Icariin ameliorates viral myocarditis by inhibiting TLR4-mediated ferroptosis
10.4103/apjtb.apjtb_588_23
- Author:
Wei Luo
1
;
Yi Lu
2
;
Jun-Hua Deng
3
;
Peng Liu
4
;
Yan Huang
5
;
Wan-Xi Liu
6
,
7
;
Chun-Li Huang
8
Author Information
1. Laboratory of the Atherosclerosis and Ischemic Cardiovascular Diseases, Department of Cardiology, Affiliated Hospital of Youjiang Medical University for Nationalities, Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China
2. Department of Critical Care Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China
3. Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China
4. Postgraduate School of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China
5. Department of Neonatology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China
6. Department of Nephrology, People&rsquo
7. s Hospital of Pubei, Qinzhou, Guangxi 535300, China
8. Urban Community Health Service Center of Youjiang District, Baise, Guangxi 533000, China
- Publication Type:Journal Article
- Keywords:
Viral myocarditis;
CVB3;
TLR4;
Ferroptosis;
Icariin
- From:Asian Pacific Journal of Tropical Biomedicine
2024;14(3):106-114
- CountryChina
- Language:English
-
Abstract:
Objective: To explore the mechanism by which icariin alleviates viral myocarditis. Methods: CVB3-induced cardiomyocytes were used as an in vitro model of viral myocarditis to assess the effects of icariin treatment on cell viability, inflammation, and apoptosis. Moreover, the effects of icariin on ferroptosis and TLR4 signaling were assessed. After AC16 cells were transfected with TLR4 overexpression plasmids, the role of TLR4 in mediating the regulatory effect of icariin in viral myocarditis was investigated. Results: Icariin significantly elevated cell viability and reduced inflammatory factors TNF-α, IL-1β, IL-6, and IL-18. Flow cytometry revealed that icariin decreased apoptosis rate, and the protein expression of Bax and cleaved caspase 3 and 9 in CVB3-induced cardiomyocytes. Additionally, it suppressed ferroptosis including lipid peroxidation and ferrous ion, as well as the TLR4 signaling. However, TLR4 overexpression abrogated the modulatory effects of icariin. Conclusions: Icariin mitigates CVB3-induced myocardial injury by inhibiting TLR4-mediated ferroptosis. Further animal study is needed to verify its efficacy.
- Full text:20240303.pdf
