维生素E对锰中毒大鼠脑损伤的保护作用
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摘要
目的探讨维生素E对锰中毒大鼠脑损伤的保护作用。方法 48只Wistar大鼠随机均分为三组。自然组每天腹腔注射生理盐水30 mg/kg;锰中毒组每天腹腔注射氯化锰溶液15mg/kg;维生素E组在锰中毒组基础上用纯净水稀释维生素E 100mg/kg灌胃给药,每天1次,共18d。比较三组大鼠Morris水迷宫实验的潜伏期时间和空间探索的平台穿越次数,采用免疫组化尼氏染色观察大鼠脑海马CA3区细胞凋亡情况。结果水迷宫实验第3、4天,锰中毒组潜伏期时间较自然组和维生素E组延长(P<0.05)。锰中毒组平台探索次数为(1.92±0.78)次,少于自然组的(3.94±1.35)次和维生素E组的(3.85±1.33)次(P<0.05)。锰中毒组凋亡细胞为(59.8±6.4)个,多于维生素E组的(15.8±5.5)个和自然组的(10.5±1.6)个(P<0.01)。结论维生素E对锰中毒大鼠的脑部损伤有保护作用,提高大鼠的学习记忆能力,减少海马CA3区细胞凋亡。
Objective To investigate the protective effect of vitamin E(VE)on the brain injury in rats with manganese poisoning.Methods Forty-eight Wistar rats were equally divided into three groups.Group A was intraperitoneally injected saline 30 mg/kg,group B was intraperitoneally injected manganese chloride 15 mg/kg and group C was intraperitoneally injected with VE 100 mg/kg on the basis of manganese poisoning,once a day for 18 days.The latent time of Morris water maze experiment and time crossing platform were compared among three groups.The cell apoptosis of hippocampus CA3 area was observed by immunohistochemical staining.Results The latent time was longer in group B than that in groups of A and C on the 3 rd and 4 th day of Morris water maze experiment(P<0.05).The time crossing platform was less and cell apoptosis was more in group B than those in groups of A and C(P<0.05 or P<0.01).Conclusion VE has a protective effect on the brain injury of rats with manganese poisoning,improves the ability of learning and memory and reduces the cell apoptosis of hippocampus CA3 area.
Objective To investigate the protective effect of vitamin E(VE)on the brain injury in rats with manganese poisoning.Methods Forty-eight Wistar rats were equally divided into three groups.Group A was intraperitoneally injected saline 30 mg/kg,group B was intraperitoneally injected manganese chloride 15 mg/kg and group C was intraperitoneally injected with VE 100 mg/kg on the basis of manganese poisoning,once a day for 18 days.The latent time of Morris water maze experiment and time crossing platform were compared among three groups.The cell apoptosis of hippocampus CA3 area was observed by immunohistochemical staining.Results The latent time was longer in group B than that in groups of A and C on the 3 rd and 4 th day of Morris water maze experiment(P<0.05).The time crossing platform was less and cell apoptosis was more in group B than those in groups of A and C(P<0.05 or P<0.01).Conclusion VE has a protective effect on the brain injury of rats with manganese poisoning,improves the ability of learning and memory and reduces the cell apoptosis of hippocampus CA3 area.
引文
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[12]Santos D,Milatovic D,Andrade V,et al.The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the rat brain[J].Toxicology,2012,292(2/3):90-98.
[13]Ye HB,Shi HB,Yin SK.Mechanisms underlying taurine protection against glutamate-induced neurotoxicity[J].Can JNeurol Sci,2013,40(5):628-634.
[14]徐冬辉,徐斌,贺安宁,等.牛磺酸和维生素C对锰致大鼠氧化损伤的拮抗作用[J].毒理学杂志,2014,28(6):457-459.
[15]Kowdley KV,Mason JB,Meydani SN,et al.Vitamin E deficiency and impaired cellular immunity related to intestinal fat malabsorption[J].Gastroenterology,1992,102(6):2139-2142.
[16]Tanyel MC,Mancano LD.Neurologic findings in vitamin Edeficiency[J].Am Fam Physician,1997,55(1):197-201.
[2]李海囡,张萍,付明.锰中毒对植物神经、神经行为功能及神经电生理影响[J].中国职业医学,2011,38(3):225-226.
[3]Ohishi T,Wang L,Akane H,et al.Reversible aberration of neurogenesis affecting late-stage differentiation in the hippocampal dentate gyrus of rat offspring after maternal exposure to manganese chloride[J].Reprod Toxicol,2012,34(3):408-419.
[4]Eriksson PS,Perfilieva E,Bj9rk-Eriksson T,et al.Neurogenesis in the adult human hippocampus[J].Nat Med,1998,4(11):1313-1317.
[5]Eirc A,Ian M,Catherine M,et al,Vitamin E and the risk of prostate cancer[J].JAMA,2011,306(14):1549-1556.
[6]程静菲,尚帅,何贵波,等.DEHP诱导的氧化应激致小鼠学习记忆能力的下降和维生素E的保护作用[J].医学研究杂志,2012,41(5):24-28.
[7]王迪雅,蔡同建,赵芳,等.维生素E抑制锰诱导的PC12细胞毒性的实验研究[J].实用预防医学,2012,19(10):1441-1444.
[8]Finkelesein Y,Zhang N,Fitsanakis VA,et al.Differential deposition of manganese in the rat brain following subchronic exposure to manganese:a T1-weighted magnetic resonance imaging study[J].Isr Med Assoc J,2008,10(11):793-798.
[9]陆彩玲,宋凌勇,唐深,等.牛磺酸改善染锰大鼠学习记忆能力的海马蛋白质组学研究[J].营养学报,2012,34(6):553-557.
[10]Sikk K,Haldre S,Aquilonius SM,et al.Manganese-induced parkinsonism in methcathinone abusers:bio-markers of exposure and follow-up[J].Eur J Neurol,2013,20(6):915-920.
[11]Li G,Pleasure SJ.Ongoing interplay between the neural network and neurogenesis in the adult hippocampus[J].Curr Opin Neurobiol,2010,20(1):126-133.
[12]Santos D,Milatovic D,Andrade V,et al.The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the rat brain[J].Toxicology,2012,292(2/3):90-98.
[13]Ye HB,Shi HB,Yin SK.Mechanisms underlying taurine protection against glutamate-induced neurotoxicity[J].Can JNeurol Sci,2013,40(5):628-634.
[14]徐冬辉,徐斌,贺安宁,等.牛磺酸和维生素C对锰致大鼠氧化损伤的拮抗作用[J].毒理学杂志,2014,28(6):457-459.
[15]Kowdley KV,Mason JB,Meydani SN,et al.Vitamin E deficiency and impaired cellular immunity related to intestinal fat malabsorption[J].Gastroenterology,1992,102(6):2139-2142.
[16]Tanyel MC,Mancano LD.Neurologic findings in vitamin Edeficiency[J].Am Fam Physician,1997,55(1):197-201.