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目的观察参葛降糖胶囊对2型糖尿病大鼠脂代谢及血清脂肪细胞因子的影响,探讨参葛降糖胶囊治疗糖尿病的作用机制。方法采用灌胃高脂高糖脂肪乳加腹腔注射小剂量链脲佐菌素(STZ),建立胰岛素抵抗糖尿病大鼠模型,将成模大鼠随机分为参葛降糖胶囊低、中、高剂量组,阳性对照组(予消渴灵)及模型组(予生理盐水),分别给予相应的干预,灌胃治疗30d。另设非糖尿病SD大鼠为正常对照组。检测各组大鼠肿瘤坏死因子(TNF)-α、瘦素(leptin)、游离脂肪酸(FFA)、甘油三酯(TG)、总胆固醇(TC)水平。结果与正常对照组比较,模型组的TNF-α、leptin、FFA、TG、TC均明显升高(P均<0.05)。参葛降糖胶囊高、中、低剂量治疗30d后,5项指标水平随药物剂量的增加而下降,除低剂量组外,均低于模型组(P均<0.05),并接近正常对照组水平(P均>0.05)。消渴灵治疗30d的阳性对照组5项指标水平均低于模型组(P均<0.05),TNF-α、leptin接近正常对照组水平(P均>0.05),但FFA、TG、TC尚高于正常对照组(P均<0.05)。结论参葛降糖胶囊可对胰岛素抵抗2型糖尿病大鼠的血脂及脂肪细胞因子水平产生影响,有可能通过调节脂代谢,改善胰岛素抵抗。
Objective To observe the effect of Shenge Jiang Jiangtang Capsule on lipid metabolism and serum adipocytokines in type 2 diabetic rats and explore its mechanism. Methods The model of insulin-resistant diabetic rats was established by intragastric administration of high-fat and high-fat lipopolysaccharide plus intraperitoneal injection of low dose streptozotocin (STZ). The rats were randomly divided into low, medium and high dose Group, positive control group (Xiaokongling) and model group (given normal saline) were given the appropriate intervention, intragastric administration for 30 days. Another non-diabetic SD rats as a normal control group. Tumor necrosis factor (TNF) -alpha, leptin, free fatty acid (FFA), triglyceride (TG) and total cholesterol (TC) were detected in each group. Results Compared with the normal control group, the levels of TNF-α, leptin, FFA, TG and TC in model group were significantly increased (all P <0.05). After 30 days of treatment, the levels of 5 indexes decreased with the increase of the drug dosage, except the low-dose group, all lower than the model group (P <0.05), and close to the normal control group Level (all P> 0.05). The levels of 5 indicators in the positive control group for 30 days of treatment with Xiaokailing were lower than those in the model group (all P <0.05), while the levels of TNF-α and leptin were close to those in the normal control group (all P> 0.05) In normal control group (all P <0.05). Conclusion GGP capsule can affect the level of blood lipids and adipocytokines in type 2 diabetic rats with insulin resistance and may improve insulin resistance by regulating lipid metabolism.