Evaluating the antioxidant-mediated neuroprotection of hamamelitannin against H₂O₂-induced oxidative damage.

Excessive generation of free radicals disrupts redox equilibrium, inducing oxidative stress. Dementia and other related neurodegenerative illnesses are important ailments associated with oxidative stress. Antioxidant treatment proves effective in reducing oxidative stress and associated neurodegeneration. This study examined the therapeutic potential of Hamamelitannin, a hydrolyzable tannin derived from the barks of L., against the hydrogen peroxide-induced oxidative stress. Hamamelitannin (10-50 μM) had no effects on the hatching, heart rates, and also no lethal malformations were observed. Hammamelitannin exposure significantly (p < 0.05) improved the alterations in swimming behavior and the cognitive impairment caused by HO in a concentration-dependent manner from 10 to 50 μM. It also showed significant restoration of antioxidant enzymes (SOD, CAT, GPx, GST, and GSH), and acetylcholinesterase activity was observed in larvae exposed to hydrogen peroxide compared to the control. Hamamelitannin lowered the MDA and nitric oxide levels in group treated with HO. The Cell death and intracellular ROS levels were assessed using acridine orange and dichlorofluorescein diacetate staining methods. Hamamelitannin significantly (p < 0.05) reduced apoptosis and ROS levels caused by hydrogen peroxide. Furthermore, Hamamelitannin upregulated the expression of antioxidant enzyme genes, indicating its potential in combating oxidative stress. These findings suggest that Hamamelitannin has substantial therapeutic value against neurological disorders associated with ROS accumulation.