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Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, Shandong 250012, China. Electronic address:
Published: March 2016
AI Article Synopsis
Article Abstract
Objective: To study the effect of levocarnitine (L-CN) on tissue inhibitor of metalloproteinase-1 (TIMP-1) and intercellular adhesion molecule-1 (ICAM-1) expression of rats with coronary heart disease and evaluate the protective effect of L-CN on myocardial cells.
Methods: High-fat diet feeding and intraperitoneal injection of pituitrin was performed on rats in model group and CHD Model of rats was built. Rats with successful model-building were selected and divided into L-CN group and Ctrl group randomly. Rats in L-CN group were given L-CN treatment, with intraperitoneal injection of 200 mg·kg(-1)·d(-1) and successive administration for 3 d. Rats in Ctrl group were given equal volumes of normal saline. Blood was collected from carotid artery at different time and expression quantity of creatine kinase-MB (CK-MB) and Troponin Ⅰ (TnⅠ) in serum was detected. Rats in each group were put to death and were separated to obtain the myocardial tissue. Real-time PCR and Western Blotting hybridization were performed to detect the TIMP-1, ICAM-1 expression in myocardial tissue in each group. Statistical analysis was employed to explore the expression changes of TIMP-1 and ICAM-1, and ELISA test was used to analyze the expression changes of myocardial necrosis marker-CK-MB and TnⅠto learn the effect of L-CN and its myocardial protective effect.
Results: The total cholesterol, triglyceride and blood glucose levels of rats in model group were significantly higher than that in control group, which indicated that due to high-fat diet feeding, blood lipid of rats in model group was obviously higher than that in control group. In myocardial tissue of rats in model group, TIMP-1 level significantly reduced and ICAM-1 level significantly increased (P < 0.01). In model group, after L-CN treatment, TIMP-1 level had double increase, while ICAM-1 level had 43% of decrease in L-CN group compared with Ctrl group. After L-CN intervention treatment, CK-MB and TnⅠ content in L-CN group relatively reduced compared with Ctrl group. The difference among groups was obvious (P < 0.01).
Conclusions: L-CN could increase the TIMP-1 expression level and inhibit the ICAM-1 expression level. L-CN has a certain myocardial protective effect.
