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beta-Caryophyllene, a natural sesquiterpene lactone attenuates hyperglycemia mediated oxidative and inflammatory stress in experimental diabetic rats

机译:β-石竹烯,一种天然的倍半萜烯内酯可减轻实验性糖尿病大鼠中高血糖介导的氧化应激和炎症应激

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Oxidative and inflammatory stress has been implicated in the onset and progression of diabetes mellitus and its complications. The present study was designed to evaluate the effect of beta-Caryophyllene (BCP) on hyperglycemia mediated oxidative and inflammatory stress in streptozotocin (STZ) induced diabetic rats. Diabetes was induced in experimental rats by a single intraperitoneal injection of STZ (40 mg/kg b.w.) dissolved in 0.1 M citrate buffer (pH 4.5). Diabetic rats exhibited increased blood glucose with significant decrease in plasma insulin levels. The activities of antioxidant enzymes and the levels of non-enzymic antioxidants were decreased while increases in the levels of lipidperoxidative markers, protein carbonyls and conjugated dienes were observed in pancreatic tissues of diabetic rats. An elevation of proinflammatory cytokines tumor necrosis factor-alpha and interleukin-6 were observed in plasma and pancreatic tissues of diabetic rats. Intragastric administration of BCP (200 mg/kg b.w) for 45 days significantly decreased glucose and increased insulin levels in diabetic rats. BCP administration significantly restored antioxidant status and decreased proinflammatory cytokines in diabetic rats. These findings were supported by histological and immunohistochemical studies. Thus, we conclude that oral administration of BCP effectively rescued beta-cells by mitigating hyperglycemia through enhancing insulin release and also averted oxidative/inflammatory stress in pancreatic tissue of diabetic rats. The efficacy of BCP was compared with glibenclamide, a standard antidiabetic drug. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
机译:氧化应激和炎性应激与糖尿病及其并发症的发作和发展有关。本研究旨在评估β-石竹烯(BCP)对链脲佐菌素(STZ)诱导的糖尿病大鼠中高血糖介导的氧化应激和炎症应激的影响。通过单次腹膜内注射溶解在0.1 M柠檬酸盐缓冲液(pH 4.5)中的STZ(40 mg / kg b.w.)诱导糖尿病。糖尿病大鼠血糖升高,血浆胰岛素水平明显降低。在糖尿病大鼠的胰腺组织中,抗氧化酶的活性和非酶性抗氧化剂的含量降低,而脂质过氧化标志物,蛋白质羰基和共轭二烯的含量则增加。在糖尿病大鼠的血浆和胰腺组织中观察到促炎细胞因子肿瘤坏死因子-α和白介素-6的升高。胃内给予BCP(200 mg / kg b.w)45天可显着降低糖尿病大鼠的血糖并增加胰岛素水平。 BCP给药可显着恢复糖尿病大鼠的抗氧化状态并减少促炎细胞因子。这些发现得到了组织学和免疫组织化学研究的支持。因此,我们得出结论,口服BCP可以通过增强胰岛素释放来缓解高血糖症,从而有效地拯救β细胞,并且还可以避免糖尿病大鼠胰腺组织中的氧化/炎症应激。将BCP的疗效与标准抗糖尿病药glibenclamide进行了比较。 (C)2016 Elsevier Ireland Ltd.保留所有权利。

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