2012Chinese Heart JournalRequires access

Effect of qidan tongmai tablet on myocardial fibrosis in postmyocardial infarction rats

LI Jun-chang

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Abstract

AIM:To investigate the effect of qidan tongmai tablet(QDTMT) on cardiac function and myocardial fibrosis in rats after myocardial infarction(MI).METHODS: Sprague Dawley(SD) rats were subjected to MI by ligating the left anterior descending coronary and randomly divided into sham group,MI group,low-dose QDTMT group(MI-QDTMTL,1.0 g/kg) and high-dose QDTMT group(MI-QDTMTH,2.0 g/kg).After 24 h of ligation,15 ml/kg saline for sham and MI groups and 1.0 g/kg or 2.0 g/kg QDTMT for MI-QDTMTL or MI-QDTMTH groups were administered twice daily.Cardiac contractile function of left ventricular end-diastolic pressure(LVEDP) and ejection factor(EF) were measured in vivo.Rats were sacrificed after 4 weeks.Collagen content in the noninfarcted area was detected by Masson' s trichrome stain.Transforming growth factor beta-1(TGF-β1),collagen type 1 and collagen type 3 mRNA expressions were examined by RT-PCR in the noninfarcted area.The hydroxyproline content of the noninfarcted tissue was measured by hydroxyproline(HYP) ELISA kit for rats.RESULTS: After 4 weeks,rat cardiac function of LVEDD and EF and the heart weight/body weight(HW/BW) index in QDTMTH group and QDTMTL group were significantly better than those in MI group(P0.01;P0.05),but poorer than those in the sham group(P0.01).Myocardial collagen content in noninfarcted area was significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.01).mRNA expression levels of TGF-β1,Col1 and Col3 in noninfarcted area were significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.01).Hydroxyproline content of the noninfarcted tissue was significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.05).CONCLUSION: In post-MI myocardial fibrosis,QDTMT improves cardiac function and reduces myocardial fibrosis by downregulating TGF-β1,Col1and Col3 expressions and decreasing the production of hydroxyproline.

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AIM:To investigate the effect of qidan tongmai tablet(QDTMT) on cardiac function and myocardial fibrosis in rats after myocardial infarction(MI).METHODS: Sprague Dawley(SD) rats were subjected to MI by ligating the left anterior descending coronary and randomly divided into sham group,MI group,low-dose QDTMT group(MI-QDTMTL,1.0 g/kg) and high-dose QDTMT group(MI-QDTMTH,2.0 g/kg).After 24 h of ligation,15 ml/kg saline for sham and MI groups and 1.0 g/kg or 2.0 g/kg QDTMT for MI-QDTMTL or MI-QDTMTH groups were administered twice daily.Cardiac contractile function of left ventricular end-diastolic pressure(LVEDP) and ejection factor(EF) were measured in vivo.Rats were sacrificed after 4 weeks.Collagen content in the noninfarcted area was detected by Masson' s trichrome stain.Transforming growth factor beta-1(TGF-β1),collagen type 1 and collagen type 3 mRNA expressions were examined by RT-PCR in the noninfarcted area.The hydroxyproline content of the noninfarcted tissue was measured by hydroxyproline(HYP) ELISA kit for rats.RESULTS: After 4 weeks,rat cardiac function of LVEDD and EF and the heart weight/body weight(HW/BW) index in QDTMTH group and QDTMTL group were significantly better than those in MI group(P0.01;P0.05),but poorer than those in the sham group(P0.01).Myocardial collagen content in noninfarcted area was significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.01).mRNA expression levels of TGF-β1,Col1 and Col3 in noninfarcted area were significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.01).Hydroxyproline content of the noninfarcted tissue was significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.05).CONCLUSION: In post-MI myocardial fibrosis,QDTMT improves cardiac function and reduces myocardial fibrosis by downregulating TGF-β1,Col1and Col3 expressions and decreasing the production of hydroxyproline.

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Available abstract

AIM:To investigate the effect of qidan tongmai tablet(QDTMT) on cardiac function and myocardial fibrosis in rats after myocardial infarction(MI).METHODS: Sprague Dawley(SD) rats were subjected to MI by ligating the left anterior descending coronary and randomly divided into sham group,MI group,low-dose QDTMT group(MI-QDTMTL,1.0 g/kg) and high-dose QDTMT group(MI-QDTMTH,2.0 g/kg).After 24 h of ligation,15 ml/kg saline for sham and MI groups and 1.0 g/kg or 2.0 g/kg QDTMT for MI-QDTMTL or MI-QDTMTH groups were administered twice daily.Cardiac contractile function of left ventricular end-diastolic pressure(LVEDP) and ejection factor(EF) were measured in vivo.Rats were sacrificed after 4 weeks.Collagen content in the noninfarcted area was detected by Masson' s trichrome stain.Transforming growth factor beta-1(TGF-β1),collagen type 1 and collagen type 3 mRNA expressions were examined by RT-PCR in the noninfarcted area.The hydroxyproline content of the noninfarcted tissue was measured by hydroxyproline(HYP) ELISA kit for rats.RESULTS: After 4 weeks,rat cardiac function of LVEDD and EF and the heart weight/body weight(HW/BW) index in QDTMTH group and QDTMTL group were significantly better than those in MI group(P0.01;P0.05),but poorer than those in the sham group(P0.01).Myocardial collagen content in noninfarcted area was significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.01).mRNA expression levels of TGF-β1,Col1 and Col3 in noninfarcted area were significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.01).Hydroxyproline content of the noninfarcted tissue was significantly inhibited in MI-QDTMTL group and MI-QDTMTH group(P0.05).CONCLUSION: In post-MI myocardial fibrosis,QDTMT improves cardiac function and reduces myocardial fibrosis by downregulating TGF-β1,Col1and Col3 expressions and decreasing the production of hydroxyproline.

Key concepts: Hydroxyproline, Medicine, Myocardial infarction, Preload, Masson's trichrome stain, Myocardial fibrosis, Internal medicine, Cardiac function curve

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