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首页> 美国卫生研究院文献>World Journal of Gastroenterology >1α 25-dihydroxyvitamin D3 prevents DNA damage and restores antioxidant enzymes in rat hepatocarcinogenesis induced by diethylnitrosamine and promoted by phenobarbital
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1α 25-dihydroxyvitamin D3 prevents DNA damage and restores antioxidant enzymes in rat hepatocarcinogenesis induced by diethylnitrosamine and promoted by phenobarbital

机译：1α25-二羟基维生素D3可防止DNA损伤并恢复由二乙基亚硝胺诱导并由苯巴比妥促进的大鼠肝癌发生中的抗氧化酶

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AIM: To investigate the chemopreventive effects of 1α, 25-dihydroxyvitamin D3 in diethylnitrosamine induced, phenobarbital promoted rat hepatocarcinogenesis.METHODS: The rats were randomly divided into 6 different groups (A-F). Groups A, C and E rats received a single intraperitoneal (i.p) injection of diethylnitrosamine (DEN) at a dose of 200 mg/kg body mass in 9 g/L NaCl solution at 4 wk of age, while group B served as normal vehicle control received normal saline once. After a brief recovery of 2 wk, all the DEN treated rats were given phenobarbital (PB) at 0.5 g/L daily in the basal diet till wk 20. Group A was DEN control. Treatment of 1α, 25-(OH)2D3 in group C was started 4 wk prior to DEN injection and continued thereafter till wk 20 at a dose of 0.3 μg/100 μL propylene glycol per one single dose (os) twice a week. Group E received the treatment of 1α, 25-(OH)2D3 at the same dose mentioned as above for 15 wk. The rats in group D and F received 1α, 25-(OH)2D3 alone as in group C without DEN injection.RESULTS: The comet assay showed statistically higher mean values for length to width ratios (L: W) of DNA mass and tailed cells (P < 0.01; P < 0.01 respectively) in DEN treated rats as compared to their normal controls. Continuous supplementation of 1α, 25-dihydroxyvitaminD3 showed a significant (P < 0.01) decrease in L:W ratio of DNA mass tailed cells. Furthermore, 1α, 25-(OH)2D3 supplementations elevated the super oxide dismutase (SOD) activity, hepatic malondialdehyde (MDA) level, reduced glutathione (GSH) and glutathione S-transferase (GST) activity (P < 0.01, P < 0.05, P < 0.05 and P < 0.05 respectively). As an endpoint marker histological changes were observed to establish the chemopreventive effects of 1α, 25-dihydroxyvitaminD3.CONCLUSION: Supplementations of 1α, 25-(OH)2D3 has a marked protection against hepatic nodulogenesis, antioxidant enzymes and DNA damages in DEN induced rat hepatocarcinogenesis promoted by phenobarbital.
机译：目的：研究1α，25-二羟基维生素D3在二乙基亚硝胺诱导的苯巴比妥促进大鼠肝癌发生中的化学预防作用。方法：将大鼠随机分为6组（A-F）。 A，C和E组大鼠在4周龄时接受了一次腹膜内（ip）腹膜内（ip）注射剂量为200 mg / kg体重的9 g / L NaCl溶液中的二乙基亚硝胺（DEN），而B组为正常媒介对照组接受一次生理盐水。短暂恢复2周后，所有的DEN处理大鼠均以基础饮食每天0.5 g / L的剂量服用苯巴比妥（PB），直到20周为止。A组为DEN对照。 C组中1α，25-（OH）2D3的治疗开始于DEN注射前4周，此后一直持续到20周，每周两次单剂量（os）的剂量为0.3μg/ 100μL丙二醇。 E组以与上述相同的剂量接受1α，25-（OH）2D3的治疗，持续15周。与未注射DEN的C组一样，D和F组的大鼠仅接受1α，25-（OH）2D3。结果：彗星试验显示出DNA质量和尾巴的长宽比（L：W）的统计学平均值较高与正常对照组相比，经DEN处理的大鼠体内的细胞（分别为P <0.01； P <0.01）。连续补充1α，25-二羟基维生素D3表明，DNA尾巴细胞的L：W比明显降低（P <0.01）。此外，添加1α，25-（OH）2D3可提高超氧化物歧化酶（SOD）活性，肝丙二醛（MDA）水平，降低谷胱甘肽（GSH）和谷胱甘肽S-转移酶（GST）活性（P <0.01，P <0.05 ，分别为P <0.05和P <0.05）。结论：补充1α，25-（OH）2D3对DEN诱导的大鼠肝癌的肝结节形成，抗氧化酶和DNA损伤具有明显的保护作用，以此作为观察终点的组织学变化以建立1α，25-dihydroxyvitaminD3的化学预防作用。由苯巴比妥促进。

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