本文關(guān)鍵詞： 末端病 TNF-α NF-κB　出處：《蘇州大學(xué)》2014年碩士論文　論文類型：學(xué)位論文

【摘要】：研究目的： 人們從分子水平進行了大量的有關(guān)TNF-α與NF-κB信號通路以及兩者之間相互關(guān)系的研究，但對于在末端病發(fā)生過程中作用的研究還處于探索階段，直接相關(guān)研究很少。TNF-α作為重要的炎癥因子，可單獨或通過與其他細胞因子的相互作用引起促進炎癥反應(yīng)。NF-κB信號通路從多方面參與末端病的形成，但這是一個復(fù)雜的細胞因子網(wǎng)絡(luò)，其具體調(diào)控及反饋調(diào)節(jié)機制、細胞因子網(wǎng)絡(luò)的交互作用、信號通路間的可能聯(lián)系尚有待逐步揭示。因而進一步加強對TNF-α介導(dǎo)的NF-κB信號轉(zhuǎn)導(dǎo)途徑的研究，尤其是TNF-α和NF-κB抑制劑進行末端病治療，可能為延緩或阻斷末端病進程提供新的嘗試，并為末端病的早期預(yù)防和臨床治療提供理論依據(jù) 研究方法： 本實驗通過大負荷跳躍運動方式建立末端病損傷模型，從炎癥因子TNF-α與NF-κB入手，探討末端病發(fā)生的分子機制。 研究方法：48只8周齡雄性SD大鼠，購買于蘇州大學(xué)動物實驗中心。大鼠隨機分為對照組和跳躍組，，對照組24只，跳躍組24只。對照組正常環(huán)境下飼養(yǎng)，跳躍組放于半自動跳躍電刺激籠內(nèi)進行為期6周的跳躍運動。每兩周取材一次，大鼠麻醉處死，取大鼠雙后足跟腱及近端跟骨區(qū)域，一組材料利用免疫組化法檢測末端組織內(nèi)TNF-α和NF-κB的蛋白含量，另外一組制作HE石蠟切片并染色觀察。觀察比較三組實驗組和對照組大鼠的跟腱末端區(qū)的病理組織變化，分析不同組大鼠的TNF-α、NF-κB的表達情況。 研究結(jié)果： (1)HE染色結(jié)果表明，跳躍組與對照組病理組織形態(tài)出現(xiàn)較大差異，且隨著造模時間延長，差異明顯增大。 (2)對照組2、4、6周大鼠肌腱、纖維及鈣化軟骨和跟骨TNF-α陽性細胞數(shù)無顯著性差異（p＞0.05），與對照組相比，跳躍2、4、6周組大鼠肌腱、纖維及鈣化軟骨和跟骨TNF-α陽性細胞數(shù)顯著增加，具有非常顯著性差異（P＜0.01）。 (3)對照組2、4、6周大鼠肌腱、纖維及鈣化軟骨和跟骨NF-κ B陽性細胞數(shù)無顯著性差異（p＞0.05），與對照組相比，跳躍2、4、6周組大鼠在肌腱、纖維及鈣化軟骨和跟骨NF-κB陽性細胞數(shù)增加顯著，，具有非常顯著性差異（P＜0.01）。 研究結(jié)論： (1)TNF-α和NF-κB對應(yīng)力刺激敏感，TNF-α和NF-κB表達升高，是末端病產(chǎn)生的機制之一。 (2)在末端區(qū)各區(qū)TNF-α和NF-κB的含量不同，其中肌腱和纖維及鈣化軟骨區(qū)偏高，骨區(qū)則偏低。
[Abstract]:Objectives of the study:. A lot of studies have been carried out on TNF- 偽 and NF- 魏 B signaling pathway and their relationship at molecular level, but the role of TNF- 偽 and NF- 魏 B in the process of terminal disease is still in the exploratory stage. As an important inflammatory factor, there are few direct correlation studies. TNF- 偽 can promote inflammatory response. NF- 魏 B signaling pathway is involved in the formation of terminal disease in many ways, either alone or through interaction with other cytokines. But this is a complex cytokine network, and its specific regulation and feedback regulation mechanisms, the interaction of cytokine networks, The possible relationship between signal pathways has yet to be gradually revealed. Therefore, the study of TNF- 偽 -mediated NF- 魏 B signal transduction pathway, especially the treatment of terminal diseases by TNF- 偽 and NF- 魏 B inhibitors, has been further strengthened. It may provide a new attempt to delay or block the progression of terminal diseases, and provide theoretical basis for early prevention and clinical treatment of terminal diseases. Research methods:. In this experiment, the model of terminal disease injury was established by means of high-load jumping exercise, and the molecular mechanism of terminal disease was discussed from the inflammatory factors TNF- 偽 and NF- 魏 B. Methods Forty eight 8-week-old male Sprague-Dawley rats were purchased from Suzhou University Animal experiment Center. The rats were randomly divided into two groups: control group (n = 24) and jumping group (n = 24). The jumping group was placed in a semi-automatic jumping electric stimulation cage for 6 weeks. The rats were anesthetized and killed every two weeks. The Achilles tendon and the proximal calcaneal area of the rats were harvested. One group of materials was used to detect the protein content of TNF- 偽 and NF- 魏 B in the terminal tissues by immunohistochemical method, the other group was made of HE paraffin sections and stained. The pathological changes of the ends of the Achilles tendon in the experimental group and the control group were observed and compared. To analyze the expression of TNF- 偽 and NF- 魏 B in different groups of rats. Results of the study:. The results of HE staining showed that the histopathology of the jumping group and the control group were significantly different, and the difference increased with the prolongation of the model making time. (2) there was no significant difference in the number of TNF- 偽 positive cells in tendon, fiber, calcified cartilage and calcaneal bone of rats in the control group at 6 weeks (P > 0.05). Compared with the control group, the number of TNF- 偽 positive cells in tendon, fiber and calcified cartilage and calcaneal bone were significantly increased in the control group. There was significant difference (P < 0.01). (3) there was no significant difference in the number of NF- 魏 B positive cells in tendon, fiber and calcified cartilage and calcaneal bone of rats in the control group at 6 weeks, and the number of NF- 魏 B positive cells in the control group was not significantly different from that in the control group (P > 0.05). The number of NF- 魏 B positive cells in fibrous and calcified cartilage and calcaneus increased significantly (P < 0.01). The study concluded that:. The increased expression of TNF- 偽 and NF- 魏 B is one of the mechanisms of terminal diseases. (2) the contents of TNF- 偽 and NF- 魏 B in the terminal region were different, in which the tendons and fibers and calcified cartilage were higher and the bone areas were lower.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：G804.2

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