柚皮苷调节溴氰菊酯暴露大鼠的记忆、焦虑、运动和情绪行为的损害;与氧化应激、乙酰胆碱酯酶和三磷酸腺苷酶有关的可能机制

Vinayagam Magendira Mani , Abdul Majeeth Mohamed Sadiq
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引用次数: 25

摘要

接触拟除虫菊酯杀虫剂会导致不良的神经发育结果,比如神经退行性疾病、低智商、广普性发育障碍、注意力问题。因此,我们研究了拟除虫菊酯溴氰菊酯暴露于乙酰胆碱酯酶、atp酶、氧化应激生物标志物与雄性Wistar大鼠行为性能受损的关系,以及饮食中黄酮类柚皮苷可能的改善机制。将成年雄性wistar大鼠分为四组。第一组:对照组;II组给予溶于玉米油中的DLM 12.8 mg/kg BW,口服(1/10 LD50),连续3周;III组口服DLM和柚皮苷(100 mg/kg BW,连续21 d)。第四组:单用柚皮甙。DLM暴露导致皮质和海马区乙酰胆碱酯酶、Na+/K+、Ca2+、Mg2+ atp酶水平降低,酶和非酶抗氧化剂活性降低,TBARS活性升高。dlm诱导的神经元改变表现为行为表现受损,如记忆、焦虑、运动和情绪行为。这也得到了大鼠皮层和海马区的组织病理学结果的支持。然而,柚皮苷治疗可以调节dlm诱导的氧化应激生物标志物、乙酰胆碱酯酶、atp酶和大鼠行为表现的异常变化。这些发现突出了柚皮苷作为神经保护剂的功效。总之,我们的结果表明DLM引起神经行为和生化改变。氧化应激、自由基机制在dlm诱导的神经毒性中起主要作用。柚皮苷具有较强的抗氧化、自由基清除和神经保护作用,可作为防治DLM毒性的理想药物。
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Naringin modulates the impairment of memory, anxiety, locomotor, and emotionality behaviors in rats exposed to deltamethrin; a possible mechanism association with oxidative stress, acetylcholinesterase and ATPase

Exposure to pyrethroid pesticides has been associated with adverse neurodevelopmental outcomes, like neurodegenerative disorder, low IQ, pervasive developmental disorder, attention problems. Thus, we investigated the relationship between pyrethroid deltamethrin exposure to acetylcholine esterase, ATPase, oxidative stress biomarkers, and impaired behavior performance, and the possible ameliorating mechanism of dietary flavonoid naringin in male Wistar rats. Adult male wistar rats were divided into four different groups. Group I: control group; group II received DLM dissolved in corn oil 12.8 mg/kg BW orally (1/10 LD50) for three weeks; group III received DLM as group II and naringin (100 mg/kg BW for 21 days) orally. Group IV: naringin alone. DLM exposure leads to reduction in the levels of acetylcholinesterase, Na+/K+, Ca2+, Mg2+ ATPase, enzymic and non-enzymic antioxidants activities in cortex and hippocampus region and increase the activities of TBARS. DLM-induced neuronal alterations was evidenced by impairment behavioral performance, like memory, anxiety, locomotor, and emotionality behaviors. This is also supported by histopathological findings of cortex and hippocampus region of rats. However, naringin treatment modulates the abnormalities of DLM-induced alterations in oxidative stress biomarkers, acetylcholine esterase, ATPase, and behavioral performance of rats. These findings highlight the efficacy of naringin as neuroprotectant. In conclusion, our results demonstrated that DLM cause neurobehavioral and biochemical alterations. Oxidative stress, free radical mechanism play major role on DLM-induced neurotoxicity. Naringin could be a suitable agent for preventing the toxicity of DLM by its potent antioxidant, free radical scavenging and neuroprotective activity.

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