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The Underlying Mechanisms of Curcumin Inhibition of Hyperglycemia and Hyperlipidemia in Rats Fed a High-Fat Diet Combined With STZ Treatment

机译:大鼠高血糖和高脂血症的姜黄素抑制的潜在机制喂养高脂饮食结合STZ治疗

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摘要

Curcumin is the main secondary metabolite of Curcuma longa and other Curcuma spp, and has been reported to have some potential in preventing and treating some physiological disorders. This study investigated the effect of curcumin in inhibiting high-fat diet and streptozotocin (STZ)-induced hyperglycemia and hyperlipidemia in rats. Twenty-six male Sprague-Dawley (SD) rats (170−190 g) were randomly divided into a standard food pellet diet group (Control group), a high-fat diet and streptozotocin group (HF + STZ group), and a high-fat diet combined with curcumin and STZ group (HF + Cur + STZ group). Compared with the HF + STZ group, the HF + Cur + STZ group exhibited significantly reduced fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), alanine aminotransferase (AST), and aspartate transaminase (ALT) levels, as well as liver coefficients. In the livers of these rats, the expression of malondialdehyde (MDA) and Bax was downregulated, whereas that of superoxide dismutase (SOD) and Bcl-2 was upregulated. Moreover, the liver histology of these rats was improved and resembled that of the control rats. These results suggest that curcumin prevents high-fat diet and STZ-induced hyperglycemia and hyperlipidemia, mainly via anti-oxidant and anti-apoptotic mechanisms in the liver.
机译:姜黄素是Curcuma Longa和其他Curcuma SPP的主要次生代谢物,并据报道据报道有可能预防和治疗一些生理疾病。本研究研究了姜黄素在抑制高脂饮食和链脲佐菌素(STZ) - 诱导的大鼠高血糖和高脂血症中的影响。将26只雄性Sprague-Dawley(SD)大鼠(170-190g)随机分为标准食品颗粒饮食组(对照组),高脂饮食和链脲佐菌素组(HF + STZ组)和高脂 - 饮食与姜黄素和STZ组(HF + Cur + STZ组)相结合。与HF + STZ组相比,HF +姜黄素+ STZ组表现出显著降低空腹血糖(FBG),总胆固醇(TC),甘油三酯(TG),低密度脂蛋白胆固醇(LDL-C),高密度脂蛋白胆固醇(HDL-C),丙氨酸氨基转移酶(AST)和天冬氨酸转氨酶(ALT)水平以及肝系数。在这些大鼠的肝脏,丙二醛(MDA)和Bax的表达下调,而超氧化物歧化酶(SOD)和Bcl-2上调的。此外,改善了这些大鼠的肝脏组织学并类似于对照大鼠的组织学。这些结果表明,姜黄素可防止高脂肪饮食和STZ诱导的高血糖和高脂血症,主要是肝脏中的抗氧化剂和抗凋亡机制。

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