| مستخلص: |
Objective: To investigate the regulatory effect of Qiliqiangxin Capsule on mitochondrial Ca2+ related genes in rats with myocardial infarction(MI). Methods: The rat model of MI was established by ligation of the left anterior descending coronary artery. After operation, the rats were randomly assigned to the model group, the Qiliqiangxin group and the captopril group; a sham‑operated group was also available as a control. After four weeks of treatment, the extent of infarction in rats was observed by gross cardiac structure and the morphological changes of myocardial histopathology were observed by HE staining. Detection of mitochondrial Ca2+ transport‑related genes such as inositol‑1,4,5‑trisphosphate receptor 2 (IP3R2), glucose regulated protein 75 (GRP75), voltage‑dependent anion channel 1 (VDAC1), and mitofusion 2 (Mfn2) and mitochondrial apoptosis‑related genes such as B‑cell lymphoma‑2 (Bcl‑2) and Bcl‑2 related X protein (Bax) mRNA expression changes was measured by RT‑PCR in the infarct margins of the heart; Western blot was used to detect changes in Bcl‑2, Bax protein expression in myocardial tissue. The rate of apoptosis in cardiac myocardial tissue was detected by TUNEL staining. Results: Compared with the sham group, the anterior left ventricular wall of the model group showed a large area of infarction, and the structure of myocardial tissue was disordered. The mRNA expression level of mitochondrial Ca2+ transport‑related genes such as IP3R2, GRP75, VDAC1, and Mfn2 were significantly increased (P<0.05, P<0.01);The mRNA and protein expression of Bcl‑2, a molecule related to mitochondrial apoptosis, were significantly decreased (P<0.01), while the mRNA and protein expression of Bax were significantly increased (P<0.01); and apoptosis rate was significantly increased (P<0.01). Compared with the model group, the infarct size of cardiac gross specimens in the Qiliqiangxin group and the captopril group was reduced and myocardial fibers were relatively well ordered; The mRNA expression of mitochondrial Ca2+ transport‑related genes such as IP3R2, GRP75, VDAC1, and Mfn2 were significantly reduced (P<0.01); the mRNA and protein expression of Bcl‑2, a molecule related to mitochondrial apoptosis, were increased (P<0.05, P<0.01), and the mRNA and protein expression of Bax were significantly decreased (P<0.05, P<0.01). and apoptosis rate was significantly decreased (P<0.01). Conclusion: Qiliqiangxin Capsule can improve the morphological structure of the heart of rats with MI, and its mechanism is related to regulation of the gene expression of mitochondrial Ca2+ transport complex IP3R2/GRP75/ VDAC1, thereby inhibiting apoptosis. [ABSTRACT FROM AUTHOR] |
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