CAJ | 학술논문

目的：探讨红杉醇（sequoyitol，Seq）对2型糖尿病大鼠心肌损伤的保护作用。方法：采用高脂高糖饮食加小剂量链脲佐菌素（ STZ，30 mg/kg）腹腔注射诱导2型糖尿病大鼠模型，灌服Seq[12．5、25、50 mg/（kg· d）]。治疗6周后，于末次给药后测定血糖及左心室质量指数、血清乳酸脱氢酶（LDH）、磷酸肌酸激酶（CPK）活性、C-反应蛋白（CRP）水平及心肌一氧化氮（ NO）、丙二醛（ MDA）含量；Masson染色观察大鼠心肌胶原纤维变化；免疫组化检测心肌诱导型一氧化氮合酶（ iNOS）蛋白表达。结果：Seq各剂量组能降低模型大鼠血糖及左心室质量指数，改善心肌纤维化，降低CK、LDH、CRP水平，下调心肌iNOS蛋白表达，降低心肌NO及MDA含量（ P＜0．05或P＜0．01）。结论：Seq可能通过抗氧化机制，下调心肌iNOS表达，进而对糖尿病大鼠心肌损伤产生保护作用。
목적：탐토홍삼순（sequoyitol，Seq）대2형당뇨병대서심기손상적보호작용。방법：채용고지고당음식가소제량련뇨좌균소（ STZ，30 mg/kg）복강주사유도2형당뇨병대서모형，관복Seq[12．5、25、50 mg/（kg· d）]。치료6주후，우말차급약후측정혈당급좌심실질량지수、혈청유산탈경매（LDH）、린산기산격매（CPK）활성、C-반응단백（CRP）수평급심기일양화담（ NO）、병이철（ MDA）함량；Masson염색관찰대서심기효원섬유변화；면역조화검측심기유도형일양화담합매（ iNOS）단백표체。결과：Seq각제량조능강저모형대서혈당급좌심실질량지수，개선심기섬유화，강저CK、LDH、CRP수평，하조심기iNOS단백표체，강저심기NO급MDA함량（ P＜0．05혹P＜0．01）。결론：Seq가능통과항양화궤제，하조심기iNOS표체，진이대당뇨병대서심기손상산생보호작용。
Objective:To investigate the protective effects of sequoyitol on myocardial injury in type 2 diabetic rats.Methods:The animal models of type 2 diabetes were developed by feeding with high fat and high sugar diet as well as intraperitoneal injection of small dose of streptozotocin (STZ,30 mg/kg).After administration of sequoyitol [12.5,25,50 mg/(kg· d)] for 6 weeks,the contents of blood glucose(BG)and left ventricular mass index, serum lactate dehydrogenase ( LDH ) , creatine phosphocreatine kinase(CRK),C-reactive protein(CRP),myocardial ni-tric oxide( NO) and malondialdehyde( MDA) were determined by the final treatment.Masson staining was used to detect the changes of myocardial collagen fibers,and immunohistochemistry to determine the expression of inducible nitric oxide synthase ( iNOS ) protein in the myocardium . Results:Different dosage of sequoyitol was capable of bringing down the BG levels and left ventricular mass index,improving the myocardial fibro-sis,reducing levels of CK,LDH and CRP,down-regulating the content of myocardial iNOS,NO and MDA in model rats(P<0.05 or P<0.01). Conclusion:Sequoyitol appears to be protective effects on the myocardium in type 2 diabetic rats through down-regulating the expression of myocar-dial iNOS protein and potentially lessening the myocardial damage in-duced by oxidative stress.