本文關(guān)鍵詞：神經(jīng)鈣調(diào)蛋白在促炎細(xì)胞因子誘導(dǎo)神經(jīng)元凋亡中作用機制　出處：《吉林大學(xué)》2005年博士論文　論文類型：學(xué)位論文

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【摘要】：本實驗主要利用炎癥細(xì)胞因子IL-1β和TNFα作用于原代培養(yǎng)的皮層神經(jīng)元和星形膠質(zhì)細(xì)胞,探討神經(jīng)鈣調(diào)蛋白是否參與了炎癥因子引起的神經(jīng)細(xì)胞的損傷及可能的機制。方法:用IL-1β和TNFα誘導(dǎo)培養(yǎng)大鼠皮層神經(jīng)元和星形膠質(zhì)細(xì)胞的損傷,采用四唑鹽比色法(MTT),乳酸脫氫酶釋放率(LDH)及免疫熒光方法觀察細(xì)胞生存力和損傷程度, Western blot 分析檢測p-JNK,p-ERK,NF-κB 的表達(dá)。結(jié)果:在皮層神經(jīng)細(xì)胞中,IL-1β和TNFα與正常對照組比較,均可明顯引起皮層神經(jīng)元的損傷(p0.05)。而IL-1β與CsA 聯(lián)合應(yīng)用組,皮層神經(jīng)元的生存力則明顯提高,TNFα與CsA 聯(lián)合應(yīng)用組,皮層神經(jīng)元的生存力改變不明顯。在LDH 釋放率測定試驗中,也觀察到了類似的結(jié)果。CsA 可明顯降低IL-1β引起的LDH 釋放率的增加。IL-1β與CsA 聯(lián)合作用組,與IL-1β單獨作用組比較可明顯降低LDH 的釋放率(p0.001),而TNFα與CsA 聯(lián)合作用組,與TNFα單獨作用組比較LDH 的釋放率沒有明顯改變(p0.05)。在星形膠質(zhì)細(xì)胞中炎性細(xì)胞因子IL-1β,TNFα均可引起細(xì)胞釋放LDH 增多,IL-1β與CsA 可明顯降低IL-1β引起的星形膠質(zhì)細(xì)胞生存力降低和LDH 釋放率的增加。IL-1β與CsA 聯(lián)合作用組,與IL-1β單獨作用組比較可明顯提高細(xì)胞的生存力和降低LDH 的釋放率(p0.001),而且TNFα與CsA 聯(lián)合作用組,與TNFα單獨作用組比較LDH 的釋放率可明顯降低(p0.05)。通過免疫熒光觀察發(fā)現(xiàn),皮質(zhì)神經(jīng)元中IL-1β和TNFα引起神經(jīng)元凋亡數(shù)(green)和死亡數(shù)(red)的細(xì)胞數(shù)均明顯增多,與正常對照組比較有顯著差異(p0.05)。而CsA 組神經(jīng)元凋亡及壞死數(shù)量均比IL-1β和TNFα損傷組少。CsA 與IL-1β聯(lián)合應(yīng)用組,神經(jīng)元凋亡和壞死率與單純
[Abstract]:In this study, the inflammatory cytokines IL-1 尾 and TNF 偽 were used in primary cultured cortical neurons and astrocytes. To investigate whether calmodulin is involved in the injury of nerve cells induced by inflammatory factors and its possible mechanism. Methods: IL-1 尾 and TNF 偽 were used to induce the injury of cortical neurons and astrocytes in cultured rats. Cell viability and damage were observed by MTT assay, lactate dehydrogenase release rate (LDH) and immunofluorescence assay. The expression of NF- 魏 B was detected by Western blot analysis. Results: in cortical neurons. Compared with the normal control group, IL-1 尾 and TNF 偽 could significantly induce the cortical neuron injury (p0.05), while the IL-1 尾 and CsA combined treatment group. The viability of cortical neurons was significantly increased in the combination of TNF- 偽 and CsA group. The viability of cortical neurons did not change significantly. In the test of LDH release rate, there was no significant change in the viability of cortical neurons. Similar results were observed. CSA could significantly reduce the increase of LDH release rate induced by IL-1 尾. IL-1 尾 combined with CsA group. Compared with IL-1 尾 alone, the release rate of LDH was significantly decreased in TNF 偽 and CsA group. Compared with TNF 偽 alone, the release rate of LDH did not change significantly. The inflammatory cytokine IL-1 尾 was found in astrocytes. TNF 偽 could induce the increase of LDH release. IL-1 尾 and CsA significantly decreased the viability of astrocytes induced by IL-1 尾 and the increase of LDH release. Compared with the IL-1 尾 alone group, the viability of the cells and the release rate of LDH were significantly increased and the release rate of LDH was decreased. Moreover, the combination of TNF 偽 and CsA group. Compared with TNF 偽 alone, the release rate of LDH was significantly lower than that of TNF 偽 alone. In cortical neurons, the number of IL-1 尾 and TNF 偽 induced neuronal apoptosis and the number of dead neurons increased significantly. The number of apoptosis and necrosis of neurons in CsA group was less than that in IL-1 尾 and TNF 偽 injury group. CSA combined with IL-1 尾 group was significantly different from normal control group. Neuron apoptosis and necrosis rate and simple
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2005
【分類號】：R363

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本文編號：1431511