Berberine protects against palmitate induced beta cell injury via promoting mitophagy

• Published in: Genes & genomics 2022, 44(7), , pp.867-878
• Main Authors: Li, Mo, She, Jiang, Ma, Louyan, Ma, Li, Ma, Xiaorui, Zhai, Jiajia
• Format: Article
• Language: English
• Subjects: Animal Genetics and Genomics; Antioxidants; Apoptosis; Berberine; Beta cells; Biomedical and Life Sciences; Cell injury; Cell viability; Diabetes; Diabetes mellitus; Diabetes therapy; Enzymes; Human Genetics; Insulin; Insulin secretion; Life Sciences; Membrane potential; Microbial Genetics and Genomics; Mitochondria; Mitophagy; Oxidative stress; Palmitic acid; Pancreas; Pancreatic beta cells; Plant Genetics and Genomics; PTEN-induced putative kinase; Research Article; 생물학
• ISSN: 1976-9571; 2092-9293
• DOI: 10.1007/s13258-022-01250-z

Background Destruction of pancreatic beta cells is the most typical characteristic of diabetes. Objective We aimed to evaluate the effect of berberine (BBR), a bioactive isoquinoline derivative alkaloid, on beta cell injury. Methods Rodent pancreatic beta cell line INS-1 was treated with 0.5 mM palmitate (PA) for 24 h to establish an in vitro beta cell injury model. Results BBR at 5 µM promoted cell viability, inhibited cell apoptosis and enhanced insulin secretion in PA-induced INS-1 cells. BBR treatment also suppressed PA-induced oxidative stress in INS-1 cells, as evidenced by the decreased ROS production and increased activities of antioxidant enzymes. In addition, suppressed ATP production and reduced mitochondrial membrane potential were restored by BBR in PA-treated INS-1 cells. It was further determined that BBR affected the expressions of mitophagy-associated proteins, suggesting that BBR promoted mitophagy in PA-exposed INS-1 cells. Meanwhile, we found that BBR facilitated nuclear expression and DNA-binding activity of Nrf2, an antioxidative protein that can regulate mitophagy. Finally, a rescue experiment was performed and the results demonstrated that the effect of BBR on cell viability, apoptosis and mitochondrial function in PA-induced INS-1 cells were cancelled by PINK1 knockdown. Conclusions BBR protects islet β cells from PA-induced injury, and this protective effect may be achieved by regulating mitophagy. The present study may provide a novel therapeutic strategy for β cell injury in diabetes mellitus.