5’-磷酸腺苷诱导的低温抗炎机制的初步研究

发布时间：2018-01-03 19:23

本文关键词：5’-磷酸腺苷诱导的低温抗炎机制的初步研究　出处：《青岛大学》2014年硕士论文　论文类型：学位论文

【摘要】：目的：应用5’-磷酸腺苷(5'-AMP)诱导低温作用于LPS诱导的大鼠炎症动物模型,分析ERK1/2、JNK、p38和NF-κB四条信号通路,明确5’-磷酸腺苷(5'-AMP)诱导低温抗炎的可能机制。方法：将成年健康的Wistar随机分为四组：空白对照组、LPS阳性对照组、5'-AMP低温预防治疗组、5'-AMP低温治疗组。每组12只大鼠。每组大鼠在注射LPS6h和12h后眼静脉丛取血保存,在LPS注射12h后取肺组织,分别冻存和福尔马林固定。ELISA法测定血清中CD14、CRP和MCP-1的表达水平,免疫组化法观察TLR4在肺组织中的表达情况,Western Blot技术测定ERKl/2、JNK、p38和NF-κB四条信号通路总蛋白和磷酸化蛋白的水平。将36只Wistar大鼠随机分为三组：LPS炎症组、5'-AMP低温预防治疗组、5'-AMP低温治疗组,每组12只大鼠,进行生存分析,记录每组12h内大鼠的生存率,重复三次。结果：实验结果表明,与LPS组相比,无论是5'-AMP低温预防组还是5'-AMP低温治疗组,都能显著地降低血清中CD14和CRP的表达水平。免疫组化结果显示,肺组织中TLR4的表达量LPS组显著高于5'-AMP低温干预组。Western Blot结果显示,5'-AMP诱导的低温能够抑制炎症信号通路ERK1/2、JNK、p38和NF-κB的激活。另外,5'-AMP低温治疗组和5'-AMP低温预防组大鼠的生存率和生存时间显著高于LPS炎症组,且5'-AMP低温预防组的效果优于5'-AMP低温治疗组。结论：5'-AMP诱导的低温能够通过降低炎症因子表达水平及抑制炎症信号通路ERKl/2, p38, JNK和NF-κB的激活而发挥抗炎作用,保护炎症模型动物组织器官免受损伤。
[Abstract]:Objective: to investigate the effects of hypothermia on LPS induced inflammation in rats and analyze the ERK1 / 2 JNK induced by 5-adenosine phosphate (AMP). Four signaling pathways p38 and NF- 魏 B were used to clarify the possible mechanism of hypothermia and anti-inflammation induced by adenosine 5-phosphate (AMP). Methods: adult healthy Wistar were randomly divided into four groups: the blank control group, the LPS-positive control group, and the hypothermia prophylaxis group. 5 Group A MP hypothermia treatment group, 12 rats in each group. Each group of rats were injected with LPS6h and 12 hours after the blood preservation of the ocular venous plexus, 12 hours after LPS injection of lung tissue. The expression levels of CD14CRP and MCP-1 in serum were determined by frozen storage and formalin fixed. The expression of TLR4 in lung tissue was observed by immunohistochemical method. The levels of total protein and phosphorylated protein in four signal pathways of ERKL / 2 JNKK p38 and NF- 魏 B were measured by Western Blot technique. Thirty-six Wistar rats were randomly divided into three groups (n = 12 in each group). The survival rate of each group within 12 hours was recorded and repeated three times. Results: the results showed that, compared with the LPS group, the hypothermia prevention group and the hypothermia treatment group were 5o AMP and 5A MP respectively. The expression of CD14 and CRP in serum was significantly decreased. The expression of TLR4 in lung tissue in LPS group was significantly higher than that in 5- AMP hypothermia group. Western Blot showed that the expression of TLR4 in lung tissue was significantly higher than that in control group. 5The hypothermia induced by AMP can inhibit the activation of ERK1 / 2 JNKP38 and NF- 魏 B. The survival rate and survival time of rats in the hypothermia treatment group and the hypothermia prevention group were significantly higher than those in the LPS inflammation group. And the effect of 5-AMP hypothermia prevention group was better than that of 5-AMP hypothermia treatment group. Conclusion the hypothermia induced by W5 / AMP can reduce the level of inflammatory factor expression and inhibit the inflammatory signaling pathway ERKL / 2, p38. The activation of JNK and NF- 魏 B plays an anti-inflammatory effect and protects tissues and organs from injury in inflammatory model animals.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2014
【分类号】：R563.8

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