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首页> 外文期刊>Cell & Bioscience >Ginkgetin aglycone ameliorates LPS-induced acute kidney injury by activating SIRT1 via inhibiting the NF-κB signaling pathway
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Ginkgetin aglycone ameliorates LPS-induced acute kidney injury by activating SIRT1 via inhibiting the NF-κB signaling pathway

机译：银杏苷元通过抑制NF-κB信号通路激活SIRT1，减轻LPS诱导的急性肾脏损伤

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Background Ginkgetin aglycone (GA), a novel Ginkgo biloba extract (GBE) by acid hydrolysis and recrystallization, is characterized by higher liposolubility and antioxidation than classical GBEs. There is no study depicting the functional role of GA in acute kidney injury (AKI). Here, we firstly reported the protective effect of GA on lipopolysaccharide (LPS)-induced AKI and its underlying mechanism. Methods ELISA analysis was applied to measure plasma level of TNF-α and IL-6, and NF-κB activity in kidney homogenate. Renal function analysis was performed by detecting serum concentration of Kim-1 and urine level of BUN. Cell apoptosis in kidney tissues was detected by TUNEL assay and caspase-3 activity assay. qRT-PCR was conducted to determine mRNA expression of TNF-α, IL-6 and IκBα. Western blot was carried out to confirm expression of p-IκBα, SIRT1, and iNOS. Results GA administration protected mice from LPS-induced AKI by attenuating inflammatory response, renal injury, as well as tubular apoptosis both in vivo. GA suppressed inflammatory response induced by LPS in HK-2 cells. Moreover, GA upregulated SIRT1 expression and blocked the NF-κB signaling pathway in LPS-induced AKT in vivo and vitro. Furthermore, suppression of SIRT1 abated the inhibitory effect of GA on LPS-induced inflammatory response and renal injury. Conclusions GA prevented LPS-induced AKI by activating SIRT1 via inhibiting the NF-κB signaling pathway, providing new insights into the function and molecular mechanism of GA in AKI. Therefore, GA may be a promising therapeutic agent for the treatment of septic AKI.
机译：背景技术银杏苷元（GA）是一种通过酸水解和重结晶的新型银杏叶提取物（GBE），其脂溶性和抗氧化性高于传统GBE。尚无研究描述GA在急性肾损伤（AKI）中的功能作用。在这里，我们首先报道了GA对脂多糖（LPS）诱导的AKI的保护作用及其潜在机制。方法采用ELISA法测定血浆匀浆中TNF-α和IL-6的水平，以及NF-κB的活性。通过检测血清Kim-1浓度和尿液中BUN水平进行肾功能分析。通过TUNEL法和caspase-3活性法检测肾组织中的细胞凋亡。进行qRT-PCR以确定TNF-α，IL-6和IκBα的mRNA表达。进行Western印迹以确认p-IκBα，SIRT1和iNOS的表达。结果GA给药可通过减弱体内炎症反应，肾损伤以及肾小管凋亡来保护小鼠免受LPS诱导的AKI的侵害。 GA抑制了HK-2细胞中LPS诱导的炎症反应。而且，GA在体内和体外上调了LPS诱导的AKT中SIRT1的表达并阻断了NF-κB信号通路。此外，SIRT1的抑制减弱了GA对LPS诱导的炎症反应和肾损伤的抑制作用。结论GA通过抑制NF-κB信号通路激活SIRT1来预防LPS诱导的AKI，为GA在AKI中的功能和分子机制提供了新的认识。因此，GA可能是治疗脓毒症AKI的有前途的治疗剂。

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