Effect Of Taurine On The Myocardial Fibrosis In Rats

Objective To explore the effect of taurine (Tau) and its mechanism on the action ofmyocardial fibrosis in vivo and in vitro, and to offer the guidance of theory fordeveloping a new drug to prevent myocardial fibrosis and relative disease.Methods In vivo The sixty Wistar rats were randomly divided into the normalgroup, model group (isoprenaline, Iso) and three groups treated with Tau (Iso+320mg·kg^-1·d^-1, Iso+160 mg·kg^-1·d^-1 and Iso+80mg·kg^-1·d^-1). Myocardial fibrosis modelof rats were made by injecting of Iso for 7 days (5mg·kg^-1·d^-1, sc). From the next day ofmaking model, rats were treated with Tau 320, 160 and80mg·kg^-1·d^-1 ip for 14 days,meanwhile the normal and model group were injected by saline. Rats were anesthetizedby chloral hydrate, monitored in terms of myocardial indexes (heart weight body weight,HW/BW and left ventricular weight/body weight, LVW/BW); the contents ofhydroxyproline (Hyp) and malondialdehyde (MDA) and the activity of superoxidedismutase (SOD) in left ventricle were assayed with spectrophotometry, respectively;The contents of lactate dehydrogenase (LDH) and creatine kinase (CK) in bloodwere detected with automatic biochemistry, analyzer. In vitro The cultured cardiacfibroblasts (CFb) in vitro were treated with angiotensinⅡ(AngⅡ) to induceproliferative cell model. Tau was added in different dosage (160,80 and 40mmol/L) tothe cardiac fibroblasts, and cultured for 48 hours. The culture media was collected. Theeffects of Tau on proliferation of cardiac fibroblast were tested by MTT coloricmetricassay. The contents of hydroxyproline and malondialdehyde, the activity of superoxidedismutase in the culture media were assayed with spectrophotometry, respectively.Results In vivo In three groups treated with Tau 320,160 and 80 mg·kg^-1·d^-1,therewere significantly reduced in the myocardial indexes (HW/BW: P＜0.001, P＜0.001,P＜0.05; LVW/BW: P＜0.001, P＜0.01, P＜0.05) and the content of hydroxyproline(P＜0.01, P＜0.01, P＜0.05) in left ventricle. The activity of superoxide dismutase(P＜0.001, P＜0.001, P＜0.05) in left ventricle was markedly enhanced, the contents oflactate dehydrogenase and creatine kinase in blood serum (P＜0.001, P＜0.001, P＜0.05) were markedly reduced in three groups treated with Tau. The content ofmalondialdehyde in left ventricle in Tau 320 and 160 mg·kg^-1·d^-1 groups (P＜0.01,P＜0.05) was significantly decreased. In vitro Compared with the model group, cellabsorption of all groups treated with Tau was markedly decreased (P＜0.001, P＜0.01,P＜0.05), the activity of superoxide dismutase (P＜0.001, P＜0.001, P＜0.05) in the culturemedia was also increased. The contents of hydroxyproline (P＜0.001, P＜0.05)andmalondialdehyde (P＜0.001, P＜0.01) in the culture media were significantly decreasedin Tau 160 and 80mmol/L group.Conclusion Experimental result in vivo and in vitro indicated that Tau can inhibitcardiac fibroblast proliferation and collagen synthesis through antioxidation, theninhibit myocardial fibrosis and protect myocardium in rats.