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卡帕鲁塔在 2 型糖尿病相关心血管并发症中改善心肌和主动脉损伤。

Kalpaamruthaa ameliorates myocardial and aortic damage in cardiovascular complications associated with type 2 diabetes mellitus.

机构信息

Department of Medical Biochemistry, Dr. A.L.M. Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, Tamil Nadu, India.

出版信息

Can J Physiol Pharmacol. 2013 Feb;91(2):116-23. doi: 10.1139/cjpp-2012-0292. Epub 2012 Nov 1.

Abstract

Myocardial and aortic damage in cardiovascular complications (CVD) associated with type 2 diabetes mellitus and the protective efficacy of Kalpaamruthaa (KA) are evaluated in this study. CVD developed in 8 weeks after type 2 diabetes mellitus was induced by the administration of a high-fat diet for 2 weeks, and then with streptozotocin (2 × 35 mg·(kg body mass)(-1), by intraperitonal injection, at 24 h intervals) in male Sprague-Dawley rats. CVD-induced rats were treated with KA at 200 mg·(kg body mass)(-1)·(day)(-1) orally for 28 days. Increased oxidative stress in CVD-induced rats lowers antioxidant defense in the aorta. Treatment with KA reduced oxidative stress by increasing antioxidant status with decreased lipid peroxides in CVD-induced rats. Histological examination of the myocardium and aorta provided support for the cytoprotective effect of KA in CVD. Ultrastructural changes in the myocardium of CVD-induced rats were improved by KA treatment. Aortic damage was observed through decreased endothelial nitric oxide synthase and increased NADPH oxidase mRNA expressions in CVD-induced rats. KA reduced the aortic damage by ameliorating these levels back to normal. KA treatment reduced the pro-inflammatory cytokines tumor necrosis factor-α and interleukin 6 in CVD-induced rats. Immunohistochemical expressions of matrix metalloproteinase-2 and -9 were observed to be elevated in the myocardium of CVD-induced rats, but these were decreased by the administration of KA. This study demonstrates the cardiovascular protective effect of KA in type 2 diabetes.

摘要

本研究评估了心血管并发症(CVD)相关 2 型糖尿病患者的心肌和主动脉损伤,以及 Kalpaamruthaa(KA)的保护效果。2 型糖尿病是通过给予高脂肪饮食 2 周,然后在 24 小时间隔内通过腹腔内注射 2 次链脲佐菌素(2×35mg·(kg 体重)(-1))在雄性 Sprague-Dawley 大鼠中诱导的。CVD 诱导的大鼠用 KA(200mg·(kg 体重)(-1)·(天)(-1)口服治疗 28 天。CVD 诱导的大鼠氧化应激增加,降低了主动脉的抗氧化防御能力。KA 治疗通过增加抗氧化状态,降低 CVD 诱导大鼠的脂质过氧化物,减少氧化应激。心肌和主动脉的组织学检查为 KA 在 CVD 中的细胞保护作用提供了支持。KA 治疗改善了 CVD 诱导大鼠心肌的超微结构变化。CVD 诱导大鼠的主动脉损伤通过降低内皮型一氧化氮合酶和增加 NADPH 氧化酶 mRNA 表达得到改善。KA 通过将这些水平恢复正常来减轻主动脉损伤。KA 治疗降低了 CVD 诱导大鼠的促炎细胞因子肿瘤坏死因子-α和白细胞介素 6。观察到 CVD 诱导大鼠心肌中基质金属蛋白酶-2 和 -9 的免疫组织化学表达升高,但通过 KA 给药降低了这些表达。这项研究表明了 KA 在 2 型糖尿病中的心血管保护作用。

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