Nkpaa Kpobari W, Onyeso Godspower I
Environmental Toxicology Unit, Department of Biochemistry, Faculty of Science, University of Port Harcourt, P.M.B 5323, Choba, Rivers State, Nigeria.
Department of Physiology, College of Medicine, Rivers State University, Port Harcourt, P.M.B 5080, Rivers State, Nigeria.
Neurosci Lett. 2018 Aug 24;682:92-99. doi: 10.1016/j.neulet.2018.06.023. Epub 2018 Jun 13.
Studies have shown that high exposure to fluoride (NaF) induces neurotoxicity. Rutin (RUT), a citrus flavonoid, has been reported to have antioxidant, anti-inflammatory and anti-apoptotic properties. The aim of this study was to investigate the neuroprotective mechanism(s) of RUT on NaF - induced neurotoxicity. Rats were exposed to NaF alone in drinking water at 15 mg/L alone ad libitum or orally co-treated by gavage with RUT at 50 and 100 mg/kg body weight for 31 consecutive days. A video-tracking software was used to monitor the motor and locomotive behavior during a 5 - min trial time in a novel environment. Thereafter, acetylcholinesterase (AChE) activity, oxidative stress markers, pro-inflammatory cytokines and caspase - 3 activity were determined in the cerebrum and striatum. The result indicates that NaF - induced neurobehavioral deficits. RUT mediated the reversal of the neurobehavioral deficits and enhanced the exploratory profile of NaF - treated rats as supported by the track plot analyses. Moreover, RUT attenuated the NaF - induced inhibition of antioxidant enzymes and AChE activity and inhibits lipid peroxidation, neuro-inflammation and apoptosis in the cerebrum and striatum of the rats. Collectively, the present study demonstrated that RUT attenuates NaF - Induced toxicity in the cerebrum and striatum of rats via mechanisms involving enhancement of AChE activity, antioxidant status with concomitant inhibition of lipid peroxidation, neuro-inflammation and apoptosis in rats. RUT may be used as a neuroprotective agent against NaF - induced neurotoxicity.
研究表明，高剂量接触氟化物（氟化钠）会诱发神经毒性。芦丁（RUT）是一种柑橘类黄酮，据报道具有抗氧化、抗炎和抗凋亡特性。本研究的目的是探讨芦丁对氟化钠诱导的神经毒性的神经保护机制。大鼠自由饮用含15 mg/L氟化钠的水，或每天经口灌胃给予50和100 mg/kg体重的芦丁，连续31天。使用视频跟踪软件在新环境中的5分钟试验时间内监测运动和 locomotive行为。此后，测定大脑和纹状体中的乙酰胆碱酯酶（AChE）活性、氧化应激标志物、促炎细胞因子和半胱天冬酶-3活性。结果表明氟化钠诱导了神经行为缺陷。轨迹图分析表明，芦丁介导了神经行为缺陷的逆转，并增强了氟化钠处理大鼠的探索能力。此外，芦丁减轻了氟化钠诱导的抗氧化酶抑制和AChE活性，并抑制了大鼠大脑和纹状体中的脂质过氧化、神经炎症和细胞凋亡。总体而言，本研究表明，芦丁通过增强AChE活性、抗氧化状态，同时抑制大鼠脂质过氧化、神经炎症和细胞凋亡的机制，减轻了氟化钠对大鼠大脑和纹状体的毒性。芦丁可用作抗氟化钠诱导的神经毒性的神经保护剂。
