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.

中文翻译：

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骆驼奶通过调节大鼠脑部的氧化应激，凋亡和炎症事件，挽救了由苯丙酸菊酯引起的神经毒性损伤。

这项研究探讨了骆驼奶（CM）改善苯丙酸菊酯（FNP）诱导的大鼠神经毒性的功效。六组分别口服生理盐水，玉米油，CM（2毫升/大鼠/天），FNP（15毫克/千克体重，每天60天），CM / FNP（保护性）或FNP + CM（治疗性）。感觉运动功能，记忆，探索性和运动活动进行了评估。确定了多巴胺（DOPA）神经递质，乙酰胆碱酯酶（AChE）酶，氧化应激和炎症标志物的水平。进行了脑组织病理学和凋亡标记物的免疫组织化学检测。结果表明，暴露于FNP会导致感觉运动功能不足，记忆力减退和探索不足。DOPA和AChE水平显着降低。FNP暴露会增加一氧化氮，丙二醛，髓过氧化物酶，Caspase-3和肿瘤坏死因子-α水平下降，但白介素10，总抗氧化剂能力和Bcl-2水平下降。另外，FNP暴露引起明显的脑病。另外，在FNP治疗的大鼠的海马中观察到神经退行性改变。FNP暴露诱导脑皮质和海马组织中Bcl-2免疫标记显着减少，但Caspase-3免疫表达增加。CM可以显着抵消FNP的有害影响，尤其是在用作预防措施而不是治疗措施时。最终，这些发现证实了CM可能是针对FNP诱导的神经行为异常和神经毒性影响的生物学有效保护剂。FNP暴露引起明显的脑病。另外，在FNP治疗的大鼠的海马中观察到神经退行性改变。FNP暴露诱导脑皮质和海马组织中Bcl-2免疫标记显着减少，但Caspase-3免疫表达增加。CM可以显着抵消FNP的有害影响，尤其是在用作预防措施而不是治疗措施时。最终，这些发现证实了CM可能是针对FNP诱导的神经行为异常和神经毒性影响的生物学有效保护剂。FNP暴露引起明显的脑病。另外，在用FNP治疗的大鼠的海马中观察到神经退行性改变。FNP暴露诱导脑皮质和海马组织中Bcl-2免疫标记显着减少，但Caspase-3免疫表达增加。CM可以显着抵消FNP的有害影响，尤其是在用作预防措施而不是治疗措施时。最终，这些发现证实了CM可能是针对FNP诱导的神经行为异常和神经毒性影响的生物学有效保护剂。FNP暴露诱导脑皮质和海马组织中Bcl-2免疫标记显着减少，但Caspase-3免疫表达增加。CM可以显着抵消FNP的有害影响，尤其是在用作预防措施而不是治疗措施时。最终，这些发现证实了CM可能是针对FNP诱导的神经行为异常和神经毒性影响的生物学有效保护剂。FNP暴露诱导脑皮质和海马组织中Bcl-2免疫标记显着减少，但Caspase-3免疫表达增加。CM可以显着抵消FNP的有害影响，尤其是在用作预防措施而不是治疗措施时。最终，这些发现证实了CM可能是针对FNP诱导的神经行为异常和神经毒性影响的生物学有效保护剂。