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Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
Baicalin relieves hypoxia-aroused H9c2 cell apoptosis by activating Nrf2/HO-1-mediated HIF1α/BNIP3 pathway
Hailiang Yu1, Bin Chen1, Qi Ren2
1Department of Cardiology, Linyi Central Hospital , Linyi , China.
Insights
Baicalin, a plant flavonoid, protects heart cells from hypoxia-induced apoptosis by activating the Nrf2/HO-1 pathway, which upregulates HIF1α/BNIP3. This study reveals baicalin
Area of Science:
- Cardiovascular Biology
- Cellular Stress Response
- Pharmacology
Background:
- Myocardial ischemia, a primary cause of ischemic heart disease, leads to cardiomyocyte apoptosis.
- Baicalin, a flavonoid from plants, exhibits known cardioprotective properties.
- Hypoxia is a critical stressor inducing apoptosis in heart cells.
Purpose of the Study:
- To investigate the protective effects of baicalin against hypoxia-induced apoptosis in H9c2 cardiomyocytes.
- To elucidate the molecular pathways involved in baicalin's cardioprotective mechanism.
- To determine the role of the Nrf2/HO-1 and HIF1α/BNIP3 pathways in baicalin's action.
Main Methods:
- H9c2 cells were exposed to hypoxia with or without baicalin treatment.
- Cell viability, apoptosis, and expression of HIF1α and BNIP3 were assessed.
- RNA interference (si-HIF1α) and pathway analysis (Nrf2/HO-1) were employed to dissect the mechanism.
Main Results:
- Hypoxia significantly reduced H9c2 cell viability and induced apoptosis.
- Baicalin treatment attenuated hypoxia-induced cell death and apoptosis.
- Baicalin enhanced the activation of the HIF1α/BNIP3 pathway and the Nrf2/HO-1 pathway under hypoxic conditions.
- Silencing HIF1α diminished the protective effects of baicalin.
- The activation of the Nrf2/HO-1 pathway correlated with HIF1α upregulation and baicalin's protective function.
Conclusions:
- Baicalin effectively mitigates hypoxia-induced apoptosis in H9c2 cardiomyocytes.
- The cardioprotective effects of baicalin are mediated through the activation of the Nrf2/HO-1 pathway, leading to the upregulation of HIF1α and subsequent modulation of the HIF1α/BNIP3 pathway.
- Baicalin represents a potential therapeutic agent for ischemic heart disease.
Abstract:
Background: Myocardial ischemia is the main reason for ischemic heart disease. Baicalin is a plant-derived flavonoid with cardio-protective activity. Herein, we tested the influences of baicalin on cardiomyocytes H9c2 apoptosis aroused by hypoxia stimulation. Methods: Firstly, H9c2 cells were subjected to hypoxia and/or baicalin exposure. Cell viability and apoptosis, along with hypoxia-inducible factor 1α (HIF1α) and Bcl-2/adenovirus E1B 19-KDa interacting protein 3 (BNIP3) expressions were tested respectively. Then, si-HIF1α was transfected into H9c2 cells to probe whether up-regulation of HIF1α attended to the influences of baicalin on hypoxia-stimulated H9c2 cells. Finally, the regulatory effect of nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway on HIF1α expression was analyzed. Results: Hypoxia exposure aroused H9c2 cell viability reduction and apoptosis. Baicalin mitigated H9c2 cell viability reduction and apoptosis aroused by hypoxia. Moreover, HIF1α/BNIP3 pathway was further activated by baicalin in hypoxia-exposed H9c2 cells. Silencing HIF1α lowered the functions of baicalin on hypoxia-exposed H9c2 cells. Besides, baicalin enhanced hypoxia-caused activation of Nrf2/HO-1 pathway. Activation of Nrf2/HO-1 pathway was associated with the up-regulation of HIF1α and protective functions of baicalin on hypoxia-exposed H9c2 cells. Conclusion: Baicalin relieved cardiomyocytes H9c2 apoptosis aroused by hypoxia might be achieved through activating Nrf2/HO-1-mediated HIF1α/BNIP3 pathway. Highlights Baicalin mitigates H9c2 cell viability loss and apoptosis aroused by hypoxia; Baicalin activates HIF1a/BNIP3 pathway in hypoxia-exposed H9c2 cells; Silencing HIF1α weakens the influences of baicalin on hypoxia-exposed H9c2 cells; Baicalin promotes Nrf2/HO-1 pathway in hypoxia-exposed H9c2 cells; Promotion of Nrf2/HO-1 pathway is related to the up-regulation of HIF1α.
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