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作 者:王微[1] 刘畅[1] 应达时[1,2] 王冰梅[1]
机构地区:[1]长春中医药大学基础医学院生理教研室,长春130117 [2]长春市应氏中医门诊部,长春130022
出 处:《中药药理与临床》2016年第6期52-56,共5页Pharmacology and Clinics of Chinese Materia Medica
基 金:吉林省科技厅自然科学基金项目(20130101144JC)
摘 要:目的:研究芍药苷(Paeoniflorin)预处理对大鼠心肌缺血再灌注损伤(MIRI)的保护性作用并对其可能机制进行探讨。方法 :制备大鼠心肌缺血再灌注损伤模型,随机分为模型组、假手术组、芍药苷60mg/kg组、30mg/kg组(n=20);取心脏测定心肌梗死面积,HE染色观察组织细胞结构,免疫组化检测心肌组织中NF-κB和ICAM-1的表达;取血测定血清中LDH、AST、CK和CK-MB含量。结果:与模型组比较,芍药苷60mg/kg组和30mg/kg组心肌梗死面积均明显降低;HE染色切片提示各给药组心肌细胞损伤较模型组为轻,且具有浓度相关性;芍药苷60mg/kg组、30mg/kg组NF-κB、ICAM-1的表达明显降低;芍药苷60mg/kg组血清CK含量降低,同时该组CK-MB亦降低显著。结论:芍药苷预处理对大鼠MIRI具有保护性作用,其机制与抑制细胞膜脂质过氧化,以及通过抑制NF-κB蛋白表达进而影响受NF-κB调控的下游炎性反应途径有关。Objective: To observe the effect of paeoniflorin preconditioning on the myocardial ischemia reperfusion injury ( MIRI ) in rats and to study the mechanism. Methods: Myocardial ischemia reperfusion injury model was established in Wistar rats. The rats were randomly divided into 4 groups : model group, sham group, paeoniflorin group respectively at 60 mg/kg and 30 mg/kg dose ( n = 20 ). The area of myocardial infarction was calculated. Tissue cell structure was observed by HE staining. NF- nuclear factor kappa B and ICAM-1 expression in cardiac tissue were detected by immunohistochemistry. And the contents of LDH, AST, CK and CK-MB in serum were also measured. Results: Paeoniflorin ( 60 and 30 mg/kg) could significantly reduce the area of myocardial infarction when compared with the model group ( P 〈 0. 01 ) ; HE stained sections suggested that the myocardial cells in each paeoniflorin group were less than those in the model group, and had a concentration dependence; The expression of NF - kappa B and ICAM-1 in medium and 60 mg/kg dose group was significantly lower ( P 〈0. 05 or P 〈0.01 ) ; Paeoniflorin (60 mg/kg) could obviously inhibit the CK activities ( P 〈0.05 ) in serum of MIRI rats. The CK-MB content in paeoniflorin at 60 mg/kg dose was significantly lower than that in the model group ( P 〈 0.05 ). Conclusion: Paeoniflorin has protective effect on myocardium against ischemia reperfusion injury in rats through several pathways including ihibition of cell membrane lipid peroxidation and NF- nuclear factor kappa B expression , and Intervention of the downstream inflammatory response pathway regulated by NF- kappa B.
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