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ZH reduces IMQ-induced inflammatory responses and abnormal proliferation in mice. A Representative spleen images and spleen weight quantification. B Immunohistochemical (IHC) staining of Ki67 in skin lesions (left panel) and quantification of its AOD (right panel). C qRT-PCR analysis of Il-22 , Il-1β , Tnf-α , and Ccl20 mRNA expression in lesion skin tissues. D <t>ELISA</t> quantification of IL-22, IL-1β, TNF-α, and CCL20 protein levels in lesion skin tissues. n = 6 (biological replicates). Data are analyzed using one-way ANOVA followed Tukey’s post hoc test. ** P < 0.01 vs. Control group; # P < 0.05; ## P < 0.01 vs. IMQ group
Elisa Kit, supplied by Cusabio, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ZH reduces IMQ-induced inflammatory responses and abnormal proliferation in mice. A Representative spleen images and spleen weight quantification. B Immunohistochemical (IHC) staining of Ki67 in skin lesions (left panel) and quantification of its AOD (right panel). C qRT-PCR analysis of Il-22 , Il-1β , Tnf-α , and Ccl20 mRNA expression in lesion skin tissues. D <t>ELISA</t> quantification of IL-22, IL-1β, TNF-α, and CCL20 protein levels in lesion skin tissues. n = 6 (biological replicates). Data are analyzed using one-way ANOVA followed Tukey’s post hoc test. ** P < 0.01 vs. Control group; # P < 0.05; ## P < 0.01 vs. IMQ group
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lp 1  (DSMZ)
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Relative fitness of mock vs EIF5A knockout (KO) cells in RPMI‐8226, <t>LP‐1,</t> and JeKo‐1 cells. (A) Competition assay in RPMI‐8226 wild‐type (WT) vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 ), qVD (5 μ m ) or TG (1 n m ), N = 3. Data are presented as mean ± SEM. (B) Competition assay in LP‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (1.5 n m ), N = 4. Data are presented as mean ± SD. (C) Competition assay in JeKo‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (2.5 n m ), N = 4. Data are presented as mean ± SD.
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Relative fitness of mock vs EIF5A knockout (KO) cells in RPMI‐8226, <t>LP‐1,</t> and JeKo‐1 cells. (A) Competition assay in RPMI‐8226 wild‐type (WT) vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 ), qVD (5 μ m ) or TG (1 n m ), N = 3. Data are presented as mean ± SEM. (B) Competition assay in LP‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (1.5 n m ), N = 4. Data are presented as mean ± SD. (C) Competition assay in JeKo‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (2.5 n m ), N = 4. Data are presented as mean ± SD.
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Relative fitness of mock vs EIF5A knockout (KO) cells in RPMI‐8226, <t>LP‐1,</t> and JeKo‐1 cells. (A) Competition assay in RPMI‐8226 wild‐type (WT) vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 ), qVD (5 μ m ) or TG (1 n m ), N = 3. Data are presented as mean ± SEM. (B) Competition assay in LP‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (1.5 n m ), N = 4. Data are presented as mean ± SD. (C) Competition assay in JeKo‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (2.5 n m ), N = 4. Data are presented as mean ± SD.
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Relative fitness of mock vs EIF5A knockout (KO) cells in RPMI‐8226, <t>LP‐1,</t> and JeKo‐1 cells. (A) Competition assay in RPMI‐8226 wild‐type (WT) vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 ), qVD (5 μ m ) or TG (1 n m ), N = 3. Data are presented as mean ± SEM. (B) Competition assay in LP‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (1.5 n m ), N = 4. Data are presented as mean ± SD. (C) Competition assay in JeKo‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (2.5 n m ), N = 4. Data are presented as mean ± SD.
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Relative fitness of mock vs EIF5A knockout (KO) cells in RPMI‐8226, <t>LP‐1,</t> and JeKo‐1 cells. (A) Competition assay in RPMI‐8226 wild‐type (WT) vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 ), qVD (5 μ m ) or TG (1 n m ), N = 3. Data are presented as mean ± SEM. (B) Competition assay in LP‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (1.5 n m ), N = 4. Data are presented as mean ± SD. (C) Competition assay in JeKo‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (2.5 n m ), N = 4. Data are presented as mean ± SD.
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Image Search Results


