Hydrogen peroxide-induced oxidative stress, acetylcholinesterase inhibition, and mediated brain injury attenuated by Thymus algeriensis.

The aim of the current study was to evaluate acetylcholinesterase (AChE) inhibition, antioxidant enzyme activities, and malondialdehyde (MDA) levels induced by hydrophobic fractions of Thymus algeriensis (HFTS) growing in Tunisia. The results showed that hydrogen peroxide (HO), an oxidative stress inducer, acts by decreasing the body mass and brain mass of rats. Moreover, we found higher MDA levels in the group treated with HO (P < 0.05) and a significantly lower activity of catalase, glutathione peroxidase, glutathione S-transferase, and superoxide dismutase, as well as a reduction in reduced glutathione activity in the brain tissues of HO-treated rats when compared with those of the control group (P < 0.05); however, rats that received HFTS with HO experienced a decrease in MDA levels in the brain. In contrast, HFTS demonstrated neuroprotective effects in rat brain. Overall, exposure to HFTS prior to HO induced a marked dose-dependent increase in reactive oxygen species scavenger levels (P < 0.05) accompanied by a statistically significant decrease in MDA levels (P < 0.05) when compared with no exposure. Notably, the activity of AChE was affected by exposure to natural compounds; levels were significantly lower in HFTS-treated rats and in those treated with the combination of HFTS and a low or high dose of HO. Furthermore, histopathological analysis showed that brain injuries occurred with high doses of HO administered alone or with a low dose of HFTS, whereas a high dose of essential oil markedly alleviated neurone degeneration. The results suggest that HFTS alleviates neuroinflammation by acting as an AChE inhibitor and attenuates HO-induced brain toxicity.