ABSTRACT
Objective:To investigate the effect of Bailing capsule on myocardial fibrosis in mice with viral myocarditis(VMC) and TGF-β1-MAPK/ERK pathway. Methods:Male BALB/c mice ( n=200 ) were randomly divided into model group ( n=180 ) and control group(n=20). The model group mice were infected with Coxsackie virus B3 to prepare VMC myocardial fibrosis. The control group mice were injected with Eagle′s MEM without virus. The model was successful after two months. The survival mice were randomly divided into model group and high,middle and low dose of Bailing capsule was administered consecutively for sixty days,once a day, Cardiac ultrasound was used to test LVEDd,LVEDs,then calculate FS. The expression of type Ⅰ collagen and type Ⅲ collagen in all the mice myocardial tissue was detected by immunohistochemical methods. Masson staining for myocardial fibrosis was used to calculate the collagen volume fraction( CVF) . Western blot was used to detect the protein expression of TGF-β1 and p-ERK1/2. Results:①Compared with the control group,the CVF,typeⅠcollagen and typeⅢcollagen obviously increased,LVEDd,LVEDs increased,FS de-creased,which had statistically significance(P<0. 05).②Compared with the control group,the model group of mice had a statistically significantly higher expression of TGF-β1 and p-ERK1/2(P<0. 05).③Compared with the model group,the expression of CVF,typeⅠcollagen and type Ⅲ collagen of high and middle dose of Bailing capsule was significantly lower,LVEDd,LVEDs decreased,while FS increased(P<0. 05).④Compared with the model group,the high dose of Bailing capsule group of mice had a statistically significantly lower expression of TGF-β1 and p-ERK1/2 ( P<0. 05 ) . Conclusion:①Bailing capsule can prevent myocardial fibrosis of mice with VMC.②The activation of TGF-β1-MAPK/ERK pathway may can promote myocardial fibrosis in VMC.③Bailing capsule could prevent myocardial fibrosis,which may be related to prevention of TGF-β1-MAPK/ERK pathway.
ABSTRACT
Objective:To investigate the effect of Bailing capsule on myocardial fibrosis in mice with viral myocarditis(VMC) and TGF-β1-MAPK/ERK pathway. Methods:Male BALB/c mice ( n=200 ) were randomly divided into model group ( n=180 ) and control group(n=20). The model group mice were infected with Coxsackie virus B3 to prepare VMC myocardial fibrosis. The control group mice were injected with Eagle′s MEM without virus. The model was successful after two months. The survival mice were randomly divided into model group and high,middle and low dose of Bailing capsule was administered consecutively for sixty days,once a day, Cardiac ultrasound was used to test LVEDd,LVEDs,then calculate FS. The expression of type Ⅰ collagen and type Ⅲ collagen in all the mice myocardial tissue was detected by immunohistochemical methods. Masson staining for myocardial fibrosis was used to calculate the collagen volume fraction( CVF) . Western blot was used to detect the protein expression of TGF-β1 and p-ERK1/2. Results:①Compared with the control group,the CVF,typeⅠcollagen and typeⅢcollagen obviously increased,LVEDd,LVEDs increased,FS de-creased,which had statistically significance(P<0. 05).②Compared with the control group,the model group of mice had a statistically significantly higher expression of TGF-β1 and p-ERK1/2(P<0. 05).③Compared with the model group,the expression of CVF,typeⅠcollagen and type Ⅲ collagen of high and middle dose of Bailing capsule was significantly lower,LVEDd,LVEDs decreased,while FS increased(P<0. 05).④Compared with the model group,the high dose of Bailing capsule group of mice had a statistically significantly lower expression of TGF-β1 and p-ERK1/2 ( P<0. 05 ) . Conclusion:①Bailing capsule can prevent myocardial fibrosis of mice with VMC.②The activation of TGF-β1-MAPK/ERK pathway may can promote myocardial fibrosis in VMC.③Bailing capsule could prevent myocardial fibrosis,which may be related to prevention of TGF-β1-MAPK/ERK pathway.