Department of Cardiology, Shanxi Provincial People's Hospital, Taiyuan, Shanxi, P.R. China.
PLoS One. 2020 Nov 5;15(11):e0241007. doi: 10.1371/journal.pone.0241007. eCollection 2020.
Kaempferol, a natural flavonoid compound, possesses potent myocardial protective property in ischemia/reperfusion (I/R), but the underlying mechanism is not well understood. The present study was aimed to explore whether miR-21 contributes to the cardioprotective effect of kaempferol on hypoxia/reoxygenation (H/R)-induced H9c2 cell injury via regulating Notch/phosphatase and tensin homologue (PTEN)/Akt signaling pathway. Results revealed that kaempferol obviously attenuates H/R-induced the damages of H9c2 cells as evidence by the up-regulation of cell viability, the down-regulation of lactate dehydrogenase (LDH) activity, the reduction of apoptosis rate and pro-apoptotic protein (Bax) expression, and the increases of anti-apoptotic protein (Bcl-2) expression. In addition, kaempferol enhanced miR-21 level in H9c2 cells exposed to H/R, and inhibition of miR-21 induced by transfection with miR-21 inhibitor significantly blocked the protection of kaempferol against H/R-induced H9c2 cell injury. Furthermore, kaempferol eliminated H/R-induced oxidative stress and inflammatory response as illustrated by the decreases in reactive oxygen species generation and malondialdehyde content, the increases in antioxidant enzyme superoxide dismutase and glutathione peroxidase activities, the decreases in pro-inflammatory cytokines interleukin (IL)-1β, IL-8 and tumor necrosis factor-alpha levels, and an increase in anti-inflammatory cytokine IL-10 level, while these effects of kaempferol were all reversed by miR-21 inhibitor. Moreover, results elicited that kaempferol remarkably blocks H/R-induced the down-regulation of Notch1 expression, the up-regulation of PTEN expression, and the reduction of P-Akt/Akt, indicating that kaempferol promotes Notch1/PTEN/AKT signaling pathway, and knockdown of Notch1/PTEN/AKT signaling pathway induced by Notch1 siRNA also abolished the protection of kaempferol against H/R-induced the damage of H9c2 cells. Notably, miR-21 inhibitor alleviated the promotion of kaempferol on Notch/PTEN/Akt signaling pathways in H9c2 cells exposed to H/R. Taken together, these above findings suggested thatmiR-21 mediates the protection of kaempferol against H/R-induced H9c2 cell injuryvia promoting Notch/PTEN/Akt signaling pathway.
山奈酚是一种天然类黄酮化合物,具有很强的心肌缺血/再灌注(I/R)保护作用,但作用机制尚不清楚。本研究旨在探讨 miR-21 是否通过调节 Notch/磷酸酶和张力蛋白同源物(PTEN)/Akt 信号通路参与山奈酚对缺氧/复氧(H/R)诱导的 H9c2 细胞损伤的保护作用。结果表明,山奈酚明显减轻 H/R 诱导的 H9c2 细胞损伤,表现为细胞活力升高,乳酸脱氢酶(LDH)活性降低,凋亡率和促凋亡蛋白(Bax)表达降低,抗凋亡蛋白(Bcl-2)表达升高。此外,山奈酚增强了 H9c2 细胞暴露于 H/R 时的 miR-21 水平,而用 miR-21 抑制剂转染抑制 miR-21 显著阻断了山奈酚对 H/R 诱导的 H9c2 细胞损伤的保护作用。此外,山奈酚消除了 H/R 诱导的氧化应激和炎症反应,表现为活性氧生成和丙二醛含量减少,抗氧化酶超氧化物歧化酶和谷胱甘肽过氧化物酶活性增加,促炎细胞因子白细胞介素(IL)-1β、IL-8 和肿瘤坏死因子-α水平降低,抗炎细胞因子白细胞介素(IL)-10 水平升高,而山奈酚的这些作用均被 miR-21 抑制剂逆转。此外,结果表明,山奈酚显著阻断了 H/R 诱导的 Notch1 表达下调、PTEN 表达上调以及 P-Akt/Akt 减少,表明山奈酚促进了 Notch1/PTEN/Akt 信号通路,Notch1 siRNA 诱导的 Notch1/PTEN/Akt 信号通路阻断也消除了山奈酚对 H/R 诱导的 H9c2 细胞损伤的保护作用。值得注意的是,miR-21 抑制剂减轻了 H/R 条件下山奈酚对 Notch/PTEN/Akt 信号通路的促进作用。综上所述,这些发现表明,miR-21 通过促进 Notch/PTEN/Akt 信号通路介导山奈酚对 H/R 诱导的 H9c2 细胞损伤的保护作用。