葛根素通过调控炎性因子水平降低营养性肥胖大鼠的体质量

摘要

构建膳食诱导的SD大鼠肥胖模型,将肥胖模型大鼠随机分为3组：肥胖模型组、西布曲明阳性药组、葛根素处理组,另设基础对照组,每组6只,每天灌胃给药,每7d测定体质量。连续给药42d后,各组大鼠禁食24h,乙醚麻醉眼眶取血测血常规、血清胰岛素、血清瘦素、肿瘤坏死因子-α（TNF-α）、脂联素以及血管内皮生长因子（VEGF）水平,以研究葛根素对饮食诱导肥胖大鼠的减肥作用及对与肥胖相关细胞因子的影响。结果显示：给药处理42d,葛根素处理组与营养性肥胖模型大鼠比较,分别降低体质量21%、血糖（Glu）水平16%、低密度胆固醇（LDL-C）20%、血脂（TG）58%;依次降低SD大鼠血清中的TNF-α、VEGF、胰岛素和瘦素细胞因子水平为36%、36%、12%和70%,提高高密度胆固醇（HDL-C）26%以及脂联素水平16%。因此,葛根素具有提高抗炎因子水平、降低炎性因子的水平、改善胰岛素和瘦素抵抗的能力,并可能通过纠正肥胖导致的炎性因子失衡而降低营养性肥胖大鼠的体质量。%The purpose of the present study was to explore the effects of puerarin on weight loss and obesity-related cytokines in rats with diet-induced obesity.Male Sprague-Dawley(SD) rat models of diet-induced obesity were created and randomly divided into three groups: obesity model group,sibutramine positive control group and puerarin treatment group.In addition,a normal control group was set up.Each group consisted of 6 rats and was intragastrically administrated once daily for 42 consecutive days.During the administration period,body weight was measured once a week.Each group was fasted for 24 h after the last administration,and then anaesthetized with diethyl ether for blood sampling from the retro-orbital plexus and routine blood indexes and the levels of glucose(Glu),insulin,leptin,adiponectin,tumor necrosis factor-alpha(TNF-α),vascular endothelial growth factor(VEGF) and triglycerides(TG) in the serum of rats were assayed.After puerarin administration for 42 days,body weight was reduced by 21% when compared with the control group.The levels of Glu,low-density lipoprotein cholesterol(LDL-C),triglycerides(TG),insulin,leptin,VEGF and TNF-α were decreased by 16%,20%,58%,12%,70%,36% and 36%,respectively.The levels of high-density lipoprotein cholesterol(HDL-C) and adiponectin were increased by 26% and 16%,respectively.Therefore,puerarin can inhibit the increase of body weight,reduce the levels of LDL-C,Glu,insulin and leptin,increase the concentrations of HDL-C and adiponectin,elevate the levels of anti-inflammatory cytokines,inhibit inflammatory cytokines,and improve insulin resistance and leptin resistance in obese rats.