Buyang-Huanwu decoction blocks TGF-β/Smad pathway by inhibiting FUT8 expression in IRI mice
首发时间:2024-04-08
Abstract: In order to elucidate the mechanism of Buyang-Huanwu decoction in TGF-β/Smad signaling pathway in AKI-to-CKD mice. We constructed animal model of AKI-to-CKD by renal ischemia-reperfusion injury (IRI). We grouped the mice, assessed renal function on the 30th day after modeling, tested the level of α-SMA and TGF-β/Smad pathways, and detected the changes of Fut8 and VEGF R2 levels and core fucosylation of TGF-βRⅡ. The results show that Buyang-Huanwu decoction also down-regulates the level of Fut8 and core fucosylation of TGF-βRII, up-regulates the level of VEGF R2, inhibits the activation of TGF-β/Smad, and eases the process of IRI. These data indicate that Buyang-Huanwu decoction could inhibit the activation of TGF-β/Smad pathway by inhibiting the Fut8 and then block the pathological process of AKI-to-CKD.
keywords: Buyang-Huanwu decoction AKI-to-CKD TGF-β/Smad Fut8 IRI core fucosylation 注:本文WEN Qingsi和GUAN Qing为共一作
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补阳还五汤抑制缺血再灌注肾损伤小鼠TGF-βSmad及PDGFERK通路活化
摘要:为明确小鼠肾脏AKI-to-CKD动物模型中,补阳还五汤调控TGF-β/Smad信号通路的糖生物学相关机制。通过肾脏缺血再灌注损伤(IRI)构建AKI-to-CKD的小鼠动物模型,分组后进行造模,于造模后第30天取材评估肾功能,测定α-SMA,TGF-β/Smad通路变化;并检测肾组织Fut8和VEGF-R2水平及TGF-βRII的核心岩藻糖基化变化。结果发现,补阳还五汤下调Fut8及TGF-βRII的核心岩藻糖基化,上调VEGF-R2水平保护PTC,抑制TGF-β/Smad通路活化,减缓缺血再灌注肾损伤进程,提示补阳还五汤可通过抑制Fut8进而阻断TGF-β/Smad通路活化,来阻断IRI小鼠AKI-to-CKD的病理过程。
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补阳还五汤抑制缺血再灌注肾损伤小鼠TGF-βSmad及PDGFERK通路活化
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