中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2014年
6期
1023-1028
,共6页
Goto-Kakizaki大鼠%糖尿病, 2型%梓醇%氧化性应激
Goto-Kakizaki大鼠%糖尿病, 2型%梓醇%氧化性應激
Goto-Kakizaki대서%당뇨병, 2형%재순%양화성응격
Goto-Kakizaki rats%Diabetes mellitus,type 2%Catalpol%Oxidative stress
目的：研究梓醇对Goto-Kakizaki（ GK）大鼠主动脉的保护作用并探讨其抗氧化机制。方法：6月龄GK大鼠45只随机分为糖尿病模型组、二甲双胍（100 mg · kg-1· d-1）组以及梓醇高剂量（100 mg · kg -1· d-1）组、中剂量（50 mg· kg-1· d-1）组、低剂量（10 mg· kg-1· d-1）组，10只雄性Wistar大鼠作为对照组。各组灌胃给药12周，对照组和模型组给予等量的生理盐水。检测大鼠空腹血糖（ FBG）和血脂；检测血清活性氧（ ROS）、丙二醛（ MDA）、超氧化物歧化酶（ SOD）和总抗氧化力（ T-AOC）水平；Western blotting检测胸主动脉组织核因子E2相关因子2（Nrf2）和血红素加氧酶1（HO-1）表达；HE染色观察胸主动脉病理变化；透射电镜观察胸主动脉组织超微结构变化。结果：梓醇治疗后，血糖和血脂显著下降；血清ROS和MDA水平明显降低，SOD活性和T-AOC显著增强；胸主动脉组织Nrf2和HO-1蛋白表达明显增强；HE染色显示胸主动脉病变程度明显减轻，透射电镜观察胸主动脉超微结构损伤明显减轻。结论：梓醇能够有效保护GK大鼠胸主动脉，其机制可能与降低血糖和血脂，减轻氧化应激反应，激活Nrf2／ARE／HO-1信号通路有关。
目的：研究梓醇對Goto-Kakizaki（ GK）大鼠主動脈的保護作用併探討其抗氧化機製。方法：6月齡GK大鼠45隻隨機分為糖尿病模型組、二甲雙胍（100 mg · kg-1· d-1）組以及梓醇高劑量（100 mg · kg -1· d-1）組、中劑量（50 mg· kg-1· d-1）組、低劑量（10 mg· kg-1· d-1）組，10隻雄性Wistar大鼠作為對照組。各組灌胃給藥12週，對照組和模型組給予等量的生理鹽水。檢測大鼠空腹血糖（ FBG）和血脂；檢測血清活性氧（ ROS）、丙二醛（ MDA）、超氧化物歧化酶（ SOD）和總抗氧化力（ T-AOC）水平；Western blotting檢測胸主動脈組織覈因子E2相關因子2（Nrf2）和血紅素加氧酶1（HO-1）錶達；HE染色觀察胸主動脈病理變化；透射電鏡觀察胸主動脈組織超微結構變化。結果：梓醇治療後，血糖和血脂顯著下降；血清ROS和MDA水平明顯降低，SOD活性和T-AOC顯著增彊；胸主動脈組織Nrf2和HO-1蛋白錶達明顯增彊；HE染色顯示胸主動脈病變程度明顯減輕，透射電鏡觀察胸主動脈超微結構損傷明顯減輕。結論：梓醇能夠有效保護GK大鼠胸主動脈，其機製可能與降低血糖和血脂，減輕氧化應激反應，激活Nrf2／ARE／HO-1信號通路有關。
목적：연구재순대Goto-Kakizaki（ GK）대서주동맥적보호작용병탐토기항양화궤제。방법：6월령GK대서45지수궤분위당뇨병모형조、이갑쌍고（100 mg · kg-1· d-1）조이급재순고제량（100 mg · kg -1· d-1）조、중제량（50 mg· kg-1· d-1）조、저제량（10 mg· kg-1· d-1）조，10지웅성Wistar대서작위대조조。각조관위급약12주，대조조화모형조급여등량적생리염수。검측대서공복혈당（ FBG）화혈지；검측혈청활성양（ ROS）、병이철（ MDA）、초양화물기화매（ SOD）화총항양화력（ T-AOC）수평；Western blotting검측흉주동맥조직핵인자E2상관인자2（Nrf2）화혈홍소가양매1（HO-1）표체；HE염색관찰흉주동맥병리변화；투사전경관찰흉주동맥조직초미결구변화。결과：재순치료후，혈당화혈지현저하강；혈청ROS화MDA수평명현강저，SOD활성화T-AOC현저증강；흉주동맥조직Nrf2화HO-1단백표체명현증강；HE염색현시흉주동맥병변정도명현감경，투사전경관찰흉주동맥초미결구손상명현감경。결론：재순능구유효보호GK대서흉주동맥，기궤제가능여강저혈당화혈지，감경양화응격반응，격활Nrf2／ARE／HO-1신호통로유관。
AIM:To investigate the protective effect of catalpol on Goto-kakizaki (GK) rat aorta and to ex-plore its antioxidant mechanisms.METHODS:Six-month-old GK rats (n=45) were randomly divided into diabetic model group, metformin (100 mg· kg-1· d-1) group, and high-dose (100 mg· kg-1· d-1), medium-dose (50 mg· kg-1· d-1) and low-dose (10 mg· kg-1· d-1) catalpol groups.The healthy male Wistar rats (n=10) were used as control group.The rats in control and model groups were given a same volume of saline .All reagents were administered by oral ga-vage for 12 weeks.Blood glucose and lipids were detected by an automatic biochemical analyzer .Serum reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) levels were detected by commercial kits .The expression of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the thoracic aorta was determined by Western blotting .The pathological changes of the thoracic aorta were observed by HE staining.The ultrastructural changes of the thoracic aorta were observed under electron microscope .RESULTS:Af-ter catalpol treatment , the levels of blood glucose and blood lipids were decreased significantly , and serum levels of ROS and MDA were significantly decreased , but the activity of SOD and T-AOC were significantly enhanced .The protein ex-pression of Nrf2 and HO-1 in the thoracic aorta were significantly increased , the thoracic aortic lesions indicated by HE staining significantly reduced , and the thoracic aortic damage under ultrastructural observation was attenuated slightly . CONCLUSION:Catalpol effectively protects GK rat thoracic aorta , which may be associated with decreasing blood lipids , reducing oxidative stress and activating Nrf 2/ARE/HO-1 signaling pathways.
