Zhonghua yi xue za zhi · 2008
[Expression of tenascin-X in alcoholic cardiomyopathy and relation thereof to myocardial fibrosis: experiment with rats].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Jing Ling, Li Wei-min, Song Jian, Zhou Li-jun, Li Shuang
Аннотация
OBJECTIVE: To explore the protein expression of tenascin-X (TN-X) and the relation between TN-X and cardiac remodeling and myocardial fibrosis in alcoholic cardiomyopathy (ACM).
METHODS: 60 Wistar rats were randomly divided into 2 equal groups: alcohol-fed group fed with alcohol to establish ACM models and control group fed with common food. 6 months later the rats were killed and the cardiac structure and function, and myocardial collagen content were measured. Western blotting and immunohistochemistry were used to detect the protein expression of TN-X, and smad-3 and smad-7, the signal transduction proteins.
RESULTS: The levels of left ventricle ejection fraction (LVEF) and fraction shortening (FS) of the alcohol-fed group were both significantly lower, and the levels of left ventricle end-diastolic diameter (LVEDd) and collagen volume fraction (CVF) were both higher than those of the control group (both P < 0.05). The protein expression levels of TN-X and smad-3 of the alcohol-fed group were (88% +/- 6%, 82% +/- 8%), both significantly higher than those of the control group (33% +/- 11%, 29% +/- 8%) (both P < 0.01), and the protein expression level of smad-7 of the alcohol-fed group were (37% +/- 9%), both significantly lower than those of the control group (79% +/- 10%, P < 0.01). The protein expression of TN-X was significantly negatively correlated with LVEF, FS, and smad-7, and positively correlated with LVEDd, CVF, and smad-3 (all P < 0.01).
CONCLUSION: Protein expression of TN-X is upregulated in alcoholic cardiomyopathy which may facilitate the myocardial fibrosis in ACM.
METHODS: 60 Wistar rats were randomly divided into 2 equal groups: alcohol-fed group fed with alcohol to establish ACM models and control group fed with common food. 6 months later the rats were killed and the cardiac structure and function, and myocardial collagen content were measured. Western blotting and immunohistochemistry were used to detect the protein expression of TN-X, and smad-3 and smad-7, the signal transduction proteins.
RESULTS: The levels of left ventricle ejection fraction (LVEF) and fraction shortening (FS) of the alcohol-fed group were both significantly lower, and the levels of left ventricle end-diastolic diameter (LVEDd) and collagen volume fraction (CVF) were both higher than those of the control group (both P < 0.05). The protein expression levels of TN-X and smad-3 of the alcohol-fed group were (88% +/- 6%, 82% +/- 8%), both significantly higher than those of the control group (33% +/- 11%, 29% +/- 8%) (both P < 0.01), and the protein expression level of smad-7 of the alcohol-fed group were (37% +/- 9%), both significantly lower than those of the control group (79% +/- 10%, P < 0.01). The protein expression of TN-X was significantly negatively correlated with LVEF, FS, and smad-7, and positively correlated with LVEDd, CVF, and smad-3 (all P < 0.01).
CONCLUSION: Protein expression of TN-X is upregulated in alcoholic cardiomyopathy which may facilitate the myocardial fibrosis in ACM.