本文關(guān)鍵詞：5’-磷酸腺苷誘導(dǎo)的低溫抗炎機(jī)制的初步研究　出處：《青島大學(xué)》2014年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 磷酸 腺苷 誘導(dǎo) 低溫 抗炎 機(jī)制 初步 研究

【摘要】：目的：應(yīng)用5’-磷酸腺苷(5'-AMP)誘導(dǎo)低溫作用于LPS誘導(dǎo)的大鼠炎癥動物模型,分析ERK1/2、JNK、p38和NF-κB四條信號通路,明確5’-磷酸腺苷(5'-AMP)誘導(dǎo)低溫抗炎的可能機(jī)制。 方法：將成年健康的Wistar隨機(jī)分為四組：空白對照組、LPS陽性對照組、5'-AMP低溫預(yù)防治療組、5'-AMP低溫治療組。每組12只大鼠。每組大鼠在注射LPS6h和12h后眼靜脈叢取血保存,在LPS注射12h后取肺組織,分別凍存和福爾馬林固定。ELISA法測定血清中CD14、CRP和MCP-1的表達(dá)水平,免疫組化法觀察TLR4在肺組織中的表達(dá)情況,Western Blot技術(shù)測定ERKl/2、JNK、p38和NF-κB四條信號通路總蛋白和磷酸化蛋白的水平。 將36只Wistar大鼠隨機(jī)分為三組：LPS炎癥組、5'-AMP低溫預(yù)防治療組、5'-AMP低溫治療組,每組12只大鼠,進(jìn)行生存分析,記錄每組12h內(nèi)大鼠的生存率,重復(fù)三次。 結(jié)果：實(shí)驗(yàn)結(jié)果表明,與LPS組相比,無論是5'-AMP低溫預(yù)防組還是5'-AMP低溫治療組,都能顯著地降低血清中CD14和CRP的表達(dá)水平。免疫組化結(jié)果顯示,肺組織中TLR4的表達(dá)量LPS組顯著高于5'-AMP低溫干預(yù)組。Western Blot結(jié)果顯示,5'-AMP誘導(dǎo)的低溫能夠抑制炎癥信號通路ERK1/2、JNK、p38和NF-κB的激活。另外,5'-AMP低溫治療組和5'-AMP低溫預(yù)防組大鼠的生存率和生存時間顯著高于LPS炎癥組,且5'-AMP低溫預(yù)防組的效果優(yōu)于5'-AMP低溫治療組。 結(jié)論：5'-AMP誘導(dǎo)的低溫能夠通過降低炎癥因子表達(dá)水平及抑制炎癥信號通路ERKl/2, p38, JNK和NF-κB的激活而發(fā)揮抗炎作用,保護(hù)炎癥模型動物組織器官免受損傷。
[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.
【學(xué)位授予單位】：青島大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R563.8

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