Empagliflozin nanoparticles attenuates type2 diabetes induced cognitive impairment via oxidative stress and inflammatory pathway in high fructose diet induced hyperglycemic mice

There is snowballing evidence that type 2 diabetes (T2D) predisposes to neuropathophysiological alterations including oxidative stress and triggered inflammatory responses in brain that eventually culminates into cognitive impairment.Accumulating evidences suggest that SGLT2 inhibitor can be a promising intervention for cognitive decline in T2DM. In the present paper, the potential effects of Empagliflozin (EMPA), a SGLT2 inhibitor, against T2D induced cognitive dysfunction have been explored. The effect of EMPA on array of inflammatory mediators including Interleukin-6(IL-6), Interleukin -1 beta (IL-1 beta), and Tumour necrosis factor-alpha(TNF alpha)), neuronal proteins including glycogen synthase kinase-3 beta (GSK- 3 beta), Phosphorylated tau (p-tau), amyloid beta (A beta) (1-40, 1-42) and altered oxidative parameters including SOD, catalase, TBARS was determined in the high fructose diet induced hyperglycaemic mice. The obtained results were compared with EMPA nanoparticles (Nps) formulated in our laboratory and found that EMPA Nps significantly showed reduced levels of inflammatory mediators and oxidative stress. Further, decrease in levels of p-tau, A beta (1-40) and A beta (1-42) were also observed with EMPA nanoparticles.Thus, the study has demonstrated that EMPA Nps could be a promising therapy to alleviate the progression of cognitive decline in T2D.

Automated summary

The study explores the potential effects of the SGLT2 inhibitor Empagliflozin on cognitive dysfunction induced by T2D. The results show that EMPA Nps significantly reduce levels of inflammatory mediators and oxidative stress, as well as decrease levels of neuronal proteins and amyloid beta, suggesting a promising therapy for cognitive decline in T2D.