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绿原酸通过抑制 TLR4/NF-κB 信号通路减轻脂多糖诱导的急性肾损伤。

Chlorogenic Acid Attenuates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting TLR4/NF-κB Signal Pathway.

机构信息

Department of Nephrology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.

Department of Endocrinology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.

出版信息

Inflammation. 2017 Apr;40(2):523-529. doi: 10.1007/s10753-016-0498-9.

Abstract

Chlorogenic acid (CGA), a polyphenolic compound, exists widely in medicinal herbs, which has been shown a strong antioxidant and anti-inflammatory effect. This study investigated the protective effects and mechanism of CGA on lipopolysaccharide (LPS)-induced acute kidney injury (AKI). Treatment of CGA successfully ameliorates LPS-induced renal function and pathological damage. Moreover, CGA dose-dependently suppressed LPS-induced blood urea nitrogen (BUN), creatinine levels, and inflammatory cytokines TNF-α, IL-6, and IL-1β in serum and tissue. The relative proteins' expression of TLR4/NF-κB signal pathway was assessed by western blot analysis. Our results showed that CGA dose-dependently attenuated LPS-induced kidney histopathologic changes, serum BUN, and creatinine levels. CGA also suppressed LPS-induced TNF-α, IL-6, and IL-1β production both in serum and kidney tissues. Furthermore, our results showed that CGA significantly inhibited the LPS-induced expression of phosphorylated NF-κB p65 and IκB as well as the expression of TLR4 signal. In conclusion, our results provide a mechanistic explanation for the anti-inflammatory effects of CGA in LPS-induced AKI mice through inhibiting TLR4/NF-κB signaling pathway.

摘要

绿原酸(CGA)是一种多酚化合物,广泛存在于草药中,具有很强的抗氧化和抗炎作用。本研究探讨了 CGA 对脂多糖(LPS)诱导的急性肾损伤(AKI)的保护作用及其机制。CGA 治疗成功改善了 LPS 诱导的肾功能和病理损伤。此外,CGA 呈剂量依赖性抑制 LPS 诱导的血清和组织中血尿素氮(BUN)、肌酐水平以及炎症细胞因子 TNF-α、IL-6 和 IL-1β的产生。通过 Western blot 分析评估 TLR4/NF-κB 信号通路的相对蛋白表达。我们的结果表明,CGA 呈剂量依赖性减轻 LPS 诱导的肾脏组织病理变化、血清 BUN 和肌酐水平。CGA 还抑制了 LPS 诱导的 TNF-α、IL-6 和 IL-1β在血清和肾脏组织中的产生。此外,我们的结果表明,CGA 显著抑制了 LPS 诱导的磷酸化 NF-κB p65 和 IκB 以及 TLR4 信号的表达。总之,我们的结果通过抑制 TLR4/NF-κB 信号通路,为 CGA 在 LPS 诱导的 AKI 小鼠中的抗炎作用提供了机制解释。

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