本文選題：炎性痛及痛過敏 + 蜜蜂毒��； 參考：《河北醫(yī)科大學(xué)》2005年碩士論文

【摘要】：傳統(tǒng)觀點認為神經(jīng)元是神經(jīng)系統(tǒng)的基本功能單位,中樞神經(jīng)系統(tǒng)對傷害性刺激的感受、傳導(dǎo)以及調(diào)節(jié),都是由神經(jīng)元介導(dǎo)的。但近年來研究表明,脊髓膠質(zhì)細胞在病理性痛的產(chǎn)生和維持中發(fā)揮重要作用。很多傷害性刺激,如皮下炎性刺激、外周神經(jīng)損傷等均可以激活脊髓后角膠質(zhì)細胞。給予膠質(zhì)細胞抑制劑(如氟代檸檬酸、CNI-1493)可明顯抑制傷害性刺激引起的熱痛敏和機械性痛敏。體外實驗表明膠質(zhì)細胞可以被一些疼痛相關(guān)物質(zhì),如ATP、興奮性氨基酸(excitatoryamino acids ,EAAs)、前列腺素、P 物質(zhì)、一氧化氮等激活。激活的脊髓膠質(zhì)細胞可以產(chǎn)生許多細胞因子和神經(jīng)活性物質(zhì)促進傷害性信息的傳遞。由此可見脊髓膠質(zhì)細胞的激活在傷害性信息處理過程中發(fā)揮重要作用。但傷害性傳入引起脊髓膠質(zhì)細胞激活的機制有待闡明。 EAAs 是脊髓中介導(dǎo)傷害性信息傳遞的重要神經(jīng)遞質(zhì),可通過N-甲基-D-天門冬氨酸(N-methyl-D-asparte,NMDA )和非NMDA受體介導(dǎo)傷害性信息,其中NMDA受體除介導(dǎo)脊髓后角痛相關(guān)神經(jīng)元的興奮外,在傷害性傳入引起的脊髓后角星形膠質(zhì)細胞的激活中也發(fā)揮重要作用,但非NMDA 受體是否參與傷害性傳入引起的脊髓后角星形膠質(zhì)細胞的激活尚未見報道。 因此,本實驗通過觀察非NMDA 受體拮抗劑6-cyano-7- nitroquinoxaline-2,3-dione(CNQX)對大鼠蜜蜂毒(Bee venom,BV)炎性痛及痛過敏所致脊髓后角星形膠質(zhì)細胞膠質(zhì)原纖酸性蛋白(glial fibrillary acidic protein,GFAP)表達的影響,以及非NMDA 受體激動劑海人藻酸(kainic acid,KA)在引起傷害性感受過程中對脊髓后角星形膠質(zhì)細胞GFAP 表達的影響,探討非NMDA 受體在傷害性信息傳入所致脊髓后角星型膠質(zhì)細胞激活中的作用。 1 非NMDA 受體拮抗劑CNQX 對大鼠蜂毒炎性痛及痛過敏所致脊髓后角星形膠質(zhì)細胞GFAP 表達的影響 雄性Sprague-Dawley 大鼠77 只,體重270-280g。動物隨機分為4 組,分別為對照(Control)組、蜂毒(BV)組、BV +溶劑二甲基亞砜(DMSO)對照組、BV+CNQX 組。其中BV+CNQX 組根據(jù)CNQX 劑量分為2.5nmol、10nmol、 40nmol三個亞組。對照組足底皮下注射生理鹽水(NS)50μl,其余各組均于右后足底皮下注射BV 溶液50μl(4g·L-1)致外周炎性痛及痛過敏。BV+DMSO 組、BV+CNQX 組于足底注射蜂毒前15min 鞘內(nèi)注射10μl 溶劑(50% DMSO)或CNQX溶液。各組均于足底注射后1h 或24h 取材,免疫組化法觀察脊髓后角GFAP 表達的變化。取材前測定自發(fā)縮足反射次數(shù)(1h),并應(yīng)用溫水浴法和熱輻射法測定熱甩尾潛伏期(24h)。 結(jié)果發(fā)現(xiàn),①縮足反射足底注射蜂毒后大鼠出現(xiàn)縮足反射。鞘內(nèi)給予DMSO 對上述BV 注射引起的縮足反射次數(shù)無顯著影響(P0.05),而鞘內(nèi)給予CNQX 則可使大鼠的退縮反射次數(shù)顯著降低(P0.05),且降低的程度與CNQX劑量顯示明顯的劑量依賴性。②熱甩尾潛伏期大鼠右后足掌面皮下注射蜂毒后其熱甩尾潛伏期顯著縮短(P0.05)。
[Abstract]:The traditional view is that neurons are the basic functional units of the nervous system. The sensory, conduction and regulation of the central nervous system are mediated by neurons. However, in recent years, studies have shown that the spinal glia cells play an important role in the production and maintenance of pathological pain. Many nociceptive stimuli, such as subcutaneous inflammatory stimuli, are important. Peripheral nerve injury, such as peripheral nerve injury, can activate glial cells in the posterior horn of the spinal cord. Glial cell inhibitors (such as fluorocitric acid, CNI-1493) can obviously inhibit the thermal pain sensitivity and mechanical sensitization induced by nociceptive stimuli. In vitro experiments show that glial cells can be treated with some pain related substances, such as ATP, excitatoryamino acids, EA. As) activation of prostaglandins, substance P, nitric oxide. Activated spinal glial cells can produce many cytokines and neuroactive substances that promote the transmission of noxious information. Thus, the activation of spinal glial cells plays an important role in the process of noxious information processing. The mechanism remains to be clarified.
