated overnight at 4 °C with primary antibodies: inducible nitric oxide synthase (iNOS, A14031, ABclonal, Wuhan, China) and arginase 1 (Arg1, A1847, ABclonal).

    Techniques: Immunohistochemistry, Analysis, Expressing, H&E Stain, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Negative Control, Standard Deviation

    Establishment of the APAP-induced liver injury in mice and cell models. (A) Paraffin-embedded liver sections underwent H&E staining as well as TNF-α, IL-6 and IL-1β immunostaining; scale bars, 100 μ m. (B) Serum ALT and AST levels were measured in APAP-induced mice (n=6). (C) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from APAP-induced mouse liver tissues. (D) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in liver extracts prepared from APAP-induced mouse liver tissues. (E) Representative western blots and densitometry analysis of iNOS and NOX4 expression in liver extracts prepared from APAP-induced mouse liver tissues. (F) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in APAP-induced AML-12 cells. (G) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in APAP-induced AML-12 cells. (H) Representative western blots and densitometry analysis of iNOS and NOX4 expression in APAP-induced AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, **** P<0.0001. APAP, acetaminophen; H&E, hematoxylin and eosin; IHC, immunohistochemistry; ALT, alanine aminotransferase; AST, aspartate aminotransferase; SREBP-1, sterol regulatory element-binding protein 1; PPAR-α, peroxisome proliferator-activated receptor α; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Journal: International Journal of Molecular Medicine

    Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

    doi: 10.3892/ijmm.2026.5855

    Figure Lengend Snippet: Establishment of the APAP-induced liver injury in mice and cell models. (A) Paraffin-embedded liver sections underwent H&E staining as well as TNF-α, IL-6 and IL-1β immunostaining; scale bars, 100 μ m. (B) Serum ALT and AST levels were measured in APAP-induced mice (n=6). (C) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from APAP-induced mouse liver tissues. (D) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in liver extracts prepared from APAP-induced mouse liver tissues. (E) Representative western blots and densitometry analysis of iNOS and NOX4 expression in liver extracts prepared from APAP-induced mouse liver tissues. (F) Representative western blots and densitometry analysis of TNF-α, IL-6 and IL-1β expression in APAP-induced AML-12 cells. (G) Representative western blots and densitometry analysis of SREBP-1, PPAR-α and Fasn expression in APAP-induced AML-12 cells. (H) Representative western blots and densitometry analysis of iNOS and NOX4 expression in APAP-induced AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, **** P<0.0001. APAP, acetaminophen; H&E, hematoxylin and eosin; IHC, immunohistochemistry; ALT, alanine aminotransferase; AST, aspartate aminotransferase; SREBP-1, sterol regulatory element-binding protein 1; PPAR-α, peroxisome proliferator-activated receptor α; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Article Snippet: The anti-p38γ (cat. no. 20184-1-AP), anti-IL-6 (cat. no. 21865-1-AP), anti-IL-1β (cat. no. 16806-1-AP), anti-albumin (cat. no. 16475-1-AP), Akt (cat. no. 10176-2-AP), anti-phosphorylated (p-)Akt (cat. no. 66444-1-Ig), anti-TNF-α (cat. no. 17590-1-AP), anti-peroxisome proliferator-activated receptor (PPAR)-α (cat. no. 66826-1-Ig), anti-sterol regulatory element-binding protein (SREBP)-1 (cat. no. 14088-1-AP) and anti-Fasn (cat. no. 10624-2-AP) antibodies were purchased from Proteintech Group, Inc. Anti-NADPH oxidase 4 (NOX4) (cat. no. A11274) and anti-inducible nitric oxide synthase (iNOS) (cat. no. A14031) were purchased from ABclonal Biotech Co., Ltd. Anti-β-actin (cat. no. AF7018), anti-PI3K (cat. no. AF3241) and anti-p-PI3K (cat. no. AF6241) were purchased from Affinity Biosciences, Ltd. ELISA kits for IL-1β (cat. no. MLB00C-1), IL-6 (cat. no. M6000B-1) and TNF-α (cat. no. MTA00B-1) were purchased R&D Systems, Inc.

