Luteolin inhibits Ang Ⅱ-induced cardiomyocyte hypertrophy in H9c2 cells through Nrf2/HO-1 pathway
10.3760/cma.j.cn121382-20250124-00208
- VernacularTitle:木犀草素通过Nrf2/HO-1通路抑制Ang Ⅱ诱导心肌H9c2细胞肥大
- Author:
Jia YAO
1
;
Yuxia GAO
Author Information
1. 天津医科大学总医院心血管内科，天津 300070
- Keywords:
Luteolin;
Cardiomyocyte hypertrophy;
Oxidative stress;
Nuclear factor-erythroid 2-related factor 2;
Heme oxygenase-1
- From:
International Journal of Biomedical Engineering
2025;48(2):158-164
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of luteolin on angiotensin Ⅱ (Ang Ⅱ)-induced cardiomyocyte hypertrophy in H9c2 cells and to reveal its potential mechanism.Methods:After H9c2 cells were cultured, they were divided into 0, 1, 2 and 4 μmol/L luteolin groups according to different cell treatment conditions. H9c2 cells were stimulated by Ang II to establish a cardiomyocyte hypertrophy model, which was divided into control group, Ang II group and luteolin+Ang II group. Cell survival rates were assessed by cell counting kit-8 assay. The degrees of cell hypertrophy were assessed by phalloidin staining assay. The levels of cellular oxidative stress were assessed by the 2′,7′-dichlorodihydrofluorescein diacetate fluorescent probe assay and thiobarbituric acid assay. The expression of apoptotic protein B-cell lymphoma-2 associated X protein (Bax), cleaved cysteine aspartic acid specific protease-3 (cleaved Caspase-3) and nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway proteins were assessed by Western blotting. The datas were analyzed by t test and one-way analysis of variance. Results:The survival rates of H9c2 cells in the 0, 1, 2, and 4 μmol/L luteolin group were 97.31%, 95.65%, 94.64%, and 93.27%, respectively. The degree of hypertrophy and the fluorescence intensity of H9c2 cells in Ang Ⅱ group were higher than those in the control group. The degree of hypertrophy and the fluorescence intensity of H9c2 cells in the luteolin+Ang Ⅱ group were lower than those in the Ang Ⅱ group. Compared with the control group, the survival rate of H9c2 cells in Ang Ⅱ group was decreased (96.26% vs 51.68%, P<0.01), the level of malondialdehyde was increased [(1.00±0.08) nmol/mg vs (3.27±0.31) nmol/mg, P<0.01], and the relative expression levels of Bax (0.79±0.04 vs 1.55±0.09, P<0.01), cleaved Caspase-3 (0.11±0.02 vs 1.00±0.04, P<0.01), Nrf2 (0.77±0.04 vs 0.95±0.03, P<0.05), and HO-1 (0.12±0.04 vs 0.41±0.05, P<0.01) were all increased. Compared with Ang Ⅱ group, the survival rate of H9c2 cells in the luteolin+Ang Ⅱ group (81.52%) was increased ( P<0.01), the level of malondialdehyde [(1.73±0.21) nmol/mg] was decreased ( P<0.01), the relative expression levels of Bax (1.25±0.05) and cleaved Caspase-3 (0.48±0.07) were decreased ( P<0.05, 0.01), Nrf2 (1.24±0.13) and HO-1 (0.82±0.03) were increased (both P<0.01). Conclusions:Luteolin effectively inhibits Ang Ⅱ-induced cardiomyocyte hypertrophy through the Nrf2/HO-1 pathway and has potential therapeutic value.
