CAJ | 학술논문

目的：观察潜阳解毒通络方在自发性高血压大鼠(SHR)心肌组织胶原合成和心肌纤维化中的作用。方法12周龄雄性自发性高血压大鼠（SHR）分为SHR应用潜阳解毒通络方组（QYTL组）、SHR应用糜酶抑制剂组（Chy-I组）、SHR应用潜阳解毒通络方及糜酶抑制剂组（QY& Chy-I组）、SHR组，另设10只12周龄的雄性Wistar-Kyoto大鼠（WKY）为正常对照组。检测各组大鼠的收缩压、心肌胶原容积分数（CVF）、心肌血管周围胶原面积比（PVCA）和心肌糜酶及I、III型胶原mRNA表达水平。结果 QYTL组、QY& Chy-I组和Chy-I组心脏CVF、PVCA与SHR组比较显著下降（P＜0.01），与WKY组比较无显著差异。QYTL组、QY& Chy-I组和Chy-I组心肌组织I、III型胶原和糜酶mRNA表达相对含量均低于SHR组（P＜0.01），与WKY组比较无显著性差异。QYTL组、QY& Chy-I组大鼠血压与SHR比较有显著改变，Chy-I组大鼠血压与SHR比较无显著改变。结论心肌组织糜酶参与胶原的合成及细胞外基质的形成和降解，潜阳解毒通络方可能通过抑制糜酶途径改善心肌纤维化。
목적：관찰잠양해독통락방재자발성고혈압대서(SHR)심기조직효원합성화심기섬유화중적작용。방법12주령웅성자발성고혈압대서（SHR）분위SHR응용잠양해독통락방조（QYTL조）、SHR응용미매억제제조（Chy-I조）、SHR응용잠양해독통락방급미매억제제조（QY& Chy-I조）、SHR조，령설10지12주령적웅성Wistar-Kyoto대서（WKY）위정상대조조。검측각조대서적수축압、심기효원용적분수（CVF）、심기혈관주위효원면적비（PVCA）화심기미매급I、III형효원mRNA표체수평。결과 QYTL조、QY& Chy-I조화Chy-I조심장CVF、PVCA여SHR조비교현저하강（P＜0.01），여WKY조비교무현저차이。QYTL조、QY& Chy-I조화Chy-I조심기조직I、III형효원화미매mRNA표체상대함량균저우SHR조（P＜0.01），여WKY조비교무현저성차이。QYTL조、QY& Chy-I조대서혈압여SHR비교유현저개변，Chy-I조대서혈압여SHR비교무현저개변。결론심기조직미매삼여효원적합성급세포외기질적형성화강해，잠양해독통락방가능통과억제미매도경개선심기섬유화。
Objective Research of Qianyang Jiedu Tongluo(QYTL) decoction inhibition of Myocardial tissue collagen synthesis and myocardial fibrosis to explore its mechanism in spontaneously hypertensive rats.Methods Through using the method of pathology, computer analysis and reverse transcription polymerase chain reaction, the spontaneously hypertensive rats divided into QYTL group, Chy-I group, the QY& Chy-I group, SHR group, WKY group. Testing the systolic pressure, CVF, PVCA, the myocardial chymase and collagen I and III mRNA expression.Results Compared with the WKY group, CVF and PVCA mRNA expression was significantly inhibited (P<0.01) in QYTL group, Chy-I group, the QY& Chy-I group. Compared with the SHR group, the myocardial chymase and collagen I and III mRNA expression was significantly inhibited (P<0.01) in QYTL group, Chy-I group, the QY& Chy-I group. Compared with the SHR group, the systolic pressure was significantly inhibited (P<0.01) in QYTL group and the QY& Chy-I group.Conclusion The myocardial chymase involved in the synthesis of collagen, the formation and degradation of ECM, and promote myocardial fibrosis in spontaneously hypertensive rats, while QYTL could Inhibition myocardial fibrosis through the way of Inhibiting the myocardial chymase.