摘要
目的研究脱氢紫堇碱(DHC)对内毒素血症大鼠心肌保护作用,并探讨其机制。方法 50只雄性Wistar大鼠随机分为对照组、模型组和DHC低、中、高剂量组,每组10只,通过尾静脉注入脂多糖(LPS)建立内毒素血症大鼠心肌损伤模型,以低、中、高剂量的DHC分别进行干预,在用药后1 h采用酶速率法检测血清心肌酶(CK)、心肌同工酶(CK-MB)、心肌肌钙蛋白(TnI)含量,ELISA法检测血清肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)含量,光镜观察大鼠心肌组织的病理学变化。结果与对照组相比较,LPS模型组CK、CK-MB、TnI明显上升,DHC低、中剂量组中CK、CK-MB、TnI明显下降(P<0.05),高剂量组与模型组相比无明显差异。LPS模型组、DHC干预组的TNF-α、IL-1β的含量均有显著增加(P<0.01),DHC低、中、高剂量组与LPS模型组相比显著减少(P<0.01)。光镜观察发现模型组大鼠心肌组织炎症反明显,心肌组织较多炎症细胞浸润;脱氢紫堇碱低、中剂量组大鼠心肌组织炎症反应较轻,心肌组织有少量炎症细胞浸润;高剂量组大鼠心肌组织炎症坏死程度介于模型组和中剂量组之间。结论 DHC能有效抑制内毒素血症大鼠心肌组织炎症反应,减轻心肌损伤,在低、中剂量时效果明显。
Objective： To study myocardial protective effect of dehydrogenation corydaline on rats with endotoxemia and to explore its mechanism. Methods： 50 male Wistar rats were randomly divided into five groups： NS control group,LPS model group,DHC low dose group,DHC medium dose group,and DHC high dose group,10 rats in each group. Lipopolysaccharide （LPS） was injected through tail vein to establish myocardium injury rat model which was intervened by low,medium and high doses of DHC. 1 hour after the medication,CK enzyme, CKMB serum enzyme and TnI levels were measured by enzyme rate method,TNF-α and IL-1β levels by ELISA method, and pathological changes of myocardial tissue by optical microscopy. Results： Compared with NS control group, CK, CKMB and TnI levels in LPS model group increased remarkably. Meanwhile, CK, CKMB and TnI levels in low and medium dose groups decreased significantly （P〈0.05）. There were no significantly differences in high dose group and in LPS model group. TNF-α and IL-1β levels in DHC intervention group and in LPS model group significantly increased （P〈0.01）. Compared with with model group,TNF-α and IL-1β levels in DHC low, medium and high dose groups significantly reduced （P〈0.01 ）. There were obvious myocardium tissue inflammation and inflammatory cell infdtration under the optical microscopy in model group. There were less myocardium inflammation and inflammatory cell infiltration in low and medium-dose groups by comparison. The cardiac tissue inflammation and necrosis in high-dose group was between model group and medium-dose groups. Conclusion： Dehydrogenation corydaline can inhibit myocardial tissue inflammation and reduce myocardial injury,especially in low and medium-dose groups.
出处
《中国中医急症》
2014年第5期830-831,848,共3页
Journal of Emergency in Traditional Chinese Medicine
基金
浙江省中医药管理局项目(2011za034)
关键词
脱氢紫堇碱
内毒素血症
心肌酶
炎症因子
Dehydrogenation corydaline
Endotoxemia
Myocardial enzyme
Inflammatory cytokines
