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目的探讨成纤维细胞生长因子诱-导早期反应蛋白14(Fn14)在自发性高血压大鼠心肌纤维化中的作用及培哚普利的干预结果。方法18只6周龄雄性自发性高血压大鼠(SHR)随机分为高血压组(SHR-C组)和培哚普利组(SHR-P组),每组9只;另取9只同龄雄性Wistar Kyoto大鼠作为正常组(WKY组),SHR-P组给予培哚普利治疗24周。实验前后测量室间隔及左室后壁背向散射积分平均强度(AII)、校正的声学强度(CAI)与峰峰强度(PPI)等超声心动图指标。24周后,处死大鼠,测量心脏重量指数(HWI),masson染色检测胶原的表达,免疫组化法检测Fn14的表达。结果30周龄时,与WKY组相比,SHR-C组HWI显著升高、Fn14表达增高(P均<0.01),室间隔及左室后壁AII、CAI明显增大(P均<0.01),PPI明显减小(P<0.01);与SHR-C组相比,SHR-P组HWI显著降低、Fn14表达降低(P均<0.01),室间隔及左室后壁AII、CAI减小(P<0.05),PPI增大(P<0.05)。Fn14表达量与胶原纤维的量呈正相关(r=0.954,P<0.01)。结论Fn14可能参与SHR心肌纤维化,培哚普利可能通过抑制其表达来减轻心肌纤维化。
Objective To investigate the role of fibronectin-induced early reactive protein 14 (Fn14) in myocardial fibrosis in spontaneously hypertensive rats and the result of perindopril intervention. Methods Eighteen 6-week-old male spontaneous hypertensive rats (SHR) were randomly divided into hypertension group (SHR-C group) and perindopril group (SHR-P group) The same age male Wistar Kyoto rats as the normal group (WKY group), SHR-P group given perindopril treatment for 24 weeks. Before and after the experiment, the mean value of AII, corrected CAI and PPI of the left ventricular and posterior wall were measured. The echocardiographic parameters were measured. After 24 weeks, the rats were killed, the heart weight index (HWI) was measured, the expression of collagen was detected by masson staining, and the expression of Fn14 was detected by immunohistochemistry. Results Compared with WKY group, the HWI of SHR-C group was significantly increased (P <0.01), and the AII and CAI of the posterior wall of left ventricular were significantly increased at 30 weeks of age (all P <0.01) (P <0.01). Compared with SHR-C group, the HWI of SHR-P group was significantly decreased and the expression of Fnl4 was decreased (all P <0.01), while the AII and CAI of the posterior interventricular septum and left ventricle were decreased P <0.05), PPI increased (P <0.05). Fn14 expression was positively correlated with the amount of collagen fibers (r = 0.954, P <0.01). Conclusion Fn14 may be involved in cardiac fibrosis in SHR. Perindopril may reduce myocardial fibrosis by inhibiting its expression.