CAJ | 학술논문

目的：观察黄连解毒汤对2型糖尿病大鼠空腹血糖(FBG)、空腹胰岛素(FINS)及腹主动脉血管内皮形态、缺氧诱导因子-1α(HIF-1α)表达的影响,并探讨其作用机制。方法采用小剂量链脲佐菌素腹腔注射联合高糖高脂饲料喂养Wistar大鼠,建立2型糖尿病模型。随机将大鼠分为空白组、模型组、对照组和治疗组。空白组、模型组灌服生理盐水,对照组灌胃二甲双胍,治疗组灌胃黄连解毒汤。6周后检测FBG、FINS,采用免疫组织化学法测定腹主动脉HIF-1α表达,HE染色法观察腹主动脉血管内皮形态变化。结果与模型组、对照组比较,治疗组腹主动脉HIF-1α表达、FBG均明显降低(P＜0.01),FINS明显升高(P＜0.01),腹主动脉血管内皮细胞的损伤得到明显改善。结论黄连解毒汤对损伤的血管内皮细胞有保护作用,其机制可能是通过抑制HIF-1α表达实现的。
목적：관찰황련해독탕대2형당뇨병대서공복혈당(FBG)、공복이도소(FINS)급복주동맥혈관내피형태、결양유도인자-1α(HIF-1α)표체적영향,병탐토기작용궤제。방법채용소제량련뇨좌균소복강주사연합고당고지사료위양Wistar대서,건립2형당뇨병모형。수궤장대서분위공백조、모형조、대조조화치료조。공백조、모형조관복생리염수,대조조관위이갑쌍고,치료조관위황련해독탕。6주후검측FBG、FINS,채용면역조직화학법측정복주동맥HIF-1α표체,HE염색법관찰복주동맥혈관내피형태변화。결과여모형조、대조조비교,치료조복주동맥HIF-1α표체、FBG균명현강저(P＜0.01),FINS명현승고(P＜0.01),복주동맥혈관내피세포적손상득도명현개선。결론황련해독탕대손상적혈관내피세포유보호작용,기궤제가능시통과억제HIF-1α표체실현적。
Objective To observe effects of Huanglian Jiedu Decoction on fasting blood glucose (FBG), fasting insulin (FINS), abdominal aortic morphology and expression of HIF-1α in the abdominal aorta in rats with type 2 diabetes. Methods The rat model of type 2 diabetes was established by intravenous injection of streptozotocin and feeding with high sugar and high fat diet. Rats were randomly divided into blank group, model group, control group and treatment group. The blank group and model group were given normal saline by gavage, the control group was given metformin, and the treatment group was given Huanglian Jiedu Decoction. Six weeks later, the levels of FBG and FINS were determined. Immunohistochemical method was used to determine the expression of HIF-1α in abdominal aorta and HE staining method to observe the changes of abdominal aortic morphology. Results Compared with model group and control group, abdominal aorta of HIF-1α and FBG level of treatment group were significantly decreased (P <0.01), FINS significantly increased (P <0.01), and abdominal aortic endothelial cell injury was significantly improved. Conclusion Huanglian Jiedu Decoction has a protective effect on the injury of vascular endothelium, and its mechanism may be related with inhibiting the expression of HIF-1α.