ZH reduces IMQ-induced inflammatory responses and abnormal proliferation in mice. A Representative spleen images and spleen weight quantification. B Immunohistochemical (IHC) staining of Ki67 in skin lesions (left panel) and quantification of its AOD (right panel). C qRT-PCR analysis of Il-22 , Il-1β , Tnf-α , and Ccl20 mRNA expression in lesion skin tissues. D ELISA quantification of IL-22, IL-1β, TNF-α, and CCL20 protein levels in lesion skin tissues. n = 6 (biological replicates). Data are analyzed using one-way ANOVA followed Tukey’s post hoc test. ** P < 0.01 vs. Control group; # P < 0.05; ## P < 0.01 vs. IMQ group

Journal: Archives of Microbiology

Article Title: Zhuhuang Granules alleviate psoriatic inflammation via restoring gut microbiota balance and enhancing intestinal barrier integrity

doi: 10.1007/s00203-026-05231-8

Figure Lengend Snippet: ZH reduces IMQ-induced inflammatory responses and abnormal proliferation in mice. A Representative spleen images and spleen weight quantification. B Immunohistochemical (IHC) staining of Ki67 in skin lesions (left panel) and quantification of its AOD (right panel). C qRT-PCR analysis of Il-22 , Il-1β , Tnf-α , and Ccl20 mRNA expression in lesion skin tissues. D ELISA quantification of IL-22, IL-1β, TNF-α, and CCL20 protein levels in lesion skin tissues. n = 6 (biological replicates). Data are analyzed using one-way ANOVA followed Tukey’s post hoc test. ** P < 0.01 vs. Control group; # P < 0.05; ## P < 0.01 vs. IMQ group

Article Snippet: An ELISA kit (Cat. #CSB-E13066m, Cusabio) was used to quantify serum lipopolysaccharide (LPS) levels.

Techniques: Immunohistochemical staining, Immunohistochemistry, Quantitative RT-PCR, Analysis, Expressing, Enzyme-linked Immunosorbent Assay, Control

Gut microbiota depletion attenuates the therapeutic effects of ZH against IMQ-induced psoriasis-like inflammation. A Schematic diagram of the experimental design for antibiotic-mediated gut microbiota depletion and subsequent establishment of the IMQ-induced psoriasis-like dermatitis model. B Quantification of fecal bacterial abundance by qPCR to assess the efficacy of antibiotic-mediated gut microbiota depletion. C Representative images of dorsal skin lesions in mice from the indicated groups. D PASI scores for scaling, erythema, thickness, and total scores. E Representative images of spleens (left) and quantification of spleen weight (right). F Representative images of H&E-stained dorsal skin sections (left) and quantification of epidermal thickness (right). G Representative immunohistochemical staining of Ki67 in dorsal skin lesions (left) and quantification of Ki67-positive cells (right). H Relative mRNA expression levels of Il-22 , Il-1β , Tnf-α , and Ccl20 in dorsal skin lesions determined by qPCR. I Protein levels of IL-22, TNF-α, IL-1β, and CCL20 in dorsal skin lesions determined by ELISA. For panels B, the Control and ABX groups each contained 12 mice before randomization; for panels C-I, mice were randomly allocated into four groups ( n = 6 per group): IMQ, IMQ + ABX, IMQ + M-ZH, and IMQ + M-ZH + ABX. Data are analyzed using one-way ANOVA followed Tukey’s post hoc test. * P < 0.05, ** P < 0.01 vs. IMQ group; # P < 0.05, ## P < 0.01 vs. IMQ + ABX group; & P < 0.05, && P < 0.01 vs. IMQ + M-ZH group