    Techniques: Staining, Immunostaining, Western Blot, Expressing, Immunohistochemistry, Binding Assay

    p38γ knockdown inhibits oxidative stress and lipid accumulation in APAP-induced AML-12 cells. Intracellular (A) MDA, (B) GSH and (C) SOD activities were assayed in AML-12 cells transfected with p38γ siRNA and pEGFP-C1-p38γ according to the manufacturer's instructions (n=3). (D) Representative images of Oil red O staining of AML12 cells transfected with p38γ siRNA and pEGFP-C1-p38γ; scale bar, 100 μ m. (E) Reactive oxygen species production was detected by DCF, DHE and MitoSOX assay after overexpression and knockdown of p38γ. Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells following p38γ (F) knockdown and (G) overexpression. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; siRNA, small interfering RNA; NC, negative control; DCF, 2',7'-dichlorofluorescein; DHE, dihydroethidium; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Journal: International Journal of Molecular Medicine

    Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

    doi: 10.3892/ijmm.2026.5855

    Figure Lengend Snippet: p38γ knockdown inhibits oxidative stress and lipid accumulation in APAP-induced AML-12 cells. Intracellular (A) MDA, (B) GSH and (C) SOD activities were assayed in AML-12 cells transfected with p38γ siRNA and pEGFP-C1-p38γ according to the manufacturer's instructions (n=3). (D) Representative images of Oil red O staining of AML12 cells transfected with p38γ siRNA and pEGFP-C1-p38γ; scale bar, 100 μ m. (E) Reactive oxygen species production was detected by DCF, DHE and MitoSOX assay after overexpression and knockdown of p38γ. Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells following p38γ (F) knockdown and (G) overexpression. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; siRNA, small interfering RNA; NC, negative control; DCF, 2',7'-dichlorofluorescein; DHE, dihydroethidium; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Article Snippet: The anti-p38γ (cat. no. 20184-1-AP), anti-IL-6 (cat. no. 21865-1-AP), anti-IL-1β (cat. no. 16806-1-AP), anti-albumin (cat. no. 16475-1-AP), Akt (cat. no. 10176-2-AP), anti-phosphorylated (p-)Akt (cat. no. 66444-1-Ig), anti-TNF-α (cat. no. 17590-1-AP), anti-peroxisome proliferator-activated receptor (PPAR)-α (cat. no. 66826-1-Ig), anti-sterol regulatory element-binding protein (SREBP)-1 (cat. no. 14088-1-AP) and anti-Fasn (cat. no. 10624-2-AP) antibodies were purchased from Proteintech Group, Inc. Anti-NADPH oxidase 4 (NOX4) (cat. no. A11274) and anti-inducible nitric oxide synthase (iNOS) (cat. no. A14031) were purchased from ABclonal Biotech Co., Ltd. Anti-β-actin (cat. no. AF7018), anti-PI3K (cat. no. AF3241) and anti-p-PI3K (cat. no. AF6241) were purchased from Affinity Biosciences, Ltd. ELISA kits for IL-1β (cat. no. MLB00C-1), IL-6 (cat. no. M6000B-1) and TNF-α (cat. no. MTA00B-1) were purchased R&D Systems, Inc.

    Techniques: Knockdown, Transfection, Staining, Mitosox Assay, Over Expression, Western Blot, Expressing, Small Interfering RNA, Negative Control, Binding Assay

    p38γ is a direct target of miR-125. (A) TargetScan was used to predict that p38γ possesses binding sites for miR-125. (B) A luciferase reporter assay was performed to detect luciferase activity in the mimics NC + MUT p38γ, miR-125 mimics + MUT p38γ, mimics NC + WT p38γ and miR-125 mimics + WT p38γ groups. (C) The mRNA levels of p38γ in cells were determined by RT-qPCR. (D) Western blot analysis of p38γ expression in AML-12 cells treated with miR-125 inhibitor or miR-125 mimics. (E) Western blot analysis of iNOS, NOX4, TNF-α, IL-6 and IL-1β expression in AML-12 cells. (F) The miR-125 expression was determined by RT-qPCR in liver injury tissues and primary hepatocytes. (G) miR-125 expression were determined by RT-qPCR in AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. ns, not significant; miR-125, microRNA-125; NC, negative control; MUT, mutant; WT, wild type; RT-qPCR, reverse transcription quantitative PCR; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4; UTR, untranslated region; APAP, acetaminophen.

