【摘要】 目的:明确α₁肾上腺素能受体（α₁-AR）激动剂苯肾上腺素（PE）在压力超负荷诱导心肌纤维化过程中的作用,观察该过程中炎症因子白细胞介素-1（IL-1）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的变化。方法:昆明（KM）小鼠49只,随机分成空白对照组、腹主动脉结扎（TAC）组和假手术组,8周后再将TAC组小鼠随机分为5组,包括TAC对照组、TAC+PE组、TAC+哌唑嗪（Praz）组、TAC+普萘洛尔（Prop）组和TAC+卡维地洛（Carv）组,分别给予不同的药物处理3周后,测定小鼠左心室组织胶原容积积分（CVF）、羟脯氨酸含量以及炎症因子IL-1、IL-6和TNF-α的表达变化。结果:TAC 8周后,小鼠出现明显心肌纤维化,左心室组织CVF、羟脯氨酸含量以及IL-1、IL-6和TNF-α的表达均较空白对照组显著增高（P<0.01）;与TAC组相比,TAC+PE组、TAC+Prop组和TAC+Carve组的左心室CVF、羟脯氨酸含量及IL-1、IL-6、TNF-α的蛋白表达均明显降低（P<0.01）,而TAC+Praz组的左心室CVF、羟脯氨酸含量及IL-1、IL-6、TNF-α表达变化不明显（P>0.05）;与TAC+PE组相比,TAC+Prop组左心室CVF、羟脯氨酸含量差异无统计学意义,但IL-1、IL-6和TNF-α的蛋白表达显著降低（P<0.05）。结论:PE通过激活α₁-AR,可改善压力超负荷诱导的心肌纤维化和炎症因子IL-1、IL-6及TNF-α的表达,α₁-AR可能是心肌纤维化的防御因素。更多还原

【Abstract】 Objective:To explicit phenylephrine(PE), α1-adrenergic receptor(α1-AR) on myocardial fibrosis regulation and interleukin-1(IL-1), IL-6, tumor necrosis factor-α(TNF-α) expressions in pressure overloaded mice.Methods:A total of 49 KM mice were randomly divided into 3 groups: Blank control group, n=7, Sham operation group, n=7, Transverse abdominal aortic constriction(TAC) group, n=35, and 8 weeks later, the mice in TAC group were further divided into 5 sub-groups as TAC control, TAC+PE, TAC+Praz, TAC+Prop, TAC+Carv sub-groups, n=5 in each sub-group, and the animals were respectively treated for 3 weeks. Left ventricular collagen volume fraction(CVE), hydroxyproline content and IL-1, IL-6, TNF-α expressions were examined respectively.Results: By 8 weeks treatment, compared with Blank control group, TAC group had obvious myocardial fibrosis, increased hydroxyproline content and IL-1, IL-6, TNF-α expressions, P<0.001. Compared with TAC control sub-group, TAC+PE, AC+Prop, TAC+Carv sub-groups showed decreased CVF, hydroxyproline content and IL-1, IL-6, TNF-α expressions, P<0.001, while the above changes were not obvious in TAC+Praz sub-group, P>0.05; CVE and hydroxyproline content were similar between TAC+PE and TAC+Prop sub-groups, while the expressions of IL-1, IL-6 and TNF-α were obviously decreased in TAC+Prop sub-group, P<0.05.Conclusion: PE may improve myocardial fibrosis and IL-1, IL-6, TNF-α expressions by activating α1-AR in pressure overloaded mice, α1-AR might be a defending factor for myocardial fibrosis.更多还原