Background: Oxidative stress is caused due to the overproduction of the reactive oxygen
species (ROS) and the disturbance developed in the antioxidant potential of biochemical processes.
ROS mostly form in the brain due to the high consumption of oxygen and the insufficiency of endogenous
antioxidant resistance mechanisms. Cytochrome P450 2E1 has an excessive percentage of
NADPH oxidase activity, which causes the production of ROS and increases oxidative stress.
Objectives: We have studied the effect of ethyl acetate extract of Achyranthes Aspera (EAAA) on ROS
in the brain of diabetes-induced rats. We have also investigated the possible molecular mechanism of
reduction in ROS through molecular docking.
Methods: To study the oxidative stress induced by ROS in diabetic rats, we estimated the ROS in rat
brain through flow cytometry. The oral dose of EAAA 50mg/kg and 100 mg/kg was given to diabetesinduced
rats. Results were articulated as mean ± standard deviation (SD). Data were analyzed using
analysis of variance (ANOVA) followed by Bonferroni as a post hoc test. We performed molecular
docking of flavonoids on CYP2E1 to study the inhibitory potential.
Results: The results have shown that EAAA reduces the generation of ROS in the diabetes-induced rat
in a dose-dependent manner. The oral dose of EAAA 50mg/kg and 100 mg/kg was given to the rats
and the ROS generation got affected accordingly. Luteolin, quercetin, and apigenin inhibited the
CYP2E1 very effectively. Luteolin formed 4 hydrogen bonds with CYP2E1, which indicated its potential
inhibition. Although, luteolin and apigenin showed a very good binding affinity with the enzyme.
Conclusion: From the present work, we have concluded that the ethyl acetate extract of achyrantesaspera
can effectively inhibit the ROS generation in the diabetes-induced rats by inhibiting the activity