    Journal: International Journal of Molecular Medicine

    Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

    doi: 10.3892/ijmm.2026.5855

    Figure Lengend Snippet: p38γ is a direct target of miR-125. (A) TargetScan was used to predict that p38γ possesses binding sites for miR-125. (B) A luciferase reporter assay was performed to detect luciferase activity in the mimics NC + MUT p38γ, miR-125 mimics + MUT p38γ, mimics NC + WT p38γ and miR-125 mimics + WT p38γ groups. (C) The mRNA levels of p38γ in cells were determined by RT-qPCR. (D) Western blot analysis of p38γ expression in AML-12 cells treated with miR-125 inhibitor or miR-125 mimics. (E) Western blot analysis of iNOS, NOX4, TNF-α, IL-6 and IL-1β expression in AML-12 cells. (F) The miR-125 expression was determined by RT-qPCR in liver injury tissues and primary hepatocytes. (G) miR-125 expression were determined by RT-qPCR in AML-12 cells. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. ns, not significant; miR-125, microRNA-125; NC, negative control; MUT, mutant; WT, wild type; RT-qPCR, reverse transcription quantitative PCR; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4; UTR, untranslated region; APAP, acetaminophen.

    Article Snippet: The anti-p38γ (cat. no. 20184-1-AP), anti-IL-6 (cat. no. 21865-1-AP), anti-IL-1β (cat. no. 16806-1-AP), anti-albumin (cat. no. 16475-1-AP), Akt (cat. no. 10176-2-AP), anti-phosphorylated (p-)Akt (cat. no. 66444-1-Ig), anti-TNF-α (cat. no. 17590-1-AP), anti-peroxisome proliferator-activated receptor (PPAR)-α (cat. no. 66826-1-Ig), anti-sterol regulatory element-binding protein (SREBP)-1 (cat. no. 14088-1-AP) and anti-Fasn (cat. no. 10624-2-AP) antibodies were purchased from Proteintech Group, Inc. Anti-NADPH oxidase 4 (NOX4) (cat. no. A11274) and anti-inducible nitric oxide synthase (iNOS) (cat. no. A14031) were purchased from ABclonal Biotech Co., Ltd. Anti-β-actin (cat. no. AF7018), anti-PI3K (cat. no. AF3241) and anti-p-PI3K (cat. no. AF6241) were purchased from Affinity Biosciences, Ltd. ELISA kits for IL-1β (cat. no. MLB00C-1), IL-6 (cat. no. M6000B-1) and TNF-α (cat. no. MTA00B-1) were purchased R&D Systems, Inc.

    Techniques: Binding Assay, Luciferase, Reporter Assay, Activity Assay, Quantitative RT-PCR, Western Blot, Expressing, Negative Control, Mutagenesis, Reverse Transcription, Real-time Polymerase Chain Reaction

    miR-125 inhibits oxidative stress and lipid accumulation by targeting p38γ. Intracellular levels of (A) MDA and (C) GSH and (B) activity of SOD were assessed in AML-12 cells. (D) Representative images of Oil red O staining of AML12 cells; scale bar, 100 μ m. (E) Reactive oxygen species production was detected using DCF, DHE and MitoSOX assays following overexpression and knockdown of miR-125. Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells treated with (F) miR-125 inhibitor and (G) miR-125 mimics. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; DCF, 2',7'-dichlorofluorescein; DHE, dihydroethidium; PPAR-α, peroxisome proliferator-activated receptor-α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Journal: International Journal of Molecular Medicine

    Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

    doi: 10.3892/ijmm.2026.5855

    Figure Lengend Snippet: miR-125 inhibits oxidative stress and lipid accumulation by targeting p38γ. Intracellular levels of (A) MDA and (C) GSH and (B) activity of SOD were assessed in AML-12 cells. (D) Representative images of Oil red O staining of AML12 cells; scale bar, 100 μ m. (E) Reactive oxygen species production was detected using DCF, DHE and MitoSOX assays following overexpression and knockdown of miR-125. Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells treated with (F) miR-125 inhibitor and (G) miR-125 mimics. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; DCF, 2',7'-dichlorofluorescein; DHE, dihydroethidium; PPAR-α, peroxisome proliferator-activated receptor-α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Article Snippet: The anti-p38γ (cat. no. 20184-1-AP), anti-IL-6 (cat. no. 21865-1-AP), anti-IL-1β (cat. no. 16806-1-AP), anti-albumin (cat. no. 16475-1-AP), Akt (cat. no. 10176-2-AP), anti-phosphorylated (p-)Akt (cat. no. 66444-1-Ig), anti-TNF-α (cat. no. 17590-1-AP), anti-peroxisome proliferator-activated receptor (PPAR)-α (cat. no. 66826-1-Ig), anti-sterol regulatory element-binding protein (SREBP)-1 (cat. no. 14088-1-AP) and anti-Fasn (cat. no. 10624-2-AP) antibodies were purchased from Proteintech Group, Inc. Anti-NADPH oxidase 4 (NOX4) (cat. no. A11274) and anti-inducible nitric oxide synthase (iNOS) (cat. no. A14031) were purchased from ABclonal Biotech Co., Ltd. Anti-β-actin (cat. no. AF7018), anti-PI3K (cat. no. AF3241) and anti-p-PI3K (cat. no. AF6241) were purchased from Affinity Biosciences, Ltd. ELISA kits for IL-1β (cat. no. MLB00C-1), IL-6 (cat. no. M6000B-1) and TNF-α (cat. no. MTA00B-1) were purchased R&D Systems, Inc.

