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出 处:《中国实验方剂学杂志》2013年第3期201-204,共4页Chinese Journal of Experimental Traditional Medical Formulae
基 金:广西中医药大学校级重点课题(ZD06008);教育部新世纪优秀人才支持计划(教技函2010-14号;NCET-10-0093)
摘 要:目的:探讨灯盏乙素对L-甲状腺素(L-Thy)诱导的大鼠实验性心肌肥厚的影响及其可能作用机制。方法:将大鼠随机分为正常组、模型组、卡托普利组(25 mg.kg-1)、灯盏乙素高、中、低剂量组(100,50,25 mg.kg-1)共6组。除正常组外,其余各组连续10 d ip L-Thy诱导心肌肥厚性损伤,造模的同时ig相应的药物进行治疗。观察大鼠的心脏质量指数、血清天冬氨酸转氨酶(AST)、乳酸脱氢酶(LDH)、肌酸激酶(CK)活性、左心室心肌匀浆中胶原含量及心肌病理变化。结果:L-Thy损伤模型组全心质量指数、左心室质量指数、血清AST,LDH,CK活性、左心室胶原含量均较正常组明显升高(P<0.01),病理切片显示心肌细胞肥大,胶原增多。与模型组相比,灯盏乙素各剂量组能明显降低左心室质量指数(P<0.05);低剂量组能明显降低血清AST活性(P<0.05),中、低剂量组能明显降低LDH活性(P<0.05),灯盏乙素各剂量组均能显著降低CK活性(P<0.01或P<0.05);高剂量组能降低左心室胶原含量(P<0.05),心肌病理改变明显减轻。结论:灯盏乙素能显著抑制甲状腺素所致的大鼠心肌肥厚,对心肌具有明显的保护作用。Objective: To observe the protective effect and mechanism of scutellarin (Scu) on hypertrophic cardiomyopathy induced by L-thyroxine (L-Thy) in rats. Method: The rats were randomly divided into six groups: normal group, model group, eaptopril group (25 mg ·kg-1 ) , Scu-high, medium and low-dose group (100, 50, 25 mg .kg-1 ). Except normal group, rats were treated by ip of L-Thy to establish cardiac hypertophic model and treated with corresponding drugs via ig at the same time. The change of cardiac indexes, the activity of creatine kinase (CK), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) in plasma, the content of hydroxproline (Hyp) in left ventricle, morphological changes of cardiac tissue were measured. Result: Compared with normal group, the cardiac indexes, the activity of CK, LDH, AST in plasma, the content of Hyp in left ventricle were significantly increased (P 〈 0.01 ) ; the myocardial hypertrophy and myocardial fibrosis were appeared in model group. Compared with model group, Scu each groups can significantly decreased the left ventricular mass indexes (P 〈 0.05) ; Scu each groups can significantly decreased the activity of CK, LDH, AST; Scu high-dose group could significantly decreased the content of Hyp (P 〈 0.05 ) and markedly inhibited myocardial hypertrophy. Conclusion: Scu could prevent cardiac hypertrophy induced by L-Thy and protect cardiac tissue from injury.
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