CAJ | 학술논문

目的：观察非酶糖化与糖尿病视网膜细胞凋亡的关系以及非酶糖化抑制剂氨基胍和具有非酶糖化抑制作用的川芎嗪对糖尿病视网膜病变的治疗作用。方法雄性Wistar大鼠40只，随机平均分为4组，正常对照组、糖尿病组、糖尿病氨基胍（100mg· kg-1· d-1）治疗组、糖尿病川芎嗪（150mg· kg-1· d-1）治疗组，除正常对照组，其余实验组分别腹腔注射链脲佐菌素（60mg/kg）诱发糖尿病。16周后，处死大鼠，分离主动脉，测定组织非酶糖化，观察bcl-2，bax的表达，电镜观察细胞凋亡的形态学变化。结果①治疗16周结束，糖尿病各实验组大鼠体重低于正常对照组（P＜0．01），糖尿病各实验组间体重比较差异无统计学意义（P＞0．05）。②糖尿病各实验组血糖水平高于正常对照组（P＜0．01），氨基胍治疗组与川芎嗪治疗组血糖与治疗前比较，差异无统计学意义（P＞0．05）。③与正常对照组相比，糖尿病组非酶糖化明显升高（P＜0．01），氨基胍治疗组、川芎嗪治疗组较糖尿病组非酶糖化降低（P＜0．01）。④透射电镜下见糖尿病组大鼠视网膜神经节细胞呈典型的凋亡形态学改变，氨基胍治疗组、川芎嗪治疗组大鼠细胞凋亡改变减轻。结论非酶糖化抑制剂氨基胍、川芎嗪抑制非酶糖化、抑制细胞凋亡，延缓糖尿病视网膜病变发展。
목적：관찰비매당화여당뇨병시망막세포조망적관계이급비매당화억제제안기고화구유비매당화억제작용적천궁진대당뇨병시망막병변적치료작용。방법웅성Wistar대서40지，수궤평균분위4조，정상대조조、당뇨병조、당뇨병안기고（100mg· kg-1· d-1）치료조、당뇨병천궁진（150mg· kg-1· d-1）치료조，제정상대조조，기여실험조분별복강주사련뇨좌균소（60mg/kg）유발당뇨병。16주후，처사대서，분리주동맥，측정조직비매당화，관찰bcl-2，bax적표체，전경관찰세포조망적형태학변화。결과①치료16주결속，당뇨병각실험조대서체중저우정상대조조（P＜0．01），당뇨병각실험조간체중비교차이무통계학의의（P＞0．05）。②당뇨병각실험조혈당수평고우정상대조조（P＜0．01），안기고치료조여천궁진치료조혈당여치료전비교，차이무통계학의의（P＞0．05）。③여정상대조조상비，당뇨병조비매당화명현승고（P＜0．01），안기고치료조、천궁진치료조교당뇨병조비매당화강저（P＜0．01）。④투사전경하견당뇨병조대서시망막신경절세포정전형적조망형태학개변，안기고치료조、천궁진치료조대서세포조망개변감경。결론비매당화억제제안기고、천궁진억제비매당화、억제세포조망，연완당뇨병시망막병변발전。
Objective By studying the relationship between nonenzymatic glycation ,apoptosis relative protein bcl-2,bax and dia-betic retinopathy ,to explore the treatment effect of nonenzymatic glycation inhibitors on diabetic retinopathy .Methods Forty male Wistar rats were randomly divided into the following groups:group control rats,group diabetic rats,group diabetic rats treated with amioguanidine (100mg · kg -1· d-1),group diabetic rats treated with ligustrazine(150mg· kg-1· d-1).These rats were induced hyperglycemia by intraperitoneal injection of streptozotocin 60mg/kg.At the end of treatment the rats were sacrificed to measure tissue nonenzymatic glycation ,bcl-2,bax pro-tein expression ,and to observe retina pathology and apoptosis .Results ①Comparing to control group ,the diabetic rat retina tissue nonenzy-matic glycation was apparently higher (P<0.01).②After 16 weeks treatment,nonenzymatic glycation in group treated with amioguanidine and group treated with ligustrazine was more significantly decreased than that of diabetic group (P<0.01).③The retina bcl-2 protein expres-sion in diabetic group were significantly decreased and Bax protein expression were significantly increased .After 16 weeks treatment of ami-oguanidine and ligustrazine ,the bcl-2 protein expression were significantly increased and bax protein expression were decreased .④The retina apoptosis changes of diabetic group were observed in transmission electron microscope ,and those morphology changes were lessen in two treat-ment groups.Conclusion ①By regulating bcl-2 and Bax expression ,nonenzymatic glycation increase the apoptosis to induce diabetic reti-nopathy .②Nonenzymatic glycation inhibitors regulate bax ,bcl-2 expression to inhibit apoptosis ,then to improve diabetic retina structure and function,and to delay the development of diabetic retinopathy .