Related Experiment Video
Updated: Mar 26, 2026
Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
Phycocyanin prevents methylglyoxal-induced mitochondrial-dependent apoptosis in INS-1 cells by Nrf2
Yingnv Gao1, Chen Liu1, Guoqing Wan1
1School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China. ouyu2008@126.com.
Abstract:
Methylglyoxal (MG) is a reactive dicarbonyl compound, whose abnormal accumulation in diabetic patients exerts deleterious effects on cells and tissues. The β-cell is the main target cell of Type 2 diabetes, and its insulin secretion injury and cell apoptosis can be due to mitochondrial dysfunction. Previous studies have demonstrated MG induced β-cell apoptosis. However, little is known about the effect of MG on β-cell mitochondrial dysfunction. Phycocyanin (PC) has been demonstrated to possess various biological activities including the effects on diabetic models in vivo. The aim of this study was to determine the protective effect of PC against methylglyoxal (MG)-induced dysfunction in pancreatic β-cell INS-1 and also the mechanism. We demonstrated that MG induced mitochondrial dysfunction by the decline in ATP levels, and the increase of the level of intracellular reactive oxygen species (ROS). Furthermore, MG released cytochrome c and apoptosis-inducing factor (AIF) from the mitochondrion, induced changes in the expression of Bcl-2 family members, activated caspases and increased PARP cleavage. Interestingly, PC activated nuclear erythroid-related factor 2 (Nrf2), and Nrf2 activation as well as antioxidant enzymes HO-1 and glyoxalase 1 (Glo-1) were confirmed to be involved in the mechanisms underlying the protection of PC by RNA interference. Altogether, these results demonstrated that PC prevented mitochondrial-dependent apoptosis in MG-induced INS-1 cells and the effect was associated with Nrf2 activation.
Insights
Phycocyanin (PC) protects pancreatic beta cells from methylglyoxal (MG)-induced apoptosis by preventing mitochondrial dysfunction. PC activates the Nrf2 pathway, reducing oxidative stress and preserving beta cell function in Type 2 diabetes models.
Area of Science:
- Cell Biology
- Biochemistry
- Endocrinology
Background:
- Methylglyoxal (MG), a reactive dicarbonyl compound, accumulates in diabetes and causes pancreatic beta-cell damage.
- Beta-cell dysfunction and apoptosis are key features of Type 2 diabetes, often linked to mitochondrial dysfunction.
- Phycocyanin (PC) exhibits diverse biological activities, including potential benefits in diabetic models.
Purpose of the Study:
- To investigate the protective effects of Phycocyanin (PC) against methylglyoxal (MG)-induced pancreatic beta-cell (INS-1) dysfunction.
- To elucidate the underlying mechanisms of PC's protective action against MG-induced mitochondrial damage and apoptosis.
Main Methods:
- Assessment of mitochondrial dysfunction markers: ATP levels, intracellular reactive oxygen species (ROS).
- Analysis of apoptosis pathways: cytochrome c and AIF release, Bcl-2 family expression, caspase activation, PARP cleavage.
- Investigation of PC's mechanism: Nrf2 activation, HO-1 and Glo-1 expression, RNA interference.
Main Results:
- MG induced mitochondrial dysfunction, characterized by decreased ATP and increased ROS levels in INS-1 cells.
- MG triggered mitochondrial-dependent apoptosis, involving cytochrome c/AIF release and caspase activation.
- PC treatment attenuated MG-induced apoptosis and mitochondrial dysfunction, linked to Nrf2 activation and increased HO-1/Glo-1 expression.
Conclusions:
- Phycocyanin (PC) demonstrates a protective effect against methylglyoxal (MG)-induced mitochondrial dysfunction and apoptosis in pancreatic beta cells.
- The protective mechanism of PC involves the activation of the Nrf2 pathway, leading to enhanced antioxidant enzyme activity.
- PC holds potential for therapeutic intervention in Type 2 diabetes by safeguarding beta-cell function from glycation stress.
