肺炎大鼠心肌TNF-α、IL-6mRNA表达及腺苷对其影响

Effect of adenosine on myocardial expression of TNF-α, IL-6 mRNA in rats with pneumonia

目的 :观察金葡菌感染大鼠肺炎时心肌组织TNF -α、IL - 6mRNA表达 ,以及腺苷对其影响。方法 :5 0只SD大鼠被随机分为 5组 ,为对照组、肺炎组和腺苷治疗A、B、C组。金葡菌经气管插管注入复制肺炎大鼠模型 ,于注菌后第 2、3、4d静脉点滴腺苷治疗 ,每天 90min ,剂量分别为 5 0、10 0、15 0 μg·kg-1·min-1。第 5d处死大鼠 ,立即取心脏液氮保存 ,心肌组织用于病理检测和采用RT -PCR方法检测TNF -α、IL - 6mRNA的表达。结果 :(1)肺炎组心肌中TNF -α、IL - 6mRNA的表达显著高于对照组 (均P <0 0 1) ;(2 )腺苷治疗B、C组心肌中TNF -α、IL - 6mRNA的表达低于肺炎组 (P <0 0 1) ,且治疗C组心肌IL - 6mRNA表达低于治疗B组 (P <0 0 1) ;而A组心肌中TNF -α、IL- 6mRNA的表达与肺炎组无明显差异 (P >0 0 5 ) ;(3)腺苷治疗可以减轻心肌的病理损伤 (P <0 0 1)。结论 :金葡菌感染大鼠肺炎可致心肌损害 ,细胞炎症因子IL - 6和TNF -α参与心肌损伤的发生和发展 ,外源性腺苷治疗可抑制炎症因子TNF -α、IL - 6的分泌 ,从而有利于减轻炎症和保护心肌。

AIM: To observe the expression of TNF-α, I L-6 mRNA in injured myocardium caused by infectious pneumonia and the effects of exogenous adenosine.METHODS: Fifty rats were divided into five experimental groups at random. The model of pneumonia was replicated by the inj ection of staphylococcus aureus into the windpipe of rats. Adenosine-treated ra ts (A,B and C group) received daily injection of adenosine at different dosages (50, 100 and 150 μg·kg -1 ·min -1 for 90 min) for 3 days. All rat s were killed on the fifth day. Pathological examination of myocardium were don e and TNF-α, IL-6 mRNA expression were detected by reverse transcription poly m erase chain reaction (RT-PCR). RESULTS: (1) Significant increa se in TNF-α, IL-6 mRNA expression was observed in myocardium of pneumonic rats compared with control group ( P< 0 01, respectively). (2) TNF-α and IL-6 m RNA expression were significantly decreased in adenosine-treated rats (B,C group s) compared with pneumonia group ( P <0 01, respectively). Compared with pne umonia group, however, there were no statistically significant difference in ad enosine-treated A group ( P >0 05). IL-6 mRNA expression in adenosine-treated C group was lower than that in adenosine-treated B group ( P <0 01). (3)Ex ogenous adenosine reduced pathological changes of injuried myocardium caused by infectious pneumonia. CONCLUSIONS: TNF-α, IL-6 may be involve d in the development of myocardial injury in rats with pneumonia. Exogenous adeno sine inhibited inflammatory by down-regulating TNF-α, IL-6 expression, and the n protected against myocardium injury in rats with pneumonia.