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目的:研究荔枝核有效部位群(含总皂苷、黄酮和鞣质)改善2型糖尿病胰岛素抵抗的作用及机制。方法:建立高脂饮食加链脲佐菌素诱导2型糖尿病大鼠动物模型,随机分为模型组、荔枝核有效部位群高剂量组(1.87 g/kg)、荔枝核有效部位群低剂量组(0.47 g/kg)及盐酸罗格列酮组(3.87×10-3g/kg),另设正常对照组,给药4 w,观察荔枝核有效部位群对实验大鼠糖脂代谢、胰岛素抵抗和胰组织病理改变及超微结构的影响,检测各组大鼠胰组织GRP78、CHOP mRNA表达变化。结果:荔枝核有效部位群高剂量可降低大鼠空腹血糖(FBG)和血清甘油三酯(TG)水平并提高口服糖耐量(P<0.05或P<0.01);荔枝核有效部位群高、低剂量能显著提高胰岛素敏感指数(ISI),降低稳态胰岛素抵抗指数(HOMA-IR)(P<0.05或P<0.01),明显改善大鼠胰腺组织的病理损伤,并促进内质网、线粒体等损伤细胞器的修复;与模型组比较,荔枝核有效部位群高、低剂量组胰腺组织GRP78 mRNA及高剂量组CHOP mRNA表达水平均显著降低(P<0.01)。结论:荔枝核有效部位群具有改善糖脂代谢、提高胰岛素敏感性、改善胰岛素抵抗和治疗2型糖尿病作用,其机制与抑制胰组织内质网应激关键基因GRP78及CHOP的mRNA表达有关。
Objective: To study the effect and mechanism of effective parts of litchi (including total saponin, flavonoid and tannin) in improving insulin resistance in type 2 diabetes mellitus. Methods: Animal models of type 2 diabetic rats induced by high-fat diet and streptozotocin (STZ) were established and randomly divided into model group, high-dose litchi group (1.87 g / kg), low- (0.47 g / kg) and rosiglitazone hydrochloride group (3.87 × 10-3 g / kg). The normal control group was given another 4 weeks. The effective area of litchi nucleus on the metabolism of glucose and lipid, insulin resistance And histopathological changes and ultrastructure of pancreatic tissue, the changes of the expression of GRP78 and CHOP mRNA in the pancreatic tissue of each group were detected. Results: High dose of Litchi chinensis could reduce fasting blood glucose (FBG) and serum triglyceride (TG) levels and increase oral glucose tolerance (P <0.05 or P <0.01) Dose significantly increased insulin sensitivity index (ISI) and decreased homeostasis insulin resistance index (HOMA-IR) (P <0.05 or P <0.01), and significantly improved the pathological injury of rat pancreatic tissue and promoted endoplasmic reticulum, mitochondria, etc. Compared with model group, GRP78 mRNA expression in high and low dose group and CHOP mRNA expression level in high dose group were significantly decreased (P <0.01) compared with model group. CONCLUSION: The effective part of litchi nucleus has the effects of improving glucose and lipid metabolism, improving insulin sensitivity, improving insulin resistance and treating type 2 diabetes mellitus. Its mechanism is related to inhibiting the mRNA expression of GRP78 and CHOP, which are the key genes of endoplasmic reticulum stress in pancreatic tissue.