摘要
目的探究替米沙坦对病毒性心肌炎小鼠炎性损伤的改善作用及机制。方法用腹腔接种柯萨奇病毒B3(CVB3)的方法构建病毒性心肌炎小鼠模型,然后随机分为模型组(n=20)及实验组(n=20),另选20只雄性BALB/c小鼠为对照组。实验组予以灌胃替米沙坦10 mg·kg~(-1),模型组及对照组则灌胃等体积0. 9%Na Cl,共4周。比较3组小鼠心肌组织炎性因子、脂联素(APN)含量及心肌组织APN蛋白表达。结果给药4周后,对照组、模型组和实验组心肌组织匀浆中IL-6分别为(56. 44±12. 41),(137. 06±16. 82),(83. 21±14. 21)pg·mg~(-1); TNF-α分别为(23. 84±8. 54),(105. 41±14. 08),(44. 95±12. 01)pg·mg~(-1); APN分别为(7. 11±0. 08),(5. 94±0. 09),(8. 03±0. 07)μg·mg~(-1),差异均有统计学意义(均P <0. 05)。结论替米沙坦可有效改善病毒性心肌炎小鼠炎性损伤,其作用机制可能与上调心肌组织APN表达相关。
Objective To explore the effect of telmisartan on the inflammatory injury of viral myocarditis mice and the underlying mechanism.Methods Viral myocarditis model was established by Coxsackievirus B3( CVB3) intraperitoneally inoculation. The mice were randomly divided into model group( n = 20) and test group( n = 20). A total of 20 male BALB/c mice were assigned to control group. The test group was given oral administration of telmisartan 10 mg·kg~(-1) once daily,while the model group and the control group were treated with equal amount of 0. 9%NaCl for 4 weeks. The inflammatory factors,adiponectin( APN) content and APN protein expression were compared among 3 groups. Results After 4 weeks of treatment,there were significant differences among the control group,model group and test group in APN [( 7. 11 ± 0. 08)μg·mg~(-1) vs( 5. 94 ± 0. 09) μg·mg~(-1) vs( 8. 03 ± 0. 07) μg·mg~(-1)],IL-6 [( 56. 44 ± 12. 41) pg·mg~(-1) vs( 137. 06 ± 16. 82) pg ·mg~(-1) vs( 83. 21 ± 14. 21) pg·mg~(-1)],TNF-α [( 23. 84 ± 8. 54) pg·mg~(-1) vs( 105. 41 ± 14. 08) pg · mg~(-1) vs( 44. 95 ± 12. 01) pg · mg~(-1)( P < 0. 05). Conclusion Telmisartan can improve the inflammatory injury of viral myocarditis mice effectively,and the action mechanism maybe related to the up-regulation of APN protein expression in myocardial tissue.
引文
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