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.

p38 丝裂原活化蛋白激酶 (MAPK) 通路是一种重要的细胞内信号通路，可导致促炎介质的表达增加。我们之前的研究表明，p38 MAPK 通路在妊娠晚期急性胰腺炎 (APIP) 的急性肾损伤 (ARI) 中发生了变化，而 p38 MAPK 在 APIP 诱导的 ARI 中的作用却知之甚少。本研究旨在调查 p38 MAPK 信号通路的参与以及 SB203580（一种 p38 MAPK 在 APIP 中的 ARI 抑制剂）的保护作用。24只妊娠晚期SD大鼠随机分为4组：正常组（N）、假手术组（SO）、急性坏死性胰腺炎（ANP）组和p38 MAPK抑制剂（SB203580）治疗组（T） . 结果表明，血清淀粉酶、脂肪酶、尿素、T组的p38抑制剂和肌酐水平明显低于ANP组。此外，磷酸化 p38 和髓过氧化物酶 (MPO)、肿瘤坏死因子 α (TNF-α)、白细胞介素 (IL)-1β、IL-6、核因子 kappa-B (NF-κB)、caspase-3 和T组的末端脱氧核苷酸TUNEL阳性细胞明显低于ANP组。我们的研究结果表明，SB203580 可以通过抑制 P38 MAPK 信号通路和阻断 APIP 中的炎症反应来抑制肾损伤。T组的末端脱氧核苷酸TUNEL阳性细胞明显低于ANP组。我们的研究结果表明，SB203580 可以通过抑制 P38 MAPK 信号通路和阻断 APIP 中的炎症反应来抑制肾损伤。T组的末端脱氧核苷酸TUNEL阳性细胞明显低于ANP组。我们的研究结果表明，SB203580 可以通过抑制 P38 MAPK 信号通路和阻断 APIP 中的炎症反应来抑制肾损伤。