Abstract
Hyperglycemia, as well as diabetes mellitus, has been shown to trigger cardiac cell apoptosis. We have previously demonstrated that myricitrin prevents endothelial cell apoptosis. However, whether myricitrin can attenuate H9c2 cell apoptosis remains unknown. In this study, we established an experiment model in H9c2 cells exposed to high glucose. We tested the hypothesis that myricitrin may inhibit high glucose (HG)-induced cardiac cell apoptosis as determined by TUNEL staining. Furthermore, myricitrin promoted antioxidative enzyme production, suppressed high glucose-induced reactive oxygen species (ROS) production and decreased mitochondrial membrane potential (MMP) in H9c2 cells. This agent significantly inhibited apoptotic protein expression, activated Akt and facilitated the transcription of NF-E2-related factor 2 (Nrf2)-mediated protein (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1) expression as determined by Western blotting. Significantly, an Akt inhibitor (LY294002) or HO-1 inhibitor (ZnPP) not only inhibited myricitrin-induced HO-1/NQO-1 upregulation but also alleviated its anti-apoptotic effects. In summary, these observations demonstrate that myricitrin activates Nrf2-mediated anti-oxidant signaling and attenuates H9c2 cell apoptosis induced by high glucose via activation of Akt signaling.
Highlights
Diabetes mellitus (DM) is a chronic complex disease and is a leading cause of morbidity and mortality worldwide
We investigated the potential role of myricitrin against high glucose-induced
Myricitrin had no toxic impact on H9c2 cells (Figure S1B)
Summary
Diabetes mellitus (DM) is a chronic complex disease and is a leading cause of morbidity and mortality worldwide. The strategies to anti-inflammatory properties, has recently attracted much attention been demonstrated that reduce oxidative stress-induced apoptosis remain limited InHeme addition, studies have an shown that the activation of nuclear anti-inflammatory properties, has recently attracted much attention [10] It has been demonstrated (Nrf2) can promote HO-1 expression [12]. Deficiency of Nrf hinders HO-1 expression and that induction of HO-1 plays a crucial role in unconjugated bilirubin-mediated vascular benefits in aggravates oxidative stress both during myocardial hypertrophy induced by angiotensin II [13] and in diabetic mice [11].
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