EAAs is an important neurotransmitter for the transmission of nociceptive information in the spinal cord, which mediates nociceptive information through the N- methyl -D- aspartate (N-methyl-D-asparte, NMDA) and non NMDA receptors, in which the NMDA receptor activates the astrocytes in the posterior horn of the spinal cord caused by nociceptive afferent in addition to the excitation of the spinal cord hornpain related neurons. It also plays an important role. However, whether the non NMDA receptor participates in the activation of astrocytes in spinal dorsal horn induced by noxious afferent has not been reported.
Therefore, we observed the non NMDA receptor antagonist 6-cyano-7-.
The effect of nitroquinoxaline-2,3-dione (CNQX) on the expression of glial fibrillary acidic protein (glial fibrillary acidic protein, GFAP) of astrocytes in the posterior horn of the spinal cord caused by Bee venom (BV) and pain allergy, and the non NMDA receptor agonist, sea human alginic acid (kainic), in the process of causing injury to the spinal cord in the spinal cord The effect of non NMDA receptor on the activation of astrocytes in spinal dorsal horn induced by noxious information was explored by GFAP expression in the posterior horn astrocytes.
1 Effect of non NMDA receptor antagonist CNQX on GFAP expression in astrocytes of spinal dorsal horn in rats with bee venom inflammatory pain and hyperalgesia
77 male Sprague-Dawley rats and weight 270-280g. animals were randomly divided into 4 groups: control (Control) group, bee venom (BV) group, BV + solvent two methyl sulfoxide (DMSO) control group, BV+CNQX group. The BV+CNQX group was divided into 2.5nmol, 10nmol, 40nmol three subgroups according to the CNQX dosage. The control group subcutaneous injection of saline 50 um, the rest All groups were subcutaneously injected into the right posterior foot by subcutaneous injection of BV solution 50 u l (4G. L-1) to peripheral inflammatory pain and hyperalgesia in.BV+DMSO group. Group BV+CNQX was injected with 10 u l solvent (50% DMSO) or CNQX solution in the 15min sheath before injection of bee venom in the foot. All groups were taken after the plantar injection 1H or 24h, the changes of the posterior horn of the spinal cord were observed by immunohistochemical method. The number of spontaneous retraction reflex (1H) was measured, and the thermal flick latency (24h) was measured by warm water bath and thermal radiation.
The results showed that the contraction foot reflex was found in the rats after the foot injection of the foot, and the intrathecal administration of DMSO had no significant effect on the times of the reflexes caused by the BV injection (P0.05), while the intrathecal CNQX could significantly reduce the number of retraction reflex (P0.05) in the rats (P0.05), and the degree of reduction was significantly dependent on the dose of CNQX. (2) the latent period of heat tail flick was significantly shortened (P0.05) after the injection of bee venom from the right posterior foot palmar skin in the thermal tail flick incubation period.
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2005
【分類號】：R363

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本文編號：1979812