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Qiliqiangxin reduced cardiomyocytes apotosis and improved heart function in infarcted heart through Pink1/Parkin -mediated mitochondrial autophagy.
BMC Complement Med Ther. 2020 Jul 02; 20(1):203.BC

Abstract

BACKGROUND

Qiliqiangxin (QLQX) is a preparation refined from a traditional Chinese medicine compound. It plays an important role in protecting cardiac function after myocardial infarction (MI). However, the underline mechanism of QLQX action is not clear. The purpose of this study was to detect the effects of QLQX on mitophagy after MI.

METHODS

Male FVB/NJ mice aged 8-10 weeks were underwent left coronary artery ligation and were orally administered either QLQX (0.25 g/kg/d) or saline. Twenty-eight days after surgical operation, the cardiac function of mice was detected by echocardiography. Electron Microscopy was used to observe the microstructure of cardiomyocytes. Myocardial apoptosis was examined by TdT-mediated dUTP Nick-End Labeling (TUNEL) and western blot. H9c2 cells were cultured in a hypoxic incubator chamber (5% CO2, 1% O2, 94% N2) for 12 h and pretreated with or without QLQX (0.5 mg/mL). The cell apoptosis, reactive oxygen species (ROS), mitochondrial membrane potential and mitophagy were detected.

RESULTS

When compared to sham group, the cardiac function of MI mice decreased significantly, and their cardiomyocyte apoptosis and mitochondrial damage were more serious. These MI-induced cardiac changes could be reversed by QLQX treatment. In vitro experiments also confirmed that QLQX could protect cardiomyocytes from hypoxia-induced apoptosis and mitochondrial damage. Further study indicated that QLQX could increase the expression of Pink1 and Parkin in cardiomyocytes.

CONCLUSION

Qiliqiangxin could reduce cardiomyocytes apotosis and improved heart function in infarcted heart through Pink1-mediated mitochondrial autophagy.

Authors+Show Affiliations

Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Cardiovascular Department, Hubei University of Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Ultrasonography Department, Hubei University of Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Ultrasonography Department, Hubei University of Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Laboratory Department of the First Affiliated Hospital of Guizhou Medical University, Guiyang, 550000, Guizhou, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China.Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China. dyywzx@163.com. Biomedical Research Institute, Hubei University of Medicine, Taihe Hospital, Hubei University of Medicine, Shiyan, 442000, Hubei, China. dyywzx@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32615967

Citation

Zhou, Junyang, et al. "Qiliqiangxin Reduced Cardiomyocytes Apotosis and Improved Heart Function in Infarcted Heart Through Pink1/Parkin -mediated Mitochondrial Autophagy." BMC Complementary Medicine and Therapies, vol. 20, no. 1, 2020, p. 203.
Zhou J, Wang Z, He Y, et al. Qiliqiangxin reduced cardiomyocytes apotosis and improved heart function in infarcted heart through Pink1/Parkin -mediated mitochondrial autophagy. BMC Complement Med Ther. 2020;20(1):203.
Zhou, J., Wang, Z., He, Y., Luo, X., Zhang, W., Yu, L., Chen, X., He, X., Yuan, Y., Wang, X., Guo, X., Tang, J., Zhu, M., Li, D., & Ding, Y. (2020). Qiliqiangxin reduced cardiomyocytes apotosis and improved heart function in infarcted heart through Pink1/Parkin -mediated mitochondrial autophagy. BMC Complementary Medicine and Therapies, 20(1), 203. https://doi.org/10.1186/s12906-020-02992-7
Zhou J, et al. Qiliqiangxin Reduced Cardiomyocytes Apotosis and Improved Heart Function in Infarcted Heart Through Pink1/Parkin -mediated Mitochondrial Autophagy. BMC Complement Med Ther. 2020 Jul 2;20(1):203. PubMed PMID: 32615967.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Qiliqiangxin reduced cardiomyocytes apotosis and improved heart function in infarcted heart through Pink1/Parkin -mediated mitochondrial autophagy. AU - Zhou,Junyang, AU - Wang,Zhixiao, AU - He,Yun, AU - Luo,Xinxia, AU - Zhang,Wenjun, AU - Yu,Li, AU - Chen,Xiuying, AU - He,Xiju, AU - Yuan,Yahong, AU - Wang,Xiaoli, AU - Guo,Xinrong, AU - Tang,Junming, AU - Zhu,Mingan, AU - Li,Dongsheng, AU - Ding,Yan, Y1 - 2020/07/02/ PY - 2019/08/08/received PY - 2020/06/16/accepted PY - 2020/7/4/entrez PY - 2020/7/4/pubmed PY - 2020/7/4/medline KW - Heart function KW - Mitophagy KW - Myocardial infarction KW - Qiliqiangxin SP - 203 EP - 203 JF - BMC complementary medicine and therapies JO - BMC Complement Med Ther VL - 20 IS - 1 N2 - BACKGROUND: Qiliqiangxin (QLQX) is a preparation refined from a traditional Chinese medicine compound. It plays an important role in protecting cardiac function after myocardial infarction (MI). However, the underline mechanism of QLQX action is not clear. The purpose of this study was to detect the effects of QLQX on mitophagy after MI. METHODS: Male FVB/NJ mice aged 8-10 weeks were underwent left coronary artery ligation and were orally administered either QLQX (0.25 g/kg/d) or saline. Twenty-eight days after surgical operation, the cardiac function of mice was detected by echocardiography. Electron Microscopy was used to observe the microstructure of cardiomyocytes. Myocardial apoptosis was examined by TdT-mediated dUTP Nick-End Labeling (TUNEL) and western blot. H9c2 cells were cultured in a hypoxic incubator chamber (5% CO2, 1% O2, 94% N2) for 12 h and pretreated with or without QLQX (0.5 mg/mL). The cell apoptosis, reactive oxygen species (ROS), mitochondrial membrane potential and mitophagy were detected. RESULTS: When compared to sham group, the cardiac function of MI mice decreased significantly, and their cardiomyocyte apoptosis and mitochondrial damage were more serious. These MI-induced cardiac changes could be reversed by QLQX treatment. In vitro experiments also confirmed that QLQX could protect cardiomyocytes from hypoxia-induced apoptosis and mitochondrial damage. Further study indicated that QLQX could increase the expression of Pink1 and Parkin in cardiomyocytes. CONCLUSION: Qiliqiangxin could reduce cardiomyocytes apotosis and improved heart function in infarcted heart through Pink1-mediated mitochondrial autophagy. SN - 2662-7671 UR - https://www.unboundmedicine.com/medline/citation/32615967/Qiliqiangxin_reduced_cardiomyocytes_apotosis_and_improved_heart_function_in_infarcted_heart_through_Pink1/Parkin_-mediated_mitochondrial_autophagy L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/32615967/ DB - PRIME DP - Unbound Medicine ER -
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