Journal: Antioxidants (Basel, Switzerland)

Article Title: Elamipretide(SS-31) Attenuates Idiopathic Pulmonary Fibrosis by Inhibiting the Nrf2-Dependent NLRP3 Inflammasome in Macrophages.

doi: 10.3390/antiox12122022

Figure Lengend Snippet: Figure 4. SS-31 alleviated NLRP3 inflammasome activation in macrophages. BMDMs were induced with IL-33 (10 ng/mL), LPS (100 ng/mL) plus IL-4 (10 ng/mL), followed with a treatment of saline or SS-31(10 nM) for 24 h, and then cell samples were collected. (A–F) The mRNA level of NLRP3, ASC, and caspase-1 was detected using qRT-PCR. (G,H) BMDMs were induced with IL-33 (10 ng/mL), and the protein level of NLRP3, ASC, and caspase-1 was analyzed using Western blotting quantified using ImageJ software. (I,J) BMDMs were induced with LPS (100 ng/mL) plus IL-4 (10 ng/mL), and the protein level of NLRP3, ASC, and caspase-1 was analyzed using Western blotting and quantified using ImageJ software. Data represent means ± SEM of three independent experiments, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Primary antibodies against α-smooth muscle actin (α-SMA, #19245), NLRP3 (#20836), caspase-1 (#20836), apoptosis-associated speck-like protein containing CARD (ASC, #20836), and Nrf2 (#12721) were purchased from Cell Signaling Technology (Danvers, MA, USA), and β-actin (#21338) was purchased from Signalway Antibody (College Park City, MD, USA).

Techniques: Activation Assay, Saline, Quantitative RT-PCR, Western Blot, Software

Journal: Antioxidants (Basel, Switzerland)

Article Title: Elamipretide(SS-31) Attenuates Idiopathic Pulmonary Fibrosis by Inhibiting the Nrf2-Dependent NLRP3 Inflammasome in Macrophages.

doi: 10.3390/antiox12122022

Figure Lengend Snippet: Figure 5. SS-31 alleviated NLRP3 inflammasome activation in mice. C57BL/6 mice were i.t. chal- lenged with saline or BLM (1.4 U/kg) for 3 and 7 days followed by i.p. injection of SS-31 (5 mg/kg) every other day. (A–C) The mRNA level of NLRP3, ASC, and caspase-1 was detected using qRT-PCR. (D–G) The protein level of NLRP3, ASC, and caspase-1 was analyzed using Western blotting and quantified using ImageJ software. Data represent means ± SEM, N = 6–8 mice for each group, * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: Primary antibodies against α-smooth muscle actin (α-SMA, #19245), NLRP3 (#20836), caspase-1 (#20836), apoptosis-associated speck-like protein containing CARD (ASC, #20836), and Nrf2 (#12721) were purchased from Cell Signaling Technology (Danvers, MA, USA), and β-actin (#21338) was purchased from Signalway Antibody (College Park City, MD, USA).

Techniques: Activation Assay, Saline, Injection, Quantitative RT-PCR, Western Blot, Software

Journal: Antioxidants (Basel, Switzerland)

Article Title: Elamipretide(SS-31) Attenuates Idiopathic Pulmonary Fibrosis by Inhibiting the Nrf2-Dependent NLRP3 Inflammasome in Macrophages.

doi: 10.3390/antiox12122022

Figure Lengend Snippet: Figure 7. SS-31 treatment did not affect NLRP3 inflammasome in Nrf2−/−macrophages. Nrf2−/− BMDMs were induced with IL-33 (10 ng/mL) and LPS (100 ng/mL) plus IL-4 (10 ng/mL), followed by treatment with saline or SS-31 (10 nM) for 24 h, and then cell samples were collected. (A–J) The mRNA level of NLRP3, ASC, caspase-1, IL-18, and IL-1β was detected using qRT-PCR. (K–N) The protein level of NLRP3, ASC, and caspase-1 was analyzed using Western blotting and quantified using ImageJ software. Data represent means ± SEM of three independent experiments, * p < 0.05, ** p < 0.01, *** p < 0.001, ns >= 0.05.

Article Snippet: Primary antibodies against α-smooth muscle actin (α-SMA, #19245), NLRP3 (#20836), caspase-1 (#20836), apoptosis-associated speck-like protein containing CARD (ASC, #20836), and Nrf2 (#12721) were purchased from Cell Signaling Technology (Danvers, MA, USA), and β-actin (#21338) was purchased from Signalway Antibody (College Park City, MD, USA).