Journal: Archives of Microbiology

Article Title: Zhuhuang Granules alleviate psoriatic inflammation via restoring gut microbiota balance and enhancing intestinal barrier integrity

doi: 10.1007/s00203-026-05231-8

Figure Lengend Snippet: Gut microbiota depletion attenuates the therapeutic effects of ZH against IMQ-induced psoriasis-like inflammation. A Schematic diagram of the experimental design for antibiotic-mediated gut microbiota depletion and subsequent establishment of the IMQ-induced psoriasis-like dermatitis model. B Quantification of fecal bacterial abundance by qPCR to assess the efficacy of antibiotic-mediated gut microbiota depletion. C Representative images of dorsal skin lesions in mice from the indicated groups. D PASI scores for scaling, erythema, thickness, and total scores. E Representative images of spleens (left) and quantification of spleen weight (right). F Representative images of H&E-stained dorsal skin sections (left) and quantification of epidermal thickness (right). G Representative immunohistochemical staining of Ki67 in dorsal skin lesions (left) and quantification of Ki67-positive cells (right). H Relative mRNA expression levels of Il-22 , Il-1β , Tnf-α , and Ccl20 in dorsal skin lesions determined by qPCR. I Protein levels of IL-22, TNF-α, IL-1β, and CCL20 in dorsal skin lesions determined by ELISA. For panels B, the Control and ABX groups each contained 12 mice before randomization; for panels C-I, mice were randomly allocated into four groups ( n = 6 per group): IMQ, IMQ + ABX, IMQ + M-ZH, and IMQ + M-ZH + ABX. Data are analyzed using one-way ANOVA followed Tukey’s post hoc test. * P < 0.05, ** P < 0.01 vs. IMQ group; # P < 0.05, ## P < 0.01 vs. IMQ + ABX group; & P < 0.05, && P < 0.01 vs. IMQ + M-ZH group

Article Snippet: An ELISA kit (Cat. #CSB-E13066m, Cusabio) was used to quantify serum lipopolysaccharide (LPS) levels.

Techniques: Staining, Immunohistochemical staining, Expressing, Enzyme-linked Immunosorbent Assay, Control

Relative fitness of mock vs EIF5A knockout (KO) cells in RPMI‐8226, LP‐1, and JeKo‐1 cells. (A) Competition assay in RPMI‐8226 wild‐type (WT) vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 ), qVD (5 μ m ) or TG (1 n m ), N = 3. Data are presented as mean ± SEM. (B) Competition assay in LP‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (1.5 n m ), N = 4. Data are presented as mean ± SD. (C) Competition assay in JeKo‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (2.5 n m ), N = 4. Data are presented as mean ± SD.

Journal: Molecular Oncology

Article Title: A role for eIF5A in translational control of stress‐inducible proteins in multiple myeloma cell lines

doi: 10.1002/1878-0261.70328

Figure Lengend Snippet: Relative fitness of mock vs EIF5A knockout (KO) cells in RPMI‐8226, LP‐1, and JeKo‐1 cells. (A) Competition assay in RPMI‐8226 wild‐type (WT) vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 ), qVD (5 μ m ) or TG (1 n m ), N = 3. Data are presented as mean ± SEM. (B) Competition assay in LP‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (1.5 n m ), N = 4. Data are presented as mean ± SD. (C) Competition assay in JeKo‐1 WT vs mock or vs EIF5A KO cells under basal conditions, with doxycycline (3 days, 1 μg·mL −1 n m ) or TG (2.5 n m ), N = 4. Data are presented as mean ± SD.

Article Snippet: RPMI‐8226 cells (RRID:CVCL_0014; obtained from ATCC), LP‐1 (RRID:CVCL_0012; obtained from DSMZ) and JeKo‐1 (RRID:CVCL_1865; obtained from DSMZ) were cultured in IMDM (Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 10% fetal bovine serum and 1% penicillin–streptomycin at 37 °C and 5% CO 2 .

