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七叶皂苷A通过激活过氧化物酶体增殖物激活受体γ(PPAR-γ)抑制脂多糖(LPS)诱导的急性肾损伤。

Esculentoside A inhibits LPS-induced acute kidney injury by activating PPAR-γ.

作者信息

Chen De-Zhun, Chen Li-Qiong, Lin Meng-Xiang, Gong Yu-Qiang, Ying Bin-Yu, Wei Da-Zhen

机构信息

Department of Anesthesiology, Critical Care, and Pain Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.

Department of Anesthesiology, Critical Care, and Pain Medicine, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.

出版信息

Microb Pathog. 2017 Sep;110:208-213. doi: 10.1016/j.micpath.2017.06.037. Epub 2017 Jun 27.

DOI:10.1016/j.micpath.2017.06.037
PMID:28666844
Abstract

Acute kidney injury (AKI) is a major clinical problem associated with high morbidity and mortality. Esculentoside A (EsA), a kind of saponin isolated from the root of the Chinese herb Phytolaca esculenta, has been reported to have anti-inflammatory effect. In this study, we aimed to investigate the protective effects of EsA on LPS-induced AKI in mice. The protective effects of EsA was evaluated by detecting kidney histological change, blood urea nitrogen (BUN) and creatinine levels, and inflammatory cytokines production. The results showed that EsA significantly attenuated LPS-induced kidney histological change, as well as BUN and creatinine levels. EsA also inhibited LPS-induced TNF-α, IL-1β, and IL-6 production. LPS-induced NF-κB activation was significantly suppressed by treatment of EsA. In addition, EsA up-regulated the expression of PPAR-γ in a dose-dependent manner. In conclusion, EsA protected mice effectively from LPS-induced AKI by PPAR-γ, which subsequently inhibited LPS-induced inflammatory response.

摘要

急性肾损伤(AKI)是一个与高发病率和死亡率相关的主要临床问题。商陆皂苷甲(EsA)是从中药商陆根中分离出的一种皂苷,据报道具有抗炎作用。在本研究中,我们旨在探讨EsA对脂多糖(LPS)诱导的小鼠急性肾损伤的保护作用。通过检测肾脏组织学变化、血尿素氮(BUN)和肌酐水平以及炎性细胞因子的产生来评估EsA的保护作用。结果表明,EsA显著减轻了LPS诱导的肾脏组织学变化以及BUN和肌酐水平。EsA还抑制了LPS诱导的肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的产生。EsA处理显著抑制了LPS诱导的核因子-κB(NF-κB)激活。此外,EsA以剂量依赖性方式上调过氧化物酶体增殖物激活受体-γ(PPAR-γ)的表达。总之,EsA通过PPAR-γ有效保护小鼠免受LPS诱导的急性肾损伤,随后抑制LPS诱导的炎症反应。

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