Astaxanthin‐s‐allyl cysteine diester attenuated high glucose‐induced oxidative stress toxicity in neuronal cells through protection of mitochondria in vitro

Background Cognitive dysfunction associate with diabetes is related to high glucose‐induced oxidative stress toxicity in neuronal cells. Hence, identifying compounds that protect the neuronal cells against high glucose toxicity is important to overcome cognitive deterioration under diabetic condition. Astaxanthin‐s‐allyl cysteine diester (AST‐SAC) was synthesized by esterification of AST from the source H. pluvialis with SAC, an allyl sulfur compound found in aged garlic extract. AST‐SAC has shown antidiabetic effect in in vivo rat model. Hence, in the present study the effect of AST‐SAC against high glucose‐induced oxidative stress toxicity in neuronal cell line in in vitro was studied. Method AST‐SAC was pre‐treated to neuronal cell line and high glucose toxicity was induced. The cell viability, reactive oxidant species generation, antioxidant status and apoptosis induction was studied. Further, mitochondrial membrane potential, mitochondrial oxidative phosphorylation activity and antioxidant status of mitochondria was measured. Result High glucose‐induced toxicity increased oxidative stress and decreased over all antioxidant status of the neuronal cells. Due to which functions (membrane potential and oxidative phosphorylation) and antioxidant status of mitochondria were reduced. All these dysfunction cumulatively lead to the induction of apoptosis in neuronal cells. However, AST‐SAC pretreatment has protected the neuronal cells against high glucose‐induced apoptosis through reduction of oxidative stress and protection of mitochondrial function. Conclusion Overall AST‐SAC attenuated high‐glucose toxicity induced neuronal injury in in vitro through preservation of mitochondrial function.