Techniques: Knock-Out, Competitive Binding Assay

Inhibiting eIF5A hypusination and unfolded protein response (UPR) activity. (A) Western blot of eIF5A hypusination in RPMI‐8226 and LP‐1 cells treated with GC7 (6 μ m ), N = 3, one representative experiment is shown. (B) Quantification of A. Data are presented as mean ± SEM. (C) Expression of key UPR proteins upon in RPMI‐8226 and LP‐1 cells treated with GC7 (6 μ m ), N = 2, one representative experiment is shown. (D) Viability of RPMI‐8226 cells treated with TG (6 n m ), GC7 (6 μ m ), and qVD (5 μ m ) for 24 h. Data are presented as mean ± SEM, N = 3. (E) Viability of LP‐1 cells treated with TG (6 n m ), GC7 (6 μ m ), and qVD (5 μ m ) for 48 h. Data are presented as mean ± SEM, N = 3. (F) Western blot of eIF5A hypusination in RPMI8226 mock cells after TG treatment (24 h, 6 n m ), N = 4, one representative experiment is shown. Data are presented as mean ± SEM. (G) Western blot of eIF5A hypusination in RPMI8226 cells treated with BO (24 h, 20 n m ), N = 3, one representative experiment is shown. Data are presented as mean ± SEM. (H) Western blot of eIF5A hypusination in LP‐1 mock cells after TG treatment (24 h, 12 n m ), N = 4, one representative experiment is shown. Data are presented as mean ± SEM. P ‐values were calculated using student's t ‐tests, * P < 0.05, ** P < 0.01. TG, thapsigargin.

Journal: Molecular Oncology

Article Title: A role for eIF5A in translational control of stress‐inducible proteins in multiple myeloma cell lines

doi: 10.1002/1878-0261.70328

Figure Lengend Snippet: Inhibiting eIF5A hypusination and unfolded protein response (UPR) activity. (A) Western blot of eIF5A hypusination in RPMI‐8226 and LP‐1 cells treated with GC7 (6 μ m ), N = 3, one representative experiment is shown. (B) Quantification of A. Data are presented as mean ± SEM. (C) Expression of key UPR proteins upon in RPMI‐8226 and LP‐1 cells treated with GC7 (6 μ m ), N = 2, one representative experiment is shown. (D) Viability of RPMI‐8226 cells treated with TG (6 n m ), GC7 (6 μ m ), and qVD (5 μ m ) for 24 h. Data are presented as mean ± SEM, N = 3. (E) Viability of LP‐1 cells treated with TG (6 n m ), GC7 (6 μ m ), and qVD (5 μ m ) for 48 h. Data are presented as mean ± SEM, N = 3. (F) Western blot of eIF5A hypusination in RPMI8226 mock cells after TG treatment (24 h, 6 n m ), N = 4, one representative experiment is shown. Data are presented as mean ± SEM. (G) Western blot of eIF5A hypusination in RPMI8226 cells treated with BO (24 h, 20 n m ), N = 3, one representative experiment is shown. Data are presented as mean ± SEM. (H) Western blot of eIF5A hypusination in LP‐1 mock cells after TG treatment (24 h, 12 n m ), N = 4, one representative experiment is shown. Data are presented as mean ± SEM. P ‐values were calculated using student's t ‐tests, * P < 0.05, ** P < 0.01. TG, thapsigargin.

Article Snippet: RPMI‐8226 cells (RRID:CVCL_0014; obtained from ATCC), LP‐1 (RRID:CVCL_0012; obtained from DSMZ) and JeKo‐1 (RRID:CVCL_1865; obtained from DSMZ) were cultured in IMDM (Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 10% fetal bovine serum and 1% penicillin–streptomycin at 37 °C and 5% CO 2 .

Techniques: Activity Assay, Western Blot, Expressing