高级检索
吴小南, 林建银, 陈洁, 汪家梨. 发酵莲子乳对小鼠急性CCl4肝毒性保护作用[J]. 中国公共卫生, 2006, 22(12): 1488-1490.
引用本文: 吴小南, 林建银, 陈洁, 汪家梨. 发酵莲子乳对小鼠急性CCl4肝毒性保护作用[J]. 中国公共卫生, 2006, 22(12): 1488-1490.
shu
WU Xiaonan, LIN Jianyin, CHEN Jie, . Protective effect of lotus-seed milk fermented product on acute CCl4 hepatic toxicity in mice[J]. Chinese Journal of Public Health, 2006, 22(12): 1488-1490.
Citation: WU Xiaonan, LIN Jianyin, CHEN Jie, . Protective effect of lotus-seed milk fermented product on acute CCl4 hepatic toxicity in mice[J]. Chinese Journal of Public Health, 2006, 22(12): 1488-1490.
shu

发酵莲子乳对小鼠急性CCl4肝毒性保护作用

Protective effect of lotus-seed milk fermented product on acute CCl4 hepatic toxicity in mice

    摘要
  • 摘要:
      目的   研究发酵莲子乳(LMFP)对急性四氯化碳(CCl4)肝毒性的保护作用。
      方法   检测LMFP上清液对体外肝匀浆过氧化脂质生成量的影响。干预14 d, 一次性腹腔注射0.1%CCl4造模, 测定肝脏损伤及抗氧化指标, 肝组织切片苏木素-伊红(HE)染色及免疫组化观察。
      结果   LMFP于体外可抑制正常肝匀浆及经半胱氨酸、硫酸亚铁激发肝匀浆脂质过氧化物(LPO)的生成; 与模型组比较, LMFP干预组肝细胞肿胀, 局灶坏死, 炎细胞浸润等病理损伤减轻, Bcl-2表达增强; 肝匀浆乳酸脱氢酶(LDH)活力降低, LPO生成显著减少, 超氧化物歧化酶(SOD)活性增加(P < 0.05)。
      结论   LMFP能够通过抗氧化系统发挥作用, 减轻CCl4所致小鼠急性肝毒性。

     

    Abstract:
      Objective   To explore the protective effect and possible mechanism of Lotus-seed Milk Fer mented Product (LMFP)from acute CCl4 hepatic toxicity in mice.
      Methods   Ascertain the effect of lotus-seed milk fermented product on LPO of normal liver homogenate and normal hepatic homogenate excitated by cysteine and ferrous sulfate in vitro.Mice were fed with distilled water, 25%, 50%, 100% LMFP and VE, intraperitoneal injected Carbon Tetrachloride(CCl4)vegetal oil admixture in the 14th day.The examines assessing the degree of the hepaticacute damage and peroxidization were executed.Pathomorphological changes were detected by Haematoxylin eosin(HE)coloration and immunohistochemistry.
      Results   Lactiperoxidase(LPO)level of normal liver homogenate and hepatic homogenate excitated by cysteine and FeSO4 in LMFP groups were significantly decreased compared with the control group.Compared with the model group, Hepatocyte swell, necrosis and inflammatory cells penetration in the LMFP and VE groups were relieved, Bcl-2 express enhanced.Latic dehydrogenase(LDH)activity was decreased, LPO level was observably decreased, Superoxide dismutase(SOD)activity was significantly increased in LMFP groups.(all Significance, P < 0.05).
      Conclusion   LMFP can protect liver from acute CCl4 hepatic toxicity by the mechanism of anti-oxide system.

     

    • HTML全文
    • 参考文献(8)
    • 相关文章
    • 施引文献
  • 资源附件(0)

/

返回文章
返回