    Techniques: Activity Assay, Staining, Over Expression, Knockdown, Western Blot, Negative Control, Small Interfering RNA, Binding Assay

    miR-125 reverses APAP-induced liver injury by targeting p38γ via activation of the PI3K/AKT signaling. (A) Kyoto Encyclopedia of Genes and Genomes enrichment of the potential signaling pathways associated with significantly differentially expressed genes between the control and APAP-treated groups. Western blot analysis of p-PI3K and p-AKT expression in (B) liver injury tissues and (C) AML-12 cells. Western blot analysis of p-PI3K and p-AKT expression in AML-12 cells transfected with (D) p38γ siRNA and (E) pEGFP-C1-p38γ. Western blot analysis of p-PI3K and p-AKT expression in AML-12 cells following (F) overexpression and (G) knockdown of miR-125. (H) Chemical structure of the PI3K/AKT signaling pathway inhibitor, LY294002. (I) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells following p38γ knockdown and treatment with LY294002. (J) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells following p38γ overexpression and treatment with LY294002. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Journal: International Journal of Molecular Medicine

    Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

    doi: 10.3892/ijmm.2026.5855

    Figure Lengend Snippet: miR-125 reverses APAP-induced liver injury by targeting p38γ via activation of the PI3K/AKT signaling. (A) Kyoto Encyclopedia of Genes and Genomes enrichment of the potential signaling pathways associated with significantly differentially expressed genes between the control and APAP-treated groups. Western blot analysis of p-PI3K and p-AKT expression in (B) liver injury tissues and (C) AML-12 cells. Western blot analysis of p-PI3K and p-AKT expression in AML-12 cells transfected with (D) p38γ siRNA and (E) pEGFP-C1-p38γ. Western blot analysis of p-PI3K and p-AKT expression in AML-12 cells following (F) overexpression and (G) knockdown of miR-125. (H) Chemical structure of the PI3K/AKT signaling pathway inhibitor, LY294002. (I) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells following p38γ knockdown and treatment with LY294002. (J) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 activity in AML-12 cells following p38γ overexpression and treatment with LY294002. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; p-, phosphorylated; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Article Snippet: The anti-p38γ (cat. no. 20184-1-AP), anti-IL-6 (cat. no. 21865-1-AP), anti-IL-1β (cat. no. 16806-1-AP), anti-albumin (cat. no. 16475-1-AP), Akt (cat. no. 10176-2-AP), anti-phosphorylated (p-)Akt (cat. no. 66444-1-Ig), anti-TNF-α (cat. no. 17590-1-AP), anti-peroxisome proliferator-activated receptor (PPAR)-α (cat. no. 66826-1-Ig), anti-sterol regulatory element-binding protein (SREBP)-1 (cat. no. 14088-1-AP) and anti-Fasn (cat. no. 10624-2-AP) antibodies were purchased from Proteintech Group, Inc. Anti-NADPH oxidase 4 (NOX4) (cat. no. A11274) and anti-inducible nitric oxide synthase (iNOS) (cat. no. A14031) were purchased from ABclonal Biotech Co., Ltd. Anti-β-actin (cat. no. AF7018), anti-PI3K (cat. no. AF3241) and anti-p-PI3K (cat. no. AF6241) were purchased from Affinity Biosciences, Ltd. ELISA kits for IL-1β (cat. no. MLB00C-1), IL-6 (cat. no. M6000B-1) and TNF-α (cat. no. MTA00B-1) were purchased R&D Systems, Inc.

