Thymoquinone ameliorate oxidative stress, GABAergic neuronal depletion and memory impairment through Nrf2/ARE signaling pathway in the dentate gyrus following cypermethrin administration.

BACKGROUND: Exposure to chemical toxins, including insecticides, harms bodily organs like the brain. This study examined the neuroprotective of thymoquinone on the cypermethrin's harmful effects on the histoarchitecture of the dentate gyrus and motor deficit in the dentate gyrus. METHODS: Forty adult male rats (180-200 g) were randomly divided into 5 groups (n = 8 per group). Groups I, II, III, IV, and V received oral administration of 0.5 ml of phosphate-buffered saline, cypermethrin (20 mg/kg), thymoquinone (10 mg/kg), cypermethrin (20 mg/kg) + thymoquinone (5 mg/kg), and cypermethrin (20 mg/kg) + thymoquinone (10 mg/kg) for 14 days respectively. The novel object recognition test that assesses intermediate-term memory was done on days 14 and 21 of the experiment. At the end of these treatments, the animals were euthanized and taken for cytoarchitectural (hematoxylin and eosin; Cresyl violet) and immunohistochemical studies (Nuclear factor erythroid 2-related factor 2 (Nrf2), Parvalbumin, and B-cell lymphoma 2 (Bcl2). RESULT: The study shows that thymoquinone at 5 and 10 mg/kg improved Novelty preference and discrimination index. Thymoquinone enhanced Nissl body integrity, increased GABBAergic interneuron expression, nuclear factor erythroid 2-derived factor 2, and enhanced Bcl-2 expression in the dentate gyrus. It also improved the concentration of nuclear factor erythroid 2-derived factor 2, increased the activities of superoxide dismutase and glutathione, and decreased the concentration of malondialdehyde level against cypermethrin-induced neurotoxicity. CONCLUSION: thymoquinone could be a therapeutic agent against cypermethrin poisoning.

Honey prevents neurobehavioural deficit and oxidative stress induced by lead acetate exposure in male Wistar rats- a preliminary study.

This research sought to investigate the possible neuroprotective effects of honey against lead (Pb)-induced neurotoxicity. Twenty four male Wistar rats were divided into four groups: Control group that received 1 ml/kg distilled orally for 28 days; while groups II-IV received 0.2% lead in drinking water and 1 ml/kg of distilled water, 1 ml/kg of honey, 1.5 ml/kg of honey respectively for 28 days. Anxiety and exploratory activities were determined in the open field test. Memory function was determined using Morris water maze after which the animals were sacrificed. The brains were then excised, homogenized and Lipid peroxidation (MDA), Superoxide dismutase (SOD), Catalase, Glutathione (GSH) and Glutathione -S- Transferase (GST) activities were determined in the brains. Results showed that lead exposure causes decrease in locomotor and exploratory activities; increase anxiety, memory impairment, lipid peroxidation and decrease antioxidant activities. However, co-administration of honey with lead inhibited neurotoxicity as indicated by the improvement in memory function as evidenced by decreased latency period and increased in time spent in target quadrant in honey-fed rats compared to the lead-exposed animals. Furthermore, honey increased locomotion, exploration and decreased anxiety in lead-exposed rats as indicated by the frequency of rearing, freezing duration and the number of line crossed by animals. Also administration of honey improves antioxidant activities as shown by increased brain SOD, GST and GSH activities compared to the lead-treated groups but no significant effect on MDA level. It can be concluded that honey has neuroprotective effects against lead-induced cognitive deficit probably by enhancing antioxidant activities.