Journal: BioMed Research International

Article Title: TAK-242 Ameliorates Hepatic Fibrosis by Regulating the Liver-Gut Axis

doi: 10.1155/2022/4949148

Figure Lengend Snippet: TAK-242 alleviated liver inflammation in HF rats. (a) IHC-stained liver sections (magnification ×200). (b) chromogenic intensity of proinflammatory cytokines. (c) RT-qPCR detection of hepatic proinflammatory cytokine expression level. (d, e) Western blot detection of hepatic proinflammatory cytokine protein expression. (f) Serum IL-1 β (ng/mL). (g) Serum IL-6 (ng/mL). (h) Serum TNF- α (ng/mL). n = 8. Compared with the control group, ## P < 0.01; compared with model group, ∗ P < 0.05 and ∗∗ P < 0.01. (f–h) Green, control; red, model; blue, TAK-242.

Article Snippet: At 4°C overnight, primary antibodies TLR4 (Ptgcn, 19811-1-AP), NF- κ B p65 (Ptgcn, 10745-1-AP), MyD88 (Ptgcn, 23230-1-AP), IL-1 β (CST, #12242), IL-6 (CST, #12912), TNF- α (Ptgcn, 60291-1-Ig), and β -actin (Ptgcn, 66009-1-Ig) were mixed with 1 mL of enzyme-labeled secondary antibody.

Techniques: Staining, Quantitative RT-PCR, Expressing, Western Blot

Journal: Drug Design, Development and Therapy

Article Title: Isoliquiritigenin Attenuates UUO-Induced Renal Inflammation and Fibrosis by Inhibiting Mincle/Syk/NF-Kappa B Signaling Pathway

doi: 10.2147/DDDT.S243420

Figure Lengend Snippet: Isoliquiritigenin reduced the inflammatory response induced by LPS in BMDM. ( A – D ) ISL can reduce the mRNA expression of inflammatory cytokines in LPS-induced BMDM, including IL-1β, IL-6, TNF-α and MCP-1. ** P <0.01, vs LPS group. *** P <0.001, vs LPS group. **** P <0.0001, vs LPS group; ( E, F ) ISL reduced the secretion of IL-1β and IL-6 in supernatant of LPS-stimulated BMDM. ** P <0.01, vs LPS group; ( G ) immunofluorescence results showed that ISL inhibited the protein level of IL-1β and IL-6 in LPS-stimulated BMDM.

Article Snippet: Subsequently, the cells were treated with 0.5% Triton X-100 for 10 min at room temperature to increase the permeation of cell membrane, followed by blocking with 5% BSA for 30 min and then incubated with mouse anti- IL-1β antibody (1:200, Santa Cruz) or mouse anti-IL-6 antibody (ab9324, 1:150, CST) overnight at 4 °C.

Techniques: Expressing, Immunofluorescence

Journal: Drug Design, Development and Therapy

Article Title: Isoliquiritigenin Attenuates UUO-Induced Renal Inflammation and Fibrosis by Inhibiting Mincle/Syk/NF-Kappa B Signaling Pathway

doi: 10.2147/DDDT.S243420

Figure Lengend Snippet: Isoliquiritigenin protects the kidney by inhibiting Mincle/Syk/NF-kappa B signaling pathway and reducing the expression and secretion of inflammatory cytokines in the kidney and blood of UUO model. ( A ) Immunohistochemistry results showed that the infiltration of macrophage was significantly increased in the kidney of UUO model and ISL reduced infiltrated macrophage; ( B – F ) immunofluorescence and Western blot results showed that ISL can effectively reduce the protein level of Mincle and iNOS as well as phosphorylated Syk and NF-kappa B in the kidney of UUO model; ( G – J ) ISL strongly reduced the mRNA expression of IL-1β, IL-6, TNF-α and MCP-1 in the kidney of UUO model; ( K, L ) ISL also inhibited the secretion of IL-1β and IL-6 in the serum of UUO mice. Notes: * P <0.05, vs UUO group. ** P <0.01, vs UUO group. *** P <0.001 vs UUO group.

Article Snippet: Subsequently, the cells were treated with 0.5% Triton X-100 for 10 min at room temperature to increase the permeation of cell membrane, followed by blocking with 5% BSA for 30 min and then incubated with mouse anti- IL-1β antibody (1:200, Santa Cruz) or mouse anti-IL-6 antibody (ab9324, 1:150, CST) overnight at 4 °C.

Techniques: Expressing, Immunohistochemistry, Immunofluorescence, Western Blot

Journal: Drug Design, Development and Therapy

Article Title: Isoliquiritigenin Attenuates UUO-Induced Renal Inflammation and Fibrosis by Inhibiting Mincle/Syk/NF-Kappa B Signaling Pathway

doi: 10.2147/DDDT.S243420

Figure Lengend Snippet: Isoliquiritigenin suppressed inflammation through Mincle-dependent mechanism in BMDM cells. ( A ) In the Mincle recovery experiment, we used TDB to upregulate Mincle in ISL-treated inflammatory BMDM. The results showed that the protein level of Mincle ( B ), iNOS ( C ), phosphorylated Syk ( D ) and phosphorylated NF-kappa B ( E ) were significantly increased in ISL-treated inflammatory BMDM, suggesting ISL inhibits inflammation by suppressing Mincle; Overexpression of Mincle by administration of TDB, upregulated the expression ( F–I ) and secretion ( J–L ) of IL-1β, IL-6 and TNF-α and MCP-1 in ISL-treated inflammatory BMDM. Notes: * P <0.05, vs LPS group. ** P <0.01, vs LPS group. *** P <0.001, vs LPS group. # P <0.05, vs LPS+ISL 40μM-treated group. ## P <0.01, vs LPS+ISL 40μM-treated group. ### P <0.001, vs LPS+ISL 40μM-treated group.

Article Snippet: Subsequently, the cells were treated with 0.5% Triton X-100 for 10 min at room temperature to increase the permeation of cell membrane, followed by blocking with 5% BSA for 30 min and then incubated with mouse anti- IL-1β antibody (1:200, Santa Cruz) or mouse anti-IL-6 antibody (ab9324, 1:150, CST) overnight at 4 °C.

Techniques: Over Expression, Expressing