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Rosmarinic Acid suppressed high glucose-induced apoptosis in H9c2 cells by ameliorating the mitochondrial function
Jiayu Diao1, Jin Wei1, Rui Yan1
1Department of Cardiology, The Second Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, China.
Abstract:
Mitochondrial injury characterized by intracellular reactive oxygen species (ROS) accumulation plays a critical role in hyperglycemia-induced myocardium dysfunction. Previous studies have demonstrated that Rosmarinic Acid (RA) treatment and activating Signal transducer and activator of transcription 3 (STAT3) signaling pathway have protective effects on mitochondrial dysfunction in cardiomyocyte, but there is little data regarding cardiomyocyte under condition of high-glucose. The present study was undertaken to determine the relationship between RA and STAT3 activation, as well as their effects on high glucose-induced mitochondrial injury and apoptosis in H9c2 cardiomyocyte. Our results revealed that RA pretreatment suppressed high glucose-induced apoptosis in H9c2 cells. Moreover, the effect of RA on apoptosis was related with improved mitochondrial function, which was demonstrated by that RA attenuated high glucose-induced ROS generation, inhibited mitochondrial permeability transition pore (MPTP) activation, suppressed cytochrome c release and caspase-3 activation. In addition, the phosphorylation of STAT3 in H9c2 cells was inhibited under condition of high-glucose, but RA improved STAT3 phosphorylation. Importantly, inhibition of STAT3 expression by using STAT3-siRNA partly suppressed the effect of RA on high glucose-induced apoptosis. Taken together, pretreatment with RA suppressed high glucose-induced apoptosis in cardiomyocyte by ameliorating mitochondrial function and activating STAT3.
Insights
Rosmarinic Acid protects heart cells from high glucose damage by improving mitochondrial function and activating the STAT3 pathway. This reduces cell death and oxidative stress, offering a potential therapeutic strategy for diabetic heart conditions.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Medicine
- Cellular Signaling
Background:
- Hyperglycemia induces myocardial dysfunction via mitochondrial injury and reactive oxygen species (ROS) accumulation.
- Rosmarinic Acid (RA) and Signal transducer and activator of transcription 3 (STAT3) activation show protective effects on mitochondrial dysfunction.
- Limited data exists on RA and STAT3 in high-glucose-induced cardiomyocyte injury.
Purpose of the Study:
- To investigate the relationship between RA and STAT3 activation.
- To determine the effects of RA and STAT3 on high glucose-induced mitochondrial injury and apoptosis in H9c2 cardiomyocytes.
Main Methods:
- H9c2 cells were treated with high glucose and/or Rosmarinic Acid.
- Mitochondrial function, ROS generation, and apoptosis markers (cytochrome c, caspase-3) were assessed.
- STAT3 phosphorylation and expression were analyzed.
- STAT3 inhibition using siRNA was performed to evaluate its role.
Main Results:
- RA pretreatment inhibited high glucose-induced apoptosis and ROS generation in H9c2 cells.
- RA improved mitochondrial function by inhibiting mitochondrial permeability transition pore (MPTP) activation and cytochrome c release.
- High glucose reduced STAT3 phosphorylation, while RA treatment restored it.
- STAT3 inhibition partially reversed the protective effects of RA.
Conclusions:
- Rosmarinic Acid mitigates high glucose-induced cardiomyocyte apoptosis.
- RA ameliorates mitochondrial dysfunction and activates the STAT3 signaling pathway.
- The protective effects of RA involve the activation of STAT3.
