Angelica polysaccharide alleviates TNF-α-induced MIN6 cell damage a through theup-reegulation

被引：0

作者：

Zhao, Yingying ^{[1
]}

Lin, Chuanqian ^{[1
]}

Zhang, Xueting ^{[1
]}

Yan, Xipeng ^{[1
,2
]}

机构：

[1] Jining 1 Peoples Hosp, Dept Tradit Chinese Med, Jining, Peoples R China

[2] Jining 1 Peoples Hosp, Dept Tradit Chinese Med, 6 Jiankang Rd, Jining 272011, Shandong, Peoples R China

来源：

BIOFACTORS | 2023年 / 49卷 / 01期

关键词：

AP; miR-143; NF-kappa B; p38; MAPK; type 1 diabetes mellitus;

D O I：

暂无

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Diabetes, is the eighth cause of death worldwide, is a kind of metabolicdisease. We planned to study the potentials of the angelica polysaccharide(AP) in MIN6 cell line. Cells were induced with tumor necrosis factor alpha(TNF-alpha)dilution or APsolutions, and transfected with microRNA-143 (miR-143) as wellas the corresponding negative control (NC). Viability was assessed via CCK-8,while the apoptosis rate was tested by the Annexin V-FITC/PI as well as flowcytometer. The insulin, miR-143 and relative proteins and the inducible nitricoxide synthase (iNOS) were individually determined via GSIS assay, qRT-PCR,and western blot. TNF-alpha induced inhibition of viability and secretion of insulin,but promotion of apoptosis and iNOS, as well as NF-kappa B and p38 MAPK cascadeson MIN6 cell line. AP released TNF-alpha-resulted damage by up-regulatingmiR-143. miR-143 inhibitor partly abolished the influence of AP on MIN6cells. AP released TNF-alpha-induced injury by promoting miR-143 throughblocking NF-kappa B and p38 MAPK in the MIN6 cells.

引用

页数：11