Background: Benzodiazepines (BZDs) are a class of depressant drugs that have enjoyed widespread use
in conventional clinical management of anxiety-related conditions such as panic disorders that require
therapeutic central relaxation and sedation. Meanwhile, prolonged administration of benzodiazepines even
at low doses has however been linked to variety of undesirable effects such as discontinuation relapse with
the associated risk of abuse and dependency. Aim: This study investigated the behavioral, histological
and biochemical outcomes of long-term low dose diazepam use and explored the potential role of nigella
sativa oil (NSO) in the amelioration of the associated side effects. Methods: Adult Wistar rats (n=32)
were randomized into four groups that received normal saline; diazepam; diazepam + NSO; or NSO only,
respectively for 14 days. At the end of the period of the various exposures, the rats were taken through
behavioral paradigms after which they were sacrificed for chemical and histological profiling. Results:
diazepam-exposed rats exhibited stress-related manifestations with relatively poor performance in memory-
related tasks. Repeated diazepam ingestion reduced brain antioxidant biomarkers while causing elevation
of brain oxidative stress markers. On histological observation, mild degenerative changes were evident
in the various brain regions of the diazepam-exposed rats. Conclusion: Interventional nigella sativa oil
administration showed therapeutic potentials by mitigating and reversing the observed effects of diazepam,
largely due to its antioxidant and anti-inflammatory effects as observed in the present study.

Background: Pyrethroids pose health risks to humans. Therefore, it is imperative to assess the preventive
benefits of thymoquinone against neurotoxicity induced by cypermethrin- in the hippocampal dentate
gyrus. Methods: Forty male adult Wistar rats with an average weight of 180-200g were randomly allocated
to five (5) groups, and each comprising eight rats (n=8 per group). The groups were designated
as follows, through oral administrations for 14 days: 0.5ml phosphate- buffered saline (PBS) was given
to group one; Group two received 20mg/kg of cypermethrin (CYM); Group three received 10 mg/kg of
thymoquinone (THQ); Group four received 20 mg/kg of cypermethrin followed by 10mg/kg of thymoquinone
(CYM-10mgTHQ); and Group five received 20 mg/kg and 5mg/kg cypermethrin and thymoquinone
respectively (CYM-5 mgTHQ). Behavioral, histological, immunohistochemical, and biochemical analyses
were conducted post-treatment. Results: Cypermethrin administration caused the rise in pro-inflammatory
cytokine TNF-α, Nuclear Factor-kappa B (NF-κB) and increased expression of astrocytes, microglia, and
pro-apoptotic protein Bax. Additionally, cypermethrin reduced levels of anti-inflammatory cytokine IL-10
and acetylcholinesterase (AChE) activity. Cytoarchitectural disruption of dentate gyrus were observed.
Cognitive deficits were evident. Thymoquinone treatment attenuated TNF-α and NF-κB elevation, reduced
astrocyte, microglial, and Bax expression, and increased IL-10 and AChE. Conclusion: Thymoquinone
demonstrated anti-inflammatory and anti-apoptotic effects against cypermethrin-induced neurotoxicity,
improving cognitive function in rats.