Techniques: Saline, Quantitative RT-PCR, Western Blot, Software

Journal: Antioxidants (Basel, Switzerland)

Article Title: Elamipretide(SS-31) Attenuates Idiopathic Pulmonary Fibrosis by Inhibiting the Nrf2-Dependent NLRP3 Inflammasome in Macrophages.

doi: 10.3390/antiox12122022

Figure Lengend Snippet: Figure 8. SS-31 treatment did not affect NLRP3 inflammasome and fibrosis in BLM-induced Nrf2−/− mice. Nrf2−/−mice were i.t. challenged with saline or BLM (1.4 U/kg) for 21 days followed by i.p. injection of SS-31 (5 mg/kg) every other day. (A–E) The mRNA level of NLRP3, ASC, caspase-1, IL-1β, and IL-18 was detected using qRT-PCR. (F,G) Lung tissue sections were performed using H&E staining and Masson trichrome staining (original magnification ×400, the scale bar is 100 µm). (H,I,J) RNA was extracted from lung tissues, and the mRNA levels of α-SMA and fibronectin were detected using RT-qPCR. (K,L) The protein level of α-SMA was analyzed using Western blotting and quantified using ImageJ software. (M) Hydroxyproline was detected in different groups of mice. Data represent means ± SEM, N = 6–8 mice for each group, * p < 0.05, ** p < 0.01, ns >= 0.05.

Article Snippet: Primary antibodies against α-smooth muscle actin (α-SMA, #19245), NLRP3 (#20836), caspase-1 (#20836), apoptosis-associated speck-like protein containing CARD (ASC, #20836), and Nrf2 (#12721) were purchased from Cell Signaling Technology (Danvers, MA, USA), and β-actin (#21338) was purchased from Signalway Antibody (College Park City, MD, USA).

Techniques: Saline, Injection, Quantitative RT-PCR, Staining, Western Blot, Software

Journal: Animals : an Open Access Journal from MDPI

Article Title: Tea Polyphenols Mitigate TBBPA-Induced Renal Injury Through Modulation of ROS-PI3K/AKT-NF-κB Signalling in Carp ( Cyprinus carpio )

doi: 10.3390/ani15152307

Figure Lengend Snippet: Effects of TBBPA exposure and TPs intervention on renal necrosis of carp. ( A ) The mRNA expression of RIPK1 , RIPK3 , and MLKL genes in the kidney. ( B , C ) Expression levels of RIPK1, RIPK3, and MLKL proteins in the kidney. ( D ) AO/EB results. Orange represents apoptotic cells, and red represents necrotic cells. Magnification 10×. ( E ) The mRNA expression of RIPK1 , RIPK3 , and MLKL genes in renal primary cells. ( F , G ) Protein expression levels of RIPK1, RIPK3, and MLKL in primary renal cells. Each group included three independent biological replicates ( n = 3). Data are expressed as mean ± SEM. Analysis was performed using one-way analysis of variance (ANOVA). **, p < 0.01; ****, p < 0.0001.

Article Snippet: RIPK3 , 47928T , Cell Signaling Technology, Inc., Boston, MA, USA , 1:1000.

Techniques: Expressing

Journal: Chinese medicine

Article Title: Shen-Bai-Jie-Du decoction suppresses the progression of colorectal adenoma to carcinoma through regulating gut microbiota and short-chain fatty acids.

doi: 10.1186/s13020-024-01019-4

Figure Lengend Snippet: Fig. 9 The schematic diagram of the mechanism of SBJDD. SBJDD may exert its inhibitory effects on colorectal adenoma carcinogenesis by regulating gut microbiota, promoting the production of SCFAs, activating G protein-coupled receptors GPR43, GPR41 and GPR109a, inhibiting histone deacetylases HDAC1 and HDAC3, inducing M2-like macrophage polarization, reducing intestinal inflammation, inhibiting cancer cell proliferation and restoring intestinal barrier function

Article Snippet: Anti-GAPDH (no. 2118S), anti-β-Tubulin (no. 2146S) and Mouse Reactive M1 vs M2 Macrophage IHC Antibody Sampler Kit (no. 97624 T) were obtained from Cell Signaling Technology (Beverly, USA).

Techniques: