Camel milk rescues neurotoxic impairments induced by fenpropathrin via regulating oxidative stress, apoptotic, and inflammatory events in the brain of rats

Abstract

This study explored the camel milk (CM) efficacy to ameliorate the fenpropathrin (FNP) induced neurotoxic impacts in rats. Six groups were orally administered physiological saline, corn oil, CM (2ml/rat/day), FNP (15 mg/kg bw daily for 60 days), CM/FNP (protective) or FNP + CM (therapeutic). Sensorimotor functions, memory, exploratory, and locomotor activities were assessed. The levels of dopamine (DOPA) neurotransmitter, acetylcholinesterase (AChE) enzyme, oxidative stress, and inflammatory markers were determined. Brain histopathology and apoptotic markers immunohistochemical detection were performed. The results revealed that FNP exposure resulted in deficit sensorimotor functions, impaired memory, and less exploration. DOPA and AChE Levels were significantly reduced. FNP exposure increased nitric oxide, malondialdehyde, myeloperoxidase, Caspase-3, and tumor necrosis factor-alpha levels but interleukin 10, total antioxidant capacity, and Bcl-2 levels were declined. Also, FNP exposure induced obvious encephalopathy. Additionally, neurodegenerative changes were seen in the hippocampi of FNP-treated rats. FNP Exposure induced a significant decrease of Bcl-2 immunolabelling but Caspase-3 immunoexpression was increased in cerebral cortices and hippocampus tissues. CM significantly counteracted the FNP injurious impacts, especially when used as a prophylactic routine than a therapeutic one. Conclusively, these findings confirmed that CM could be a biologically effective protective agent against FNP induced neurobehavioral aberrations and neurotoxic impacts.

Keywords: Apoptosis; Camel milk; Dopamine; Fenpropathrin; Interleukins; Sensorimotor functions.