【摘要】 目的:观察氨基胍甘草酸对D-半乳糖诱导大鼠体内醛糖还原酶活性、糖耐量和蛋白非酶糖基化反应的作用。方法:实验于2005-06/2005-09在暨南大学药学院药理教研室实验室完成。选用6周龄清洁级SD大鼠60只,雌雄各半,取15只为正常对照组,腹腔注射生理盐水,1次/d,持续8周;其余大鼠均采用腹腔注射D-半乳糖150mg/kg,1次/d×8周致病。D-半乳糖处理大鼠2周后,将大鼠按体质量均衡数字表法随机分成模型对照组、氨基胍组和甘草酸组3组,然后继续腹腔注射D-半乳糖处理同时灌胃给予蒸馏水、氨基胍和甘草酸穴浓度均为30g/L雪300mg/kg灌胃,1次/d×6周;实验结束时,观察氨基胍和甘草酸对D-半乳糖诱导大鼠体内醛糖还原酶活性、糖耐量和蛋白非酶糖基化反应的作用。结果:实验动物60只全部进入结果分析,没有有脱失。①与正常对照组比较,D-半乳糖处理大鼠出现糖耐量减退、糖基化产物(包括糖化血红蛋白、果糖胺和晚期糖基化终产物)增高以及红细胞内醛糖还原酶活性增强(P<0.01)。②氨基胍组与模型组比较,2h血糖显著降低,可拮抗D-半乳糖诱导的糖耐量减退(P<0.01);甘草酸对糖耐量减退也有一定的改善作用,但差异未见显著性意义(P>0.05)。③氨基胍和甘草酸,均可抑制D-半乳糖诱导的醛糖还原酶活性增高(P<0.01,0.05);氨基胍能明显降低果糖胺,糖化血红蛋白和晚期糖基化终末产物含量,差异均有非常显著性意义(P<0.01);甘草酸则对果糖胺,糖化血红蛋白和晚期糖基化终末产物含量的影响不大,差异均未见显著性意义(P>0.05)。结论:氨基胍和甘草酸均能抑制D-半乳糖诱导大鼠体内增高的醛糖还原酶活性,氨基胍对D-半乳糖诱致的大鼠糖基化反应具有明显的抑制作用,而甘草酸对大鼠糖基化反应未见抑制作用。更多还原

【Abstract】 AIM:To observe the effects of aminoguanidine (AG) and glycyrrhizic acid (Gly) on the aldose reductase activity,glucose tolerance and protein non-enzymatic glycation in D-galactose (D-gal) induced rats. METHODS: The experiment was conducted in the Laboratory of Pharmacy,Pharmacy College of Jinan University between June and September 2005. Sixty male and female clean SD rats aged 6 months old were selected. Fifteen rats were taken as normal control group,which received intraperitoneal injection of normal saline once a day for 8 continuous weeks,and the rest rats were intraperitoneally injected with D-gal 150 mg/kg,once a day for 8 weeks. 2 weeks after treated with D-gal,rats were randomly divided into 3 groups: model control group,AG group and Gly group. The intraperitoneal injection of D-gal was continued,and gastric perfusion of distilled water,AG and Gly (at the concentration of 30 g/L) were given simultaneously at 300 mg/kg once a day for 6 continuous weeks. At the end of experiment,the effects of AG and Gly on aldose reductase activity,glucose tolerance and protein non-enzymatic glycation in D-gal induced rats were observed. RESULTS: A total of 60 experimental animals were involved in the analysis of results,and no one withdrew from the study.①Compared with the blank control group,the sugar tolerance and products of glycosylation (including glycosylated hemoglobin,fructosamine and end products of terminal glycosylation) as well as aldose reductase activity of akaryocyte in rats induced by D-gal were respectively reduced,enhanced and reinforced (P < 0.01).②Compared with the model group,2-hour blood glucose in the AG group was significantly decreased and the antagonistic D-gal induced glucose tolerance was reduced (P < 0.01). Gly had some amelioration effects on the reduction of glucose tolerance,while the differences were not significant (P < 0.05).③Both AG and Gly could inhibit the increase of aldose reductase activity induced by D-gal (P < 0.01,0.05),and AG could obviously reduce the contents of fructosamine,glycosylated hemoglobin and end products of terminal glycosylation with remarkable differences (P < 0.01),while the effects of Gly on fructosamine,glycosylated hemoglobin and end products of terminal glycosylation were not marked,and the differences were not significant (P > 0.05). CONCLUSION: Both AG and Gly can inhibit the enhanced aldose reductase activity in rats induced by D-gal,and AG has a remarkable inhibition effect on glycosylation in rats induced by D-gal,while the Gly can not inhibit the glycosylation in rats.更多还原