Tibetan-Origin Edible Chinese Herbal Prescription C18 Protects H9C2 Cardiomyocytes from Cobalt Chloride-induced Hypoxia Injury through the PI3K/AKT Signaling Pathway
Guoxin Chang1,2, Hongyi Xie1,2, Shu Chen3, Ruixue Wang2, Xuxin Zeng2, Dingmei Lin1,2, Zixuan Mo1,2, Jingjing Yu2, Xindan Liu2, Zhaoguang Zheng1,2,4★, Yan Wang1★★ Corresponding author
- 1Department of Traditional Chinese Medicine and Pharmacy, School of Chinese Materia Medica, Guangdong Pharmaceutical University, Guangzhou, Guangdong, PR China
- 2Department of Pharmacy, School of Medicine, Foshan University, Foshan, Guangdong, PR China
- 3Department of Drug Research, Cancer Research Institute, Foshan First People’s Hospital, Foshan, Guangdong, PR China
- 4Department of Drug Research, Foshan Newtopcome Pharmaceutical Technology Co., Ltd., Foshan, Guangdong, PR China
CORRESPONDENCE
Zhaoguang Zheng
s: Yan Wang, College of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, PR China. ; Zhaoguang Zheng, School of Medicine, Foshan University, 33 Guangyun Road, Nanhai Area, Foshan, Guangdong 528000, PR China. Email: dzhg168@126.com
Received: 03-01-2024; Accepted: 08-04-2024.
Volume 20, Issue 4 · pp. 1295–1303 · PUBLISHED 2024 · DOI: 10.1177/09731296241252202
View on Pharmacogn. Mag. original site ↗
ABSTRACT
Background: Altitude sickness is often prone to occur during tourism or work in high-altitude areas. In China, traditional Tibetan medicines have a long history of preventing or treating altitude sickness, especially altitude hypoxia, which may lead to myocardial cell apoptosis and myocardial hypoxia-reoxygenation injury. Purpose: This study investigated the effect of a Tibetan-origin edible Chinese herbal prescription (named C18) on protecting H9C2 cardiomyocytes from cobalt chloride-induced hypoxia injury and its potential mechanism. Materials and Methods: In this study, a hypoxic injury model of H9C2 cardiomyocytes induced by cobalt chloride was established first. Then the cell viability, relevant antioxidant indicators malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and protein expression (hypoxia-inducible factor 1 alpha (HIF-1α), phosphoinositide 3-kinase (PI3K), phosphorylated protein kinase B (p-AKT)) were measured after pretreatment with or without C18. At last, the specific PI3K/AKT inhibitor LY294002 was applied to verify the antihypoxia signaling pathway. Results: C18 could significantly promote normal H9C2 cardiomyocyte proliferation and inhibit apoptosis of hypoxic H9C2 cardiomyocytes, reduce the release of lactate dehydrogenase and MDA, and increase the levels of SOD and GSH-Px antioxidant enzymes. In addition, C18 could significantly downregulate the expression of HIF-1α protein and upregulate the expression of intracellular p-AKT. Moreover, these effects of C18 can be blocked by the specific PI3K/AKT inhibitor LY294002. Conclusion: C18 protects H9C2 cardiomyocytes from cobalt chloride-induced hypoxia injury through the PI3K/AKT signaling pathway.
KEYWORDS
REFERENCES
As publishedShowing references and in-text citations exactly as published.
Cite this article
SELECT FORMAT
Chang, G., Xie, H., Chen, S., Wang, R., Zeng, X., Lin, D., Mo, Z., Yu, J., Liu, X., Zheng, Z., & Wang, Y. (2024). Tibetan-Origin Edible Chinese Herbal Prescription C18 Protects H9C2 Cardiomyocytes from Cobalt Chloride-induced Hypoxia Injury through the PI3K/AKT Signaling Pathway. Pharmacognosy Magazine, 20(4), 1295–1303. https://doi.org/10.1177/09731296241252202
