Neuroprotective Effects of Virgin Coconut Oil Supplemented Diet against Sodium Benzoate-induced Acetylcholinesterase Dysfunction and Cognitive Impairment: Role of Nrf2/NfKb Signaling Pathway.

Q4 Medicine
Abraham Asuku
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Abstract

The effect of virgin coconut oil (VCO) supplemented diet on sodium benzoate (SB) - induced neurotoxicity in male Wistar rats was investigated. Twenty (20) male Wistar rats weighing 160-180g were divided into four (4) groups: Control which received 1ml of normal saline, SB-treated; received 200 mg/kg b.w, SB + Low Dose VCO-treated (SB + 5% VCO mixed with 95g of rat chow), and SB + High Dose VCO-treated (SB+ 15% VCO mixed with 85g of rat chow). The brain was processed for NRF-2, NF-kB, and acetylcholine esterase (AchE) gene expression levels. Also, the blood sample was processed for assessment of superoxide dismutase (SOD), catalase (CAT), and IL1B levels. One-way ANOVA and Tukey post hoc tests were used to analyze data. SB-treated rats with no intervention showed anxiety-like behavior and impaired memory as depicted by a significant (p<0.0001) increase in anxiety index, increase in brain NF-KB, increase in serum IL1B and increase in AchE gene expression level, reduction in the recognition ratio, decreased spontaneous alternation performance, decreased CAT and SOD levels and decreased NRF-2 expression level when compared to other groups (especially control and SB + 5% VCO). VCO supplemented diet (both 5% and 15%) significantly (p<0.0001) increased the CAT and SOD levels, increased the NRF-2 gene expression level, and significantly (p <0.0001) decreased the IL1-B level. Moreover, 5% VCO significantly (p<0.0001) decreased the anxiety index, decreased AchE and NFkB gene expression levels, increased spontaneous alternation performance, and increased recognition ratio compared to 15% VCO. VCO shows a neuroprotective effect in attenuating cognitive impairment and anxiety-like behavior in SB-induced model by modulating oxidative stress and inflammatory pathways, and also enhancing cholinergic neurotransmission. Keywords: Virgin coconut oil; sodium benzoate; acetylcholinesterase; catalase; superoxide dismutase; oxidative stress.

初椰油补充饮食对苯甲酸钠诱导的乙酰胆碱酯酶功能障碍和认知障碍的神经保护作用:Nrf2/NfKb信号通路的作用
研究了添加初榨椰子油(VCO)的日粮对苯甲酸钠(SB)诱导的雄性Wistar大鼠神经毒性的影响。20只雄性Wistar大鼠,体重160-180g,分为4组:对照组给予生理盐水1ml,SB处理;接受200mg/kg b.w,SB+低剂量VCO处理(SB+5%VCO与95g大鼠食物混合),和SB+高剂量VCO治疗(SB+15%VCO和85g大鼠饮食混合)。对大脑进行NRF-2、NF-kB和乙酰胆碱酯酶(AchE)基因表达水平的处理。此外,对血样进行处理以评估超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和IL1B水平。采用单因素方差分析和Tukey事后检验对数据进行分析。未经干预的SB治疗大鼠表现出焦虑样行为和记忆力受损,表现为焦虑指数显著(p<0.0001)增加,大脑NF-KB增加,血清IL1B增加,AchE基因表达水平增加,识别率降低,自发交替能力下降,与其他组(尤其是对照组和SB+5%VCO)相比,CAT和SOD水平降低并且NRF-2表达水平降低。添加VCO的饮食(5%和15%)显著(p<0.0001)增加了CAT和SOD水平,增加了NRF-2基因表达水平,并显著(p<0.00001)降低了IL1-B水平。此外,与15%的VCO相比,5%的VCO显著降低了焦虑指数(p<0.0001),降低了AchE和NFkB基因表达水平,提高了自发交替性能,并提高了识别率。在SB诱导的模型中,VCO通过调节氧化应激和炎症途径,以及增强胆碱能神经传递,在减轻认知障碍和焦虑样行为方面显示出神经保护作用。关键词:初榨椰子油;苯甲酸钠;乙酰胆碱酯酶;过氧化氢酶;超氧化物歧化酶;氧化应激
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来源期刊
Nigerian Journal of Physiological Sciences
Nigerian Journal of Physiological Sciences Medicine-Physiology (medical)
CiteScore
0.80
自引率
0.00%
发文量
23
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