Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, 608 002, Tamilnadu, India.
Department of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, 608 002, Tamilnadu, India.
Chem Biol Interact. 2016 Feb 5;245:50-8. doi: 10.1016/j.cbi.2015.12.019. Epub 2015 Dec 31.
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 β-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-α 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 β-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.
氧化应激和炎症反应与糖尿病及其并发症的发生和发展有关。本研究旨在评估β-石竹烯（BCP）对链脲佐菌素（STZ）诱导的糖尿病大鼠高血糖介导的氧化和炎症应激的影响。实验大鼠通过单次腹腔注射 STZ（40mg/kg b.w.）溶解在 0.1M 柠檬酸盐缓冲液（pH4.5）中诱导糖尿病。糖尿病大鼠表现出血糖升高，血浆胰岛素水平显著降低。糖尿病大鼠胰腺组织中抗氧化酶活性降低，非酶抗氧化剂水平降低，脂质过氧化标志物、蛋白羰基和共轭二烯水平升高。糖尿病大鼠血浆和胰腺组织中促炎细胞因子肿瘤坏死因子-α和白细胞介素-6水平升高。BCP（200mg/kg b.w.）灌胃 45 天可显著降低糖尿病大鼠血糖，升高胰岛素水平。BCP 给药可显著恢复糖尿病大鼠的抗氧化状态，降低促炎细胞因子。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 通过增强胰岛素释放有效挽救了β细胞，从而减轻了高血糖，并且还防止了糖尿病大鼠胰腺组织中的氧化/炎症应激。BCP 的疗效与格列本脲（一种标准的抗糖尿病药物）进行了比较。
