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Effect of Atractylenolide I on Myocardial Injury in Rats with AMI through Adjusting HIF-1α/VEGF Signaling Pathway |
MA Weiqian, et al |
Shijiazhuang Ping'an Hospital, Hebei Shijiazhuang 050000, China |
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Abstract Objective: To investigate the effect of atractylenolide I (Atr-I) on myocardial injury in acute myocardial infarction (AMI) rats by regulating hypoxia inducible factor-1 alpha (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway. Methods: Rats were separated into control group, AMI group, Atr-I group, aspirin group, BAY87-2243 group, and Atr-I+BAY87-2243 group, with 18 rats in each group. Except for the control group, rats in all other groups were used to construct AMI models through ligating the root of the left anterior descending branch of the coronary artery. After 1 hour of modeling, treatment began, and the drug was administered once a day for 7 days. Echocardiography was applied to detect changes in left ventricular short axis shortening rate (FS) and left ventricular ejection fraction (LVEF); the percentage of myocardial infarction area in rats was detected by 2,3,5-triphenyl tetrazolium chloride (TTC) staining; HE staining was applied to detect pathological changes in left ventricular myocardial tissue; TUNEL staining was applied to detect myocardial cell apoptosis; ELISA was applied to detect the levels of myoglobin (Mb), lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in left ventricular myocardial tissue; Western blot was applied to detect the expression of HIF-1α and VEGF proteins in myocardial tissue homogenate. Results: Compared with the control group, the myocardial injury was obvious in the AMI group, the FS, LVEF, the expression of HIF-1α and VEGF proteins decreased, the percentage of myocardial infarction area, the contents of Mb, LDH, TNF-α, and IL-1β increased (P<0.05); compared with the AMI group, the myocardial damage in rats in Atr-I group and aspirin group improved, the FS, LVEF, the expression of HIF-1α and VEGF proteins increased, the percentage of myocardial infarction area, the contents of Mb, LDH, TNF-α and IL-1β decreased; the corresponding indexes of BAY87-2243 group showed the opposite trend (P<0.05); compared with the Atr-I group, the myocardial injury in the Atr-I+BAY87-2243 group was exacerbated, the FS, LVEF, the expression of HIF-1α and VEGF proteins decreased, the percentage of myocardial infarction area, the contents of Mb, LDH, TNF-α, and IL-1β increased (P<0.05). Conclusion: Atr-I reduces myocardial injury in AMI rats, which may be related to the activation of the HIF-1α/VEGF signaling pathway.
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