    Techniques: Activation Assay, Protein-Protein interactions, Control, Western Blot, Expressing, Transfection, Over Expression, Knockdown, Activity Assay, Negative Control, Small Interfering RNA, Binding Assay

    miR-125 reverses APAP-induced liver injury by targeting p38γ via activation of the PI3K/AKT signaling pathway. (A) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells transfected with miR-125 inhibitor and treated with LY294002. (B) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells transfected with miR-125 mimics and then treated with LY294002. Western blot analysis of TNF-α, IL-6 and IL-1β expression in AML-12 cells transfected with (C) p38γ siRNA and (D) pEGFP-C1-p38γ and then treated with LY294002. Western blot analysis of TNF-α, IL-6 and IL-1β expression in AML-12 cells transfected with (E) miR-125 inhibitor or (F) miR-125 mimics and then treated with LY294002. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01. ns, not significant; APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Journal: International Journal of Molecular Medicine

    Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

    doi: 10.3892/ijmm.2026.5855

    Figure Lengend Snippet: miR-125 reverses APAP-induced liver injury by targeting p38γ via activation of the PI3K/AKT signaling pathway. (A) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells transfected with miR-125 inhibitor and treated with LY294002. (B) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in AML-12 cells transfected with miR-125 mimics and then treated with LY294002. Western blot analysis of TNF-α, IL-6 and IL-1β expression in AML-12 cells transfected with (C) p38γ siRNA and (D) pEGFP-C1-p38γ and then treated with LY294002. Western blot analysis of TNF-α, IL-6 and IL-1β expression in AML-12 cells transfected with (E) miR-125 inhibitor or (F) miR-125 mimics and then treated with LY294002. Data are presented as the mean ± SD of at least three repeats and were compared using a one-way ANOVA followed by Bonferroni's correction. * P<0.05, ** P<0.01. ns, not significant; APAP, acetaminophen; miR-125, microRNA-125; NC, negative control; siRNA, small interfering RNA; PPAR-α, peroxisome proliferator-activated receptor α; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Article Snippet: The anti-p38γ (cat. no. 20184-1-AP), anti-IL-6 (cat. no. 21865-1-AP), anti-IL-1β (cat. no. 16806-1-AP), anti-albumin (cat. no. 16475-1-AP), Akt (cat. no. 10176-2-AP), anti-phosphorylated (p-)Akt (cat. no. 66444-1-Ig), anti-TNF-α (cat. no. 17590-1-AP), anti-peroxisome proliferator-activated receptor (PPAR)-α (cat. no. 66826-1-Ig), anti-sterol regulatory element-binding protein (SREBP)-1 (cat. no. 14088-1-AP) and anti-Fasn (cat. no. 10624-2-AP) antibodies were purchased from Proteintech Group, Inc. Anti-NADPH oxidase 4 (NOX4) (cat. no. A11274) and anti-inducible nitric oxide synthase (iNOS) (cat. no. A14031) were purchased from ABclonal Biotech Co., Ltd. Anti-β-actin (cat. no. AF7018), anti-PI3K (cat. no. AF3241) and anti-p-PI3K (cat. no. AF6241) were purchased from Affinity Biosciences, Ltd. ELISA kits for IL-1β (cat. no. MLB00C-1), IL-6 (cat. no. M6000B-1) and TNF-α (cat. no. MTA00B-1) were purchased R&D Systems, Inc.

    Techniques: Activation Assay, Western Blot, Expressing, Transfection, Negative Control, Small Interfering RNA, Binding Assay

    p38γ knockdown attenuates liver injury in APAP-treated mice. (A) Small animal imaging analysis. (B) Fluorescence imaging analysis showed that AAV9-shRNA-p38γ was specifically located in the mouse liver tissues. (C) Immunofluorescence staining of p38γ in APAP-induced mice liver injury tissues; scale bar, 100 μ m. (D) Western blot analysis of p38γ expression in mouse liver tissues. (E) The H&E staining of liver sections; scale bar, 100 and 40 μ m. (F) IHC analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from mice liver tissues. Serum levels of (G) AST and (H) ALT were measured (n=6). Serum levels of (I) GSH, (J) MDA and (K) SOD were measured (n=3). (L) Representative images of Oil red O staining of AML-12 cells; scale bar, 100 and 40 μ m. (M) DCF analysis of reactive oxygen species production; scale bar, 100 and 40 μ m. (N) Western blot analysis of TNF-α, IL-6 and IL-1β expression in mouse liver tissues. (O) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in mouse liver tissues. Data are presented as the mean ± SD of at least three repeats and were compared using a two-tailed unpaired Student's t-test. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; AAV, adeno-associated virus; shRNA, short hairpin RNA; H&E, hematoxylin and eosin; IHC, immunohistochemistry; AST, aspartate aminotransferase; ALT, alanine aminotransferase; GSH, glutathione; MDA, malondialdehyde; SOD, superoxide dismutase; DFH, dihydrofluorescein; DCF, 2',7'-dichlorofluorescein; PPAR-α, peroxisome proliferator-activated receptor alpha; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Journal: International Journal of Molecular Medicine

