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急性病毒性心肌炎小鼠肿瘤坏死因子-α、单核细胞趋化蛋白-1的表达及卡维地洛的干预作用 被引量:7

Effect of carvedilol on expression of tumor necrosis factor-n, monocyte chemoattractant protein-1 in murine vi-ral myocarditis
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摘要 目的 探讨TNF-α、单核细胞趋化蛋白-1(MCP-1)在急性病毒性心肌炎(VMC)发病中的作用及 β受体阻滞剂卡维地洛对其影响。方法 将80只4周龄雄性Balb/c小鼠随机分为3组:心肌炎组(n=30)、卡维地洛组(n=30)和对照组(n =20),心肌炎组及卡维地洛组经腹腔接种柯萨奇病毒B 3(CVB 3)诱发急性 VMC,对照组接种不含病毒的Eagle′s液;卡维地洛组于接种病毒次日开始灌服卡维地洛5 mg/kg,心肌炎组和对照组灌服9 g/L盐水,每天2次。于接种后的第7、14天随机从各组抽取8只小鼠取血后处死,HE染色检测小鼠心肌病理积分,ELISA法检测血清TNF-α水平,RT-PCR检测心肌组织 MCP-1 mRNA 的表达。结果 心肌炎组心肌组织病理积分较对照组明显增高(P 〈0.01),卡维地洛组较心肌炎组病理积分降低(P 〈0.05);心肌炎组小鼠血清TNF-α水平较对照组升高(P 〈0.01),且与心肌病理积分呈正相关(r=0.42,P 〈0.05),卡维地洛组TNF-α水平较心肌炎组显著下降(P 〈0.05);与对照组比较,心肌炎组小鼠心肌MCP-1 mRNA表达明显增加(P 〈0.01),卡维地洛组小鼠心肌 MCP-1 mRNA 表达较心肌炎组明显下降(P 〈0.05)。结论 TNF-α 和 MCP-1参与VMC的发病过程,卡维地洛可能通过下调 TNF-α、MCP-1的过表达减轻 CVB 3感染小鼠的心肌损害,起心肌保护作用。 Objective To investigate the role of tumor necrosis factor-α(TNF-α) and monocyte chemoattrac-tant protein-1 ( MCP-1 ) in the pathogenesis of viral myocarditis (VMC) and the effect of carvedilol. Methods Eighty male Balb/c mice were randomly divided into 3 groups:control group( n = 20), myocarditis group (n = 30) and carve-dilol group (n = 30). The latter 2 groups were intraperitoneally inoculated with Coxsackie virus B3 ( CVB3 ) to induce VMC,while control group with virus-free Eagle's medium instead. Carvedilol was poured 5 mg/kg from the next day af- ter injecting virus in carvedilol group,9 g/L saline was used in control group and myocarditis group,twice a day. On the 7^th and 14^th day after inoculation,8 mice were sacrificed after taking blood sample which were randomly selected from each group. Histological cross sections of hearts were stained with hematoxylin-eosin ( HE), and the content of serum TNF-α was assayed with enzyme-linked immunoadsordent assay, while the expression of MCP-1 mRNA in myocardial tissue was detected with reverse transcriptase-polymerase chain reaction(RT-PCR) method. Results The pathological score of myocarditis group was significantly higher than that in control group(P 〈0.01 ) ,while carvedilol group was sig-nificantly lower than that in myocardial group(P 〈 0.05 ). The serum level of TNF-α of VMC mice in myocarditis was significantly higher than that in control group ( P 〈 0.01 ) and positively correlated with the pathological score of the myocardium ( r = O. 42, P 〈 0.05 ), and serum TNF-α in carvedilol group was remarkably decreased compared with myo- carditis group(P 〈0.05). The expression level of MCP-1 mRNA in myocarditis group was increased significantly com-pared with control group (P 〈 0.01 ), and remarkably decreased in carvedilol group compared with myocarditis group ( P 〈 0.05 ). Conclusions TNF-α and MCP-1 may be involved in the pathogenesis of VMC, and carvedilol may protect myoc
出处 《中华实用儿科临床杂志》 CAS CSCD 北大核心 2013年第13期1020-1022,共3页 Chinese Journal of Applied Clinical Pediatrics
关键词 卡维地洛 病毒性心肌炎 肿瘤坏死因子-Α 单核细胞趋化蛋白-1 Carvedilol Viral myocarditis Tumor necrosis factor-α Monocyte chemoattractant protein-1
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