本文選題：低氧應(yīng)激　切入點(diǎn)：冷應(yīng)激、束縛應(yīng)激　出處：《浙江大學(xué)》2005年博士論文　論文類型：學(xué)位論文

【摘要】：應(yīng)激可以引起機(jī)體內(nèi)環(huán)境平衡失調(diào),導(dǎo)致生理乃至病理性變化,例如抑制機(jī)體免疫系統(tǒng)、影響神經(jīng)系統(tǒng)的代謝和功能。低氧作為一種特殊的環(huán)境應(yīng)激,使機(jī)體器官組織乃至細(xì)胞的供氧不足,造成全身性缺氧反應(yīng)。許多研究指出缺氧和缺血性缺氧可抑制機(jī)體的免疫系統(tǒng)、抑制生長(zhǎng)、抑制甲狀腺軸和性腺軸的功能。低氧應(yīng)激可以引起中樞性免疫變化,誘導(dǎo)神經(jīng)內(nèi)分泌變化,使中樞產(chǎn)生免疫分子并參與中樞神經(jīng)系統(tǒng)的損傷、免疫炎癥和發(fā)生缺血性疾病。然而關(guān)于低氧對(duì)中樞神經(jīng)免疫作用的研究相對(duì)較少。因此,本文著重研究在持續(xù)性低氧應(yīng)激下,中樞神經(jīng)免疫的變化以及下丘腦神經(jīng)肽促腎上腺皮質(zhì)激素釋放因子(CRF)、細(xì)胞因子—白細(xì)胞介素-6(IL-6)和ET-1表達(dá)的相關(guān)性。 在神經(jīng)—內(nèi)分泌—免疫網(wǎng)絡(luò)中,神經(jīng)肽、激素和細(xì)胞因子的相互作用共同誘導(dǎo)應(yīng)激下的中樞免疫過程。CRF不僅是應(yīng)激下HPA軸的中樞始動(dòng)者,而且CRF具有炎性因子的作用直接參與中樞免疫反應(yīng),此外還參與中樞神經(jīng)系統(tǒng)的炎癥和細(xì)胞因子的產(chǎn)生等免疫調(diào)節(jié)。由中樞神經(jīng)系統(tǒng)內(nèi)激活的神經(jīng)膠質(zhì)和神經(jīng)元細(xì)胞產(chǎn)生的前炎性因子IL-6,是神經(jīng)免疫調(diào)節(jié)的信號(hào)來源。在缺血性缺氧和腦疾患中,IL-6直接參與腦損傷病理過程,導(dǎo)致神經(jīng)元細(xì)胞損傷、血腦屏障(BBB)的損壞、誘導(dǎo)腦水腫等免疫病理過程。腦內(nèi)的炎性細(xì)胞因子同時(shí)影響血管舒縮活性物質(zhì)的表達(dá),例如內(nèi)皮素(endothelin,ET)增加,引發(fā)血管收縮造成進(jìn)一步缺血性腦損傷,腦內(nèi)ET顯著升高可以誘導(dǎo)神經(jīng)細(xì)胞的損傷、引起腦水腫加劇。綜上所述,應(yīng)激下中樞的下丘腦、海馬、視上核和室旁核等相關(guān)腦區(qū)內(nèi)神經(jīng)肽、細(xì)胞因子和神經(jīng)遞質(zhì)的變化與中樞免疫調(diào)節(jié)密切相關(guān)。應(yīng)激下HPA軸和IL-6、ET之間存在相互調(diào)節(jié)共同參與中樞免疫過程。
[Abstract]:Stress can cause imbalance of environmental balance in the body, leading to physiological and even pathological changes, such as inhibiting the body's immune system, affecting the metabolism and function of the nervous system. The lack of oxygen supply to organs, tissues and cells of the body, which results in a systemic anoxic response. Many studies have shown that hypoxia and ischemic hypoxia inhibit the immune system and growth of the body. Inhibiting the function of thyroid axis and gonadal axis. Hypoxia stress can induce central immune changes, induce neuroendocrine changes, produce immune molecules in the central nervous system and participate in the damage of the central nervous system. Immune inflammation and ischemic diseases. However, there are relatively few studies on the immune effects of hypoxia on central nervous system. The changes of central nervous system immunity and the correlation between the expression of hypothalamic neuropeptide corticotropin releasing factor (CRF), cytokine interleukin-6 (IL-6) and ET-1. In neuroendocrine immune networks, the interaction of neuropeptides, hormones and cytokines induces the central immune process under stress. CRF is not only the central initiator of the HPA axis under stress. Moreover, CRF has the effect of inflammatory factor directly involved in the central immune response. In addition, it also participates in the immune regulation of inflammation and cytokine production in the central nervous system. IL-6, a proinflammatory factor produced by the activated glial and neuronal cells in the central nervous system, is the signal source of neuroimmune regulation. IL-6 is directly involved in the pathological process of brain injury in ischemic hypoxia and brain diseases. The inflammatory cytokines in the brain also affect the expression of vasomotor and vasomotor active substances, such as endothelin et. Further ischemic brain injury is caused by vasoconstriction, and a significant increase in et in the brain can induce nerve cell damage and increase brain edema. The changes of neuropeptides, cytokines and neurotransmitters in the supraoptic nucleus and paraventricular nucleus are closely related to the central immune regulation.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2005
【分類號(hào)】：R392

【引證文獻(xiàn)】

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1 楊希;慢性間歇低氧暴露對(duì)棕色田鼠親體及其子代生活史特征的影響[D];鄭州大學(xué);2011年

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本文編號(hào)：1614943