    Article Title: Hepatic p38γ exacerbates acetaminophen-induced acute liver injury via PI3K/Akt-dependent mechanisms

    doi: 10.3892/ijmm.2026.5855

    Figure Lengend Snippet: p38γ knockdown attenuates liver injury in APAP-treated mice. (A) Small animal imaging analysis. (B) Fluorescence imaging analysis showed that AAV9-shRNA-p38γ was specifically located in the mouse liver tissues. (C) Immunofluorescence staining of p38γ in APAP-induced mice liver injury tissues; scale bar, 100 μ m. (D) Western blot analysis of p38γ expression in mouse liver tissues. (E) The H&E staining of liver sections; scale bar, 100 and 40 μ m. (F) IHC analysis of TNF-α, IL-6 and IL-1β expression in liver extracts prepared from mice liver tissues. Serum levels of (G) AST and (H) ALT were measured (n=6). Serum levels of (I) GSH, (J) MDA and (K) SOD were measured (n=3). (L) Representative images of Oil red O staining of AML-12 cells; scale bar, 100 and 40 μ m. (M) DCF analysis of reactive oxygen species production; scale bar, 100 and 40 μ m. (N) Western blot analysis of TNF-α, IL-6 and IL-1β expression in mouse liver tissues. (O) Western blot analysis of PPAR-α, SREBP-1, Fasn, iNOS and NOX4 expression in mouse liver tissues. Data are presented as the mean ± SD of at least three repeats and were compared using a two-tailed unpaired Student's t-test. * P<0.05, ** P<0.01, *** P<0.001. APAP, acetaminophen; AAV, adeno-associated virus; shRNA, short hairpin RNA; H&E, hematoxylin and eosin; IHC, immunohistochemistry; AST, aspartate aminotransferase; ALT, alanine aminotransferase; GSH, glutathione; MDA, malondialdehyde; SOD, superoxide dismutase; DFH, dihydrofluorescein; DCF, 2',7'-dichlorofluorescein; PPAR-α, peroxisome proliferator-activated receptor alpha; SREBP-1, sterol regulatory element-binding protein 1; Fasn, fatty acid synthase; iNOS, inducible nitric oxide synthase; NOX4, NADPH oxidase 4.

    Article Snippet: The anti-p38γ (cat. no. 20184-1-AP), anti-IL-6 (cat. no. 21865-1-AP), anti-IL-1β (cat. no. 16806-1-AP), anti-albumin (cat. no. 16475-1-AP), Akt (cat. no. 10176-2-AP), anti-phosphorylated (p-)Akt (cat. no. 66444-1-Ig), anti-TNF-α (cat. no. 17590-1-AP), anti-peroxisome proliferator-activated receptor (PPAR)-α (cat. no. 66826-1-Ig), anti-sterol regulatory element-binding protein (SREBP)-1 (cat. no. 14088-1-AP) and anti-Fasn (cat. no. 10624-2-AP) antibodies were purchased from Proteintech Group, Inc. Anti-NADPH oxidase 4 (NOX4) (cat. no. A11274) and anti-inducible nitric oxide synthase (iNOS) (cat. no. A14031) were purchased from ABclonal Biotech Co., Ltd. Anti-β-actin (cat. no. AF7018), anti-PI3K (cat. no. AF3241) and anti-p-PI3K (cat. no. AF6241) were purchased from Affinity Biosciences, Ltd. ELISA kits for IL-1β (cat. no. MLB00C-1), IL-6 (cat. no. M6000B-1) and TNF-α (cat. no. MTA00B-1) were purchased R&D Systems, Inc.

    Techniques: Knockdown, Imaging, Fluorescence, shRNA, Immunofluorescence, Staining, Western Blot, Expressing, Two Tailed Test, Virus, Immunohistochemistry, Binding Assay