Type 1 diabetes is a chronic immune-mediated disease caused by pancreatic β-cell dysfunction with consequent severe insulin deficiency. Exacerbated blood glucose levels can cause oxidative stress in the pancreatic β-cells, which leads to inflammation, and apoptosis resulting in islet dysfunction. Although massive studies have been carried out to elucidate the causative factors for β-cell damage in diabetes, the therapeutic approach to pancreatic β-cell damage has not been extensively studied. Hence, the present study has been designed to delineate the role of gymnemic acid (GA) in protecting pancreatic β-cells in diabetic animals, with special reference to inflammation and apoptosis. Our data revealed that the treatment with GA significantly reverted the alteration in both biochemical and histochemical observations in young diabetic rats. Moreover, treatment with the GA downregulates the expression of proinflammatory markers (nuclear factor-κB, tumor necrosis factor-α, interleukin-[IL]-6, and IL-1β), proapoptotic proteins (Bax, cytochrome c, and cleaved caspase-3), as well as upregulates the expression of antiapoptotic protein Bcl-2 in diabetic rats. These findings suggest that the anti-inflammatory and antiapoptotic nature of GA mitigates β-cell damage in hyperglycemic rats.
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