文章摘要
李广军1 姜银松2 王占青2 马玉英2△ 尹彩星2.百草枯中毒大鼠TNF-α、IL-10 的表达及大黄保护作用的研究[J].,2012,12(4):649-651
百草枯中毒大鼠TNF-α、IL-10 的表达及大黄保护作用的研究
The Study on Expression of TNF-α、IL-10 in Rats with Paraquat Intoxicationand the Protection Effect of Rhubarb
  
DOI:
中文关键词: 大黄  百草枯  TNF-α  IL-10
英文关键词: Rhubarb  Paraquat  Tumor necrosis factor-α  Interleukin-10
基金项目:专利申请号:201010274655.X
作者单位
李广军1 姜银松2 王占青2 马玉英2△ 尹彩星2 临沂市罗庄区人民医院外一科 
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中文摘要:
      目的:观察大黄对急性百草枯中毒大鼠TNF- α、IL-10 的干预作用,探讨其可能的作用机制。方法:90 只SD 大鼠随机分为生 理盐水对照组(A 组)、PQ(60 mg/kg)灌胃染毒组(B 组)、生大黄(300mg/kg·d)干预组(C 组),每组30 只。中毒后6h、24h、72h 分 批处死存活的大鼠,并且检测大鼠血浆TNF- α、IL-10 水平。结果:B 组、C 组TNF-α、IL-10 水平在染毒后6h 开始升高,72h 达到高 峰,与A 组相比,差异有统计学意义(P<0.05、P<0.01),在相同时间点C 组TNF- α 和IL-10 的表达低于B 组,差异均有统计学意 义(P<0.01)。B 组、C 组血浆TNF- α、IL-10 水平与中毒时间呈显著正性相关关系(r=0.849,P<0.01;r=0.790,P<0.01;r=0.0.943,P<0. 01;r=0.892,P<0.01)。结论:大黄能够通过降低百草枯中毒大鼠体内的TNF-α、IL-10 水平,减轻百草枯对大鼠的损伤作用。
英文摘要:
      Objective: To evaluate the effect of rhubarb on tumor necrosis factor-a (TNF-α) and interleukin-10 (IL-10) in rats with paraquat intoxication, and investigate its mechanism. Methods: 90 healthy adult SD rats were randomly divided into Group A(control group n=30), Group B(poisoned group n=30 ) , Group C (rhubarb-treated group n=30 ) . Group B and C were treated intragastrically with PQ at 60 mg/kg, Group C given rhubarb at 300mg/kg. d, while only saline was treated intragastrically the other two groups . Live rats in each group were sacrificed at 6 hours,24 hours and 72 hours, for the determination of TNF-α, IL-10 in plasma of rats. Results: The leves of TNF-α, IL-10 increased at 6 hours after paraquat intoxication in Group B and Group C, and peaked at 72 hours later, with statistical difference from Group A (P<0.05, P<0.01); Compared with group B, delayed,lower increasing extent,obviously reducing tendency in group C, with statistical difference (P<0.01).As to the leves of TNF-α, IL-10and poisoning time, there were high positive correlations among them. Conclusions: Rhubarb ameliorates damage effect caused by PQ poisoning in rats by means of inhibiting the expression of TNF-α, IL-10 in turn to alleviate inflammatory reaction.
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