...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Anti-Fibrotic Effect of Plumbagin on CCl4-Lesioned Rats
【24h】

Anti-Fibrotic Effect of Plumbagin on CCl4-Lesioned Rats

机译：Plumbagin对CCl4损伤大鼠的抗纤维化作用

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background/Aims: Our previous studies have shown that plumbagin effectively inhibits hepatic stellate cell (HSC) proliferation. Thus, plumbagin-mediated anti-fibrotic effects in vivo merit further investigation. Methods: We used rat models to assess the potential benefits of plumbagin against CCl4-induced liver fibrosis. Results: The results showed that plumbagin lowered the serum concentrations of liver functional enzymes (ALT, AST, ALB, TBIL) in CCl4-fibrotic rats while reducing inflammatory cytokine levels (IL-6, TNF-α). As reflected in pathological examinations, rats that were administered plumbagin showed decreased collagen markers (HA, LN, PCIII and CIV) in liver tissues and improved hepatocellular impairments. In addition, plumbagin contributed to down-regulating NF-κB and TLR-4 mRNA in CCl4-lesioned livers. As revealed in the immunohistochemical assay, plumbagin-administered rats showed reduced levels of α-SMA and TNF-α immunoreactive cells in liver tissue. Conclusion: Collectively, these findings offer appealing evidence that plumbagin may serve as an anti-fibrotic medication through inactivating the NF-κB/TLR-4 pathway that is associated with inflammatory reactions, thereby mitigating liver fibrosis.
机译：背景/目的：我们以前的研究表明，李白素有效抑制肝星状细胞（HSC）的增殖。因此，plumbagin介导的体内抗纤维化作用值得进一步研究。方法：我们使用大鼠模型评估了铅肽对CCl 4 诱导的肝纤维化的潜在益处。结果：结果表明，铅皮降低了CCl 4 纤维化大鼠的血清肝功能酶（ALT，AST，ALB，TBIL）的浓度，同时降低了炎症细胞因子（IL-6，TNF-α）的水平。 ）。从病理学检查中可以看出，使用彭巴金定的大鼠肝脏组织中的胶原蛋白标记物（HA，LN，PCIII和CIV）减少，肝细胞损伤得到改善。此外，铅蛋白还可以下调CCl 4 病变肝脏的NF-κB和TLR-4 mRNA。如免疫组织化学测定所揭示的那样，给予铅袋素的大鼠肝组织中的α-SMA和TNF-α免疫反应细胞水平降低。结论：总的来说，这些发现提供了有吸引力的证据，表明plumbagin可以通过灭活与炎症反应相关的NF-κB/ TLR-4途径，从而减轻肝纤维化，从而作为抗纤维化药物。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号