医学
急性胰腺炎
标记法
内科学
p38丝裂原活化蛋白激酶
MAPK/ERK通路
胰腺炎
激酶
内分泌学
药理学
生物
生物化学
免疫组织化学
作者
Jiacheng Zhang,Fangchao Mei,Liang Zhao,Teng Zuo,Yu-pu Hong,Man Li,Jia Yu,Weixing Wang
标识
DOI:10.1007/s12026-021-09195-3
摘要
The p38 mitogen-activated protein kinase (MAPK) pathway is an important intracellular signalling pathway that leads to increased expression of pro-inflammatory mediators. Our previous studies have shown that the p38 MAPK pathway was changed in the acute renal injury (ARI) in acute pancreatitis in late pregnancy (APIP), whereas the role of p38 MAPK in APIP-induced ARI has been poorly understood. The present study was undertaken to investigate the participation of the p38 MAPK signalling pathway and the protective effect of SB203580, an inhibitor of p38 MAPK in ARI in APIP. Twenty-four late-gestation SD rats were randomly assigned to four groups: the normal group (N), sham-operated group (SO), acute necrotizing pancreatitis (ANP) group, and p38 MAPK inhibitor (SB203580) treatment group (T). The results showed that serum amylase, lipase, urea, and creatinine levels of p38 inhibitor of T groups were markedly lower than the ANP groups. Additionally, the expression of phosphorylated p38 and myeloperoxidase (MPO), tumour necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, nuclear factor kappa-B (NF-κB), caspase-3, and terminal deoxynucleotidyl TUNEL-positive cells was markedly lower in the T group than in the ANP group. Our results suggest that SB203580 can inhibit renal injury by inhibiting the P38 MAPK signalling pathway and blocking the inflammatory responses in APIP.
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