Protective effects of ginsenoside Rg1 on cardiac muscle of aging mice induced by D-galactose

• Main Authors: LI Geng, WANG Ziling, HOU Jiying, HUANG Caihong, XIAO Hanxianzhi, ZENG Di, JIANG Rong, WANG Lu, WANG Yaping
• Format: Article
• Language: zho
• Published: Editorial Office of Journal of Third Military Medical University 2021-06-01
• Series: Di-san junyi daxue xuebao
• Subjects: ginsenoside rg1; d-galactose; myocardium; oxidative stress injury; nrf2 signal pathway
• Online Access: http://aammt.tmmu.edu.cn/Upload/rhtml/202012240.htm

Objective To investigate the protective effects and primary mechanism of ginsenoside Rg1 on cardiac muscle of aging mice induced by D-galactose (D-gal). Methods C57BL/6 J mice were randomly divided into normal control, model, Rg1 intervention and negative control groups, with 10 animals in each group. D-gal (200 mg/kg) was injected intraperitoneally to the mice for 42 d to establish the model group, and the mice of the Rg1 intervention group was given 40 mg/kg Rg1 per day for 26 d intraperitoneally from the 16th day of model establishment. The mice of the normal control group were given same amount of normal saline for 42 d, and those of the negative control group were treated with normal saline after model establishment. On the 2nd day after treatment, the hearts were taken to measure the organ index. HE staining and transmission electron microscopy were performed to observe the morphology and micro-structures of the heart tissue from each group. The activities of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), total superoxide dismutase (T-SOD), catalase (CAT) and contents of malondialdehyde (MDA) in the myocardial tissue homogenate were tested by enzyme-labeled colorimetry; The expression levels of Nrf2, Keap1 and HO-1 in the heart tissue were detected by Western blotting. Results Compared with the control group, the model group had significantly increased heart index (P < 0.01); larger amount of deposited collagen fibers between myocardial fibers, disordered myofibril bundles, thicker myocardial fibers, and abnormally swollen mitochondria; enhanced AST and LDH activities, declined T-SOD and CAT activities, and increased MDA content (P < 0.05); remarkably down-regulation of Nrf2 and HO-1 (P < 0.05), and no changed Keap1 level. While in the Rg1 intervention group, all the above phenomena were greatly improved after the intervention, with obviously decreased heart index (P < 0.01), not notable morphological changes with normal control mice, reversed AST, LDH, T-SOD and CAT activities and MDA contents(P < 0.05), and elevated protein levels of Nrf2 and HO-1, and decreased level of Keap1 (P < 0.01). Conclusion Rg1 effectively alleviates the damage of D-gal to the morphology and ultrastructure of mouse myocardium, and its mechanism may be related to the inhibition of oxidative stress and the up-regulation of the Nrf2 antioxidant signal pathway.