The JAK2/STAT3 signaling pathway is involved in the inflammation induced by lipopolysaccharide in glomerular endothelial cells

Acta Universitatis Medicinalis Anhui 2020 03 v.55 327-332     font:big middle small

Found programs:

Authors:Liu Yan; Zhang Xiaocui; Deng Fang

Keywords:glomerular endothelial cells;JAK2;STAT3;inflammation;lipopolysaccharide

DOI:10.19405/j.cnki.issn1000-1492.2020.03.002

〔Abstract〕 Objective To investigate the potential mechanism of lipopolysaccharide(LPS)′s effect on inflammatory response of mouse glomerular endothelial cells(mGECs). Methods Isolation and culture of mGECs, CCK-8 assay and Western blot were used to determine the optimum concentration of LPS. mGECs were stimulated with LPS and incubated with JAK2 siRNA, STAT3 siRNAin vitro. The mRNA expression and secretion levels of tumor necrosis factor(TNF-α) and interleukin-6(IL-6) were detected by ELISA and qRT-PCR. JAK2 and STAT3 protein expressions and the phosphorylation level were detected respectively by Western blot. Results Compared with the control group, the expressions of JAK2 and STAT3 phosphorylation in mGECs increased in a concentration-dependent manner after LPS stimulation(P<0.05). The secretion of TNF-α, IL-6 in cell culture medium markedly increased(P<0.05). JAK2 siRNA and STAT3 siRNA could significantly inhibit the overexpression of TNF-α and IL-6 induced by LPS(P<0.05). Conclusion The JAK2/STAT3 signaling pathway is involved in the development of LPS-induced mGECs inflammation.