Effects of puerarin on expressions of leptin receptor mRNA, phosphoryla-ted Janus kinase 2/phosphorylated signal transducers and activators of transcription 3 proteins in the liver of rats with non-alcoholic fatty liver

2008 ◽  
Vol 6 (9) ◽  
pp. 921-927 ◽  
Author(s):  
PY Zheng
Keyword(s):  
Fatty Liver ◽  
Leptin Receptor ◽  
Janus Kinase ◽  
Janus Kinase 2 ◽  
Alcoholic Fatty Liver ◽  
Signal Transducers ◽  
Receptor Mrna ◽  
Transcription 3 ◽  
Signal Transducers And Activators

Cinnamic Acid Reduces Inflammation and Apoptosis in Necrotizing Enterocolitis

2021 ◽  
Vol 20 (1) ◽  
pp. 70-75
Author(s):  
Huajun Ye ◽  
Ting Zou ◽  
Xueqing Jiang ◽  
Xinran Lin ◽  
Weimin Cai
Keyword(s):  
Necrotizing Enterocolitis ◽  
Cinnamic Acid ◽  
B Cell Lymphoma ◽  
Human Colon ◽  
Janus Kinase ◽  
Janus Kinase 2 ◽  
Colon Cells ◽  
Signal Transducers ◽  
Transcription 3 ◽  
Signal Transducers And Activators

Necrotizing enterocolitis is characterized by an inflammatory condition in the intestine that could result in intestinal necrosis and cell death. Cinnamic acid, an unsaturated carboxylic acid, possesses anti-inflammatory capacity. However, the regulatory role of cinnamic acid on necrotizing enterocolitis has not been investigated yet. To this end, human fetal colon cells were incubated with increasing concentrations of lipopolysaccharides to establish a necrotizing enterocolitis cell model. Data from 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis showed that lipopolysaccharides, in a dosage-dependent manner, reduced cell viability of fetal human colon cells. Also, cinnamic acid prevented the cytotoxic effect of lipopolysaccharides on fetal human colon cells and increased the cell viability. Furthermore, cinnamic acid attenuated lipopolysaccharides-induced decrease in interleukin-10 and increase in interleukin-6 and tumor necrosis factor-α caused by lipopolysaccharides. The lipopolysaccharides-induced increase in cell apoptosis in fetal human colon cells was accompanied with upregulated B-cell lymphoma 2 protein-associated X protein and downregulated B-cell lymphoma 2 protein. These changes were reversed by cinnamic acid treatment. Lastly, expression of protein for suppressor of cytokine signaling 3 was reduced, while phosphorylation of Janus kinase 2 and signal transducers and activators of transcription 3 were enhanced in lipopolysaccharides-induced fetal human colon cells. Once again, cinnamic acid reversed the expression of suppressor of cytokine signaling 3, phospho- Janus kinase 2, and phospho-signal transducers and activators of transcription 3 in lipopolysaccharides-induced fetal human colon cells. In conclusion, cinnamic acid exerted antiapoptotic and anti-inflammatory effects and protected enterocytes against necrotizing enterocolitis through regulation of signal transducers and activators of transcription-mediated Janus kinase 2/signal transducers and activators of transcription 3 pathway.

Liraglutide Exerts Potential Anti-inflammatory Effect in Type 1 Diabetes by Inhibiting IFN-γ Production via Suppressing JAK-STAT Pathway

2019 ◽  
Vol 19 (5) ◽  
pp. 656-664
Author(s):  
Yunjuan Zhao ◽  
Yunliang Xie ◽  
Wangen Li
Keyword(s):  
Type 1 Diabetes ◽  
Signaling Pathway ◽  
Interferon Γ ◽  
Janus Kinase ◽  
Janus Kinase 2 ◽  
Signal Transducers ◽  
High Glucose Condition ◽  
Glucose Condition ◽  
Signal Transducers And Activators

Background: Type 1 diabetes is a T cell-mediated autoimmune disease. Interferon γ plays a critical role in the pathogenesis of type 1 diabetes. Signal transducer and activator of transcription transduces type I interferon cytokines in T cells, leading to Th1 cell differentiation and production of interferon γ. Recent studies suggest that liraglutide reduces the plasma concentration of C-reative protein in patients with type 1 diabetes and protects β cell function in the non-obese diabetic mouse. Objective: The study aimed to explore the effect of glucagon-like peptide-1 analogue on interferon γ production and the underlying signaling pathway in vitro. Methods: Jurkat E6-1 cells were intervened with different concentrations of glucose and liraglutide during different time periods. Protein was extracted from Jurkat E6-1 cells. The target proteins (total and activated Janus kinase 2, signal transducers and activators of transcription 4 and interferon γ) were detected by Western blot. Results: Glucose stimulates interferon γ expression and activates Janus kinase 2/signal transducers and activators of transcription 4 signaling pathway in Jurkat E6-1 cells in a concentration and timedependent manner. Under high glucose condition, liraglutide inhibits interferon γ expression and Janus kinase 2/signal transducers and activators of transcription 4 signaling pathway in Jurkat E6-1 cells in a concentration and time-dependent manner. The Janus kinase responsible for liraglutide-inhibited signal transducers and activators of transcription 4 phosphorylation is Janus kinase 2, which is also required for the interferon γ induction. Finally, we demonstrated that under high glucose condition, liraglutide inhibits interferon γ expression via Janus kinase 2/signal transducers and activators of transcription 4 signaling pathway in Jurkat E6-1 cells. Conclusion: Liraglutide inhibits Jurkat E6-1 cells to produce interferon γ via the Janus kinase/signal transducers and activators of transcription signaling pathway under high glucose condition, which implies its potential in the immunoregulatory effect of type 1 diabetes.

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