Statins have been reported to suppress CD40 expression and nuclear factor (NF)-κB activation, which are both up-regulated in the intestines following traumatic brain injury (TBI)-induced intestinal injury. In this study, we aimed to investigate the effects of the statin rosuvastatin on post-TBI jejunal injury in rats, focusing on potential mechanisms involving the CD40/NF-κB signaling pathway. The jejunal CD40 expression was determined by western blotting. The DNA-binding activity of NF-κB was assessed by electrophoretic mobility shift assays (EMSAs). The tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels were assessed by enzyme-linked immunosorbent assays (ELISAs). The severity of the jejunal mucosal injury was assessed by hematoxylin and eosin (HE) staining and histopathological evaluation. We found that the post-TBI upregulation of both CD40 expression and NF-κB activity in the jejunal tissues were significantly inhibited by rosuvastatin, while the post-TBI expression of TNF-α and IL-1β was significantly suppressed by rosuvastatin. In addition, rosuvastatin significantly ameliorated TBI-induced effects on the villus height, crypt depth, and villous surface area. Rosuvastatin suppressed TBI-induced intestinal injury in rats, which may be associated with the blockade of the CD40/NF-κB pathway.

中文翻译：

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罗苏伐他汀通过下调创伤性脑损伤后大鼠肠道的CD40途径来减轻肠道损伤。

据报道，他汀类药物可抑制CD40表达和核因子（NF）-κB活化，在颅脑外伤（TBI）引起的肠道损伤后，它们均在肠道中上调。在这项研究中，我们旨在研究他汀类药物瑞舒伐他汀对大鼠TBI空肠损伤的影响，重点研究涉及CD40 /NF-κB信号通路的潜在机制。通过蛋白质印迹法测定空肠CD40表达。NF-κB的DNA结合活性通过电泳迁移率变动分析（EMSA）进行评估。通过酶联免疫吸附测定（ELISA）评估肿瘤坏死因子（TNF）-α和白介素（IL）-1β的水平。空肠黏膜损伤的严重程度通过苏木精和曙红（HE）染色以及组织病理学评估来评估。我们发现，瑞舒伐他汀显着抑制空肠组织中CD40表达和NF-κB活性的TBI后上调，而瑞舒伐他汀显着抑制TNF-α和IL-1β的TBI后表达。此外，瑞舒伐他汀显着改善了TBI诱导的对绒毛高度，隐窝深度和绒毛表面积的影响。瑞舒伐他汀抑制TBI诱导的大鼠肠道损伤，这可能与CD40 /NF-κB通路的阻滞有关。