摘要:
目的:探讨龙须菜多糖(GPs)对D-半乳糖(D-gal)及氯化铝(AlCl3)诱导的大鼠神经毒性的保护效果。方法:采用腹腔注射D-gal及AlCl3 42 d的方法建立阿尔茨海默病(AD)大鼠模型。将大鼠分为对照组、AD组、AD+GPs(300 mg/kg,口服)组及AD+GPs(600 mg/kg,口服)组。采用Morris水迷宫(MWM)评估动物行为反应,进行海马氧化应激参数及组织病理学研究。结果:与AD组相比,口服GPs在获得性训练的第2、3及4 d显著地降低了平均逃避潜伏期(低剂量GPs组与AD组相比:相应地,P<0.05、0.05及0.01;高剂量GPs组与AD组相比:相应地,P<0.01、0.01及0.01)。在空间探索实验中,GPs组大鼠穿越平台次数极显著地高于AD组(P<0.01)。与AD组相比,低剂量及高剂量GPs均能很好地维持锥体神经元的有序排列。口服GPs可极显著地缓解海马超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性的降低(P<0.01)。此外,口服GPs还可极显著地抑制D-gal及AlCl3诱导的丙二醛(MDA)水平的升高(P<0.01)。结论:GPs可保护D-gal及AlCl3毒性所引起的大鼠认知损伤及海马组织形态学改变。GPs的神经保护效果可能通过其抗氧化及自由基清除作用来介导。
Abstract:
Objective:To explore the protective effects of Gracilaria lemaneiformis polysaccharides(GPs)on D-galactose(D-gal)and aluminumchloride(AlCl3) induced neurotoxicity in rats. Methods:Alzheimer’s disease(AD) rats was established by injecting both D-gal and AlCl3 into abdominal cavity for 42 d. Rats were divided into control group,AD group,AD+GPs(300 mg/kg,p.o.)group and AD+GPs(600 mg/kg,p.o.)group. Behavioral responses of animals were assessed in a Morris water maze(MWM). Oxidative stress parameters and histopathological studies were carried out in hippocampus. Results:Oral administration of GPs significantly decreased mean escape latency time as compared to the AD group on the second,third,fourth day of the acquisition trial(low-dose GPs group vs. the AD group:P<0.05,0.05 and 0.01,respectively;high-dose GPs group vs. the AD group:P<0.01,0.01 and 0.01,respectively). In the spatial exploration test,rats treated with GPs got higher numbers of platform crossings than that in the AD group(P<0.01). Compared with the AD group,both low-dose and high-dose GPs treatments could well maintain the ordered arrangement of pyramidal neurons. The reduction of the hippocampus superoxide dismutase(SOD)and glutathione peroxidase(GSH-Px)activities were ameliorated by oral administration of GPs(all P<0.01).Furthermore,oral administration of GPs significantly prevented D-gal and AlCl3-induced rise in malondialdehyde(MDA)level(all P<0.01). Conclusion:GPs could protect cognitive impairments and morphological alterations caused by D-gal and AlCl3 toxicity in rats. The neuroprotective effect of GPs might be mediated through its antioxidant and free radical scavenging effects.
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