摘要
目的观察地塞米松(Dexamethasone,DEX)对异丙肾上腺素(Isoprotereno,ISO)致小鼠急性心肌缺血损伤的影响并探讨其作用机制。方法 16只昆明种小鼠随机分成正常对照(control,CON)组、ISO组、地塞米松预处理(Dexamethasone pretreatment,DEX-pre)组、DEX组,每组4只。CON组、ISO组首次处理前30 min给予等量0.9%氯化钠注射液腹腔注射预处理,然后CON组给予等量0.9%氯化钠注射液腹腔注射处理,ISO组小鼠给予ISO(5 mg/kg),每日腹腔注射1次,连续3 d;DEX-pre组在首次ISO注射前30 min给予DEX(1.25 mg/kg)腹腔注射,余同ISO组;DEX组在第2天、第3天ISO注射30 min后给予DEX(1.25 mg/kg)腹腔注射,余同ISO组。检测血清谷草转氨酶(AST)、乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)了解心肌损伤;观察心肌组织的病理学改变并检测细胞因子TNF-α的变化。结果 1与CON组比较,ISO组ASL、LDH、CK均明显升高(P<0.01),CK-MP无明显改变(P>0.05);ISO组心肌损伤明显加重,形态学计分为4.0比0.0(P<0.01);ISO组血清TNF-α明显升高(P<0.05);DEX-pre组TNF-α明显下降(P<0.01)。2与ISO组比较,EX-pre组ASL、CK下降非常显著(P<0.01),LDH、CK-MP轻度下降(P<0.05);DEX-pre组心肌损伤得到明显改善,形态学计分为2.0比4.0(P<0.01);DEX-pre组血清TNF-α下降非常显著(P<0.01)。3与ISO组比较,DEX组ASL、LDH、CK、CK-MP均无明显改变(P>0.05);DEX组心肌损伤无明显变化,形态学计分为3.5比4.0(P>0.05);DEX组血清TNF-α升高非常显著(P<0.01)。结论地塞米松预处理对异丙肾上腺素致小鼠急性心肌损伤的心肌具有明显保护作用,TNF-α等细胞因子改变可能是其机制之一。
Objective To investigate potential protective effect of glucocorticoid receptor（ GR） agonist dexamethasone on isoproterenol-induced myocardial injury and the possible mechanism. Methods The sixteen mice were randomly divided into control（ CON） group（ n = 4）,ISO group（ n = 4）,Dexamethasone pretreatment（ DEX-pre） group（ n = 4） and Dexamethasone treatment（ DEX） group（ n = 4）. The mice in CON group and ISO group were given the same amount of 0. 9% sodium chloride and DEX-pre group given dexamethasone（ 1. 25 mg / kg） injection by intraperitoneal injection as a pretreatment before treatment 30 minutes. CON group was given the same amount of 0. 9% sodium chloride injection by intraperitoneal injection. ISO group,DEX-pre group and DEX group received 5 mg / kg isoproterenol hydrochloride with daily intraperitoneal injection and continuous 3 days. At the two and three days,dexamethasone（ 1. 25 mg / kg） was given after ISO injected 30 minutes in DEX group. Observe the serum ASL,LDH,CK,and CK-MP. Myocardial tissue injury was assessed by HE staining. The expression of TNF-α on serum was detected by ELISA. Results① Compared with control group,the levels of ASL,LDH and CK was significantly increased; the degree of myocardial injury were greatly deteriorated in ISO group（ P〈0. 01）. The expression of TNF-α on serum was greatly increased（ P〈0. 05） in ISO group.The expression of TNF-α on serum was significantly reduced（ P〈0. 01） in DEX-pre group. ② Compared with ISO group,the levels of ASL and CK was significantly reduced（ P〈0. 01） and the levels of LDH and CK-MP was reduced（ P〈0. 05）. The degree of myocardial injury were greatly improved（ P〈0. 01） in DEX-pre group. The expression of TNF-α on serum was significantly reduced（ P〈0. 01） in DEX-pre group. ③ Compared with ISO group,the levels of ASL,LDH,CK,CK-MP and the degree of myocardial injury weren＇t significantly difference in DEX group（ P〉0. 05）. The expression of TNF-α on serum was significantly increased（ P〈0. 01）in DEX group. Conclusion DEX pretreatment has protective effect against ISO-induced myocardial injury. The mechanism might be the changes of inflammatory cytokinesthe.
出处
《东南国防医药》
2015年第5期467-470,共4页
Military Medical Journal of Southeast China
