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Effect of Quamoclit angulata Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice.
Antioxidants ( IF 6.0 ) Pub Date : 2020-05-27 , DOI: 10.3390/antiox9060459
Ji Eun Park 1 , Heaji Lee 1 , Hyunkyung Rho 1 , Seong Min Hong 2 , Sun Yeou Kim 2 , Yunsook Lim 1
Affiliation  

Type 2 diabetes mellitus (T2DM) is caused by abnormalities of controlling blood glucose and insulin homeostasis. Especially, hyperglycemia causes hyper-inflammation through activation of NLRP3 inflammasome, which can lead to cell apoptosis, hypertrophy, and fibrosis. Quamoclit angulata (QA), one of the annual winders, has been shown ameliorative effects on diabetes. The current study investigated whether the QA extract (QAE) attenuated hyperglycemia-induced renal inflammation related to NLRP inflammasome and oxidative stress in high fat diet (HFD)-induced diabetic mice. After T2DM was induced, the mice were treated with QAE (5 or 10 mg/kg/day) by gavage for 12 weeks. The QAE supplementation reduced homeostasis model assessment insulin resistance (HOMA-IR), kidney malfunction, and glomerular hypertrophy in T2DM. Moreover, the QAE treatment significantly attenuated renal NLRP3 inflammasome dependent hyper-inflammation and consequential renal damage caused by oxidative stress, apoptosis, and fibrosis in T2DM. Furthermore, QAE normalized aberrant energy metabolism (downregulation of p-AMPK, sirtuin (SIRT)-1, and PPARγ-coactivator α (PGC-1 α)) in T2DM mice. Taken together, the results suggested that QAE as a natural product has ameliorative effects on renal damage by regulation of oxidative stress and inflammation in T2DM.

中文翻译:

补充Quamoclit Angulata提取物对2型糖尿病小鼠氧化应激和炎症对高血糖诱导的肾脏损害的影响。

2型糖尿病(T2DM)是由控制血糖和胰岛素稳态异常引起的。特别是,高血糖症通过激活NLRP3炎性小体引起高炎症,可导致细胞凋亡,肥大和纤维化。拟南芥(QA)是一年一度的绕线机之一,已显示出对糖尿病的改善作用。目前的研究调查了QA提取物(QAE)是否减轻了高脂饮食(HFD)诱导的糖尿病小鼠中与NLRP炎性体和氧化应激有关的高血糖引起的肾脏炎症。诱导T2DM后,通过强饲法对小鼠进行QAE(5或10 mg / kg /天)治疗12周。QAE补充剂可降低T2DM的稳态模型评估胰岛素抵抗(HOMA-IR),肾功能不全和肾小球肥大。此外,QAE治疗显着减轻了肾脏NLRP3炎性小体依赖性过度炎症以及由T2DM中的氧化应激,细胞凋亡和纤维化引起的肾脏损害。此外,QAE使异常的能量代谢正常化(p-AMPK,sirtuin(SIRT)-1,T2DM小鼠体内的PPARγ和共激活因子α(PGC-1α))。两者合计,结果表明,作为天然产物的QAE通过调节T2DM中的氧化应激和炎症对肾脏损害具有改善作用。
更新日期:2020-05-27
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