本文選題：電刺激 + 光損傷誘導(dǎo)感光細(xì)胞變性�。� 參考：《復(fù)旦大學(xué)》2012年博士論文

【摘要】：第一部分：電刺激促進(jìn)光損傷感光細(xì)胞存活的神經(jīng)保護(hù)作用 體外培養(yǎng)感光細(xì)胞系(661W),接種于六孔板貼壁后,放入光照培養(yǎng)箱中接受4-6h光照強(qiáng)度為15,0001ux的寬譜藍(lán)光照射。在光照后的24h進(jìn)行LDH細(xì)胞壞死測(cè)定實(shí)驗(yàn)、TUNEL凋亡染色及免疫熒光染色觀察661W的凋亡情況以及形態(tài)學(xué)改變。結(jié)果顯示：光照后,LDH實(shí)驗(yàn)顯示59.7%±2.7%的661W細(xì)胞壞死,TUNEL顯示70%左右的染色陽(yáng)性即凋亡,而免疫熒光染色則發(fā)現(xiàn)正常661W呈扁平狀,細(xì)胞之間連接緊密,但光損傷后661W突觸變細(xì)長(zhǎng),細(xì)胞失去扁平形態(tài),且細(xì)胞間隙明顯變大,表明光損傷誘導(dǎo)感光細(xì)胞凋亡模型成功建立。 利用1h雙相方波、直流電刺激(3ms,20Hz,300～1600μA)預(yù)先作用于光損傷661W和小膠質(zhì)細(xì)胞或Muller細(xì)胞共培養(yǎng)體系,并將其視為干預(yù)組；將未接受電刺激的此共培養(yǎng)體系視為未干預(yù)對(duì)照組；正常661W細(xì)胞和小膠質(zhì)細(xì)胞或Muller細(xì)胞共培養(yǎng)體系視為正常對(duì)照組。在共培養(yǎng)后3h、6h、12h、24h進(jìn)行LDH實(shí)驗(yàn),并在共培養(yǎng)后24h進(jìn)行TUNEL凋亡染色實(shí)驗(yàn)及免疫熒光染色。結(jié)果如下：LDH凋亡-時(shí)間曲線表明1000μA的電刺激預(yù)先作用于光損傷661W和小膠質(zhì)細(xì)胞共培養(yǎng)組之后,相較于未干預(yù)組相對(duì)應(yīng)時(shí)間點(diǎn)的細(xì)胞死亡率,從共培養(yǎng)后12h開始661W的細(xì)胞死亡率顯著降低,并保持相對(duì)恒定直到共培養(yǎng)后24h；同樣,1600M的電刺激預(yù)先作用于光損傷661W和Muller細(xì)胞共培養(yǎng)組之后,從共培養(yǎng)后3h開始661W的細(xì)胞死亡率顯著降低,并逐漸加大降低幅度直到共培養(yǎng)后24h。 TUNEL染色則顯示共培養(yǎng)后24h,電刺激干預(yù)組的TUNEL染色陽(yáng)性細(xì)胞比率較未干預(yù)組明顯減少。免疫熒光染色也提示了光損傷661W細(xì)胞和小膠質(zhì)細(xì)胞干預(yù)組的661W較未干預(yù)組細(xì)胞形態(tài)改變程度輕,細(xì)胞間隙更小。另一方面,我們也將電刺激總用于光損傷后單獨(dú)培養(yǎng)的661W細(xì)胞,并在相同時(shí)間節(jié)點(diǎn)進(jìn)行LDH、TUNEL及免疫熒光染色實(shí)驗(yàn),但結(jié)果與作用于共培養(yǎng)體系的電刺激不同,電刺激干預(yù)并未減輕661W細(xì)胞的凋亡。 本部分的實(shí)驗(yàn)研究結(jié)果表明,電刺激能夠減輕強(qiáng)光照射引起的感光細(xì)胞凋亡變性,但感光細(xì)胞本身對(duì)電刺激并沒有反應(yīng),可能電刺激改變了膠質(zhì)細(xì)胞的活性,而膠質(zhì)細(xì)胞活性的改變轉(zhuǎn)而影響了感光細(xì)胞的存活。 第二部分：光損傷誘導(dǎo)感光細(xì)胞變性激活視網(wǎng)膜膠質(zhì)細(xì)胞,激活的膠質(zhì)細(xì)胞進(jìn)而影響光損傷感光細(xì)胞凋亡的作用 成功建立了光損傷誘導(dǎo)感光細(xì)胞變性的模型后,我們進(jìn)一步利用膠質(zhì)細(xì)胞與光損傷感光細(xì)胞共培養(yǎng)體系(未干預(yù)組)探索小膠質(zhì)細(xì)胞和Muller細(xì)胞受光損傷感光細(xì)胞影響后的數(shù)量、形態(tài)學(xué)的改變以及相伴隨的功能的變化,同時(shí)探索平行的661W細(xì)胞的生存狀態(tài)變化。正常661W細(xì)胞和小膠質(zhì)細(xì)胞或Muller細(xì)胞共培養(yǎng)組視為正常對(duì)照組。在共培養(yǎng)24h后利用免疫熒光染色觀察兩組小膠質(zhì)細(xì)胞或Muller細(xì)胞數(shù)量及形態(tài)學(xué)的差異；同時(shí)利用Real-time PCR和Western blot法在共培養(yǎng)后3h,6h,12h,24h對(duì)兩組小膠質(zhì)細(xì)胞所分泌的促炎因子IL-1β、 TNF-α以及Muller細(xì)胞所分泌的神經(jīng)營(yíng)養(yǎng)因子BDNF、CNTF的基因表達(dá)量和蛋白分泌量?jī)山M差異以及時(shí)間趨勢(shì)變化進(jìn)行定量分析。并且運(yùn)用LDH、TUNEL及免疫熒光染色等實(shí)驗(yàn)檢測(cè)單獨(dú)培養(yǎng)光損傷661W細(xì)胞和與小膠質(zhì)細(xì)胞或Muller細(xì)胞共培養(yǎng)的661W細(xì)胞壞死和凋亡率的差異。 結(jié)果顯示：免疫細(xì)胞化學(xué)實(shí)驗(yàn)發(fā)現(xiàn)與正常661W細(xì)胞共培養(yǎng)的小膠質(zhì)細(xì)胞成靜息狀態(tài),形態(tài)成分支狀,突觸長(zhǎng),胞體較小,而與光損傷661W細(xì)胞共培養(yǎng)的小膠質(zhì)細(xì)胞成激活狀態(tài),形態(tài)成阿米巴樣或圓形,突觸短,胞體大,且數(shù)量較正常對(duì)照組增多。兩組Muller細(xì)胞的形態(tài)則無顯著差異。另外,在共培養(yǎng)后的24h,Real time PCR和Western blot顯示與光損傷661W共培養(yǎng)的小膠質(zhì)細(xì)胞IL-1β和TNF-α的基因和蛋白表達(dá)量較正常對(duì)照組顯著上升,與光損傷661W共培養(yǎng)的Muller細(xì)胞BDNF和CNTF的基因和蛋白表達(dá)量也較正常對(duì)照組明顯上調(diào)；蛋白量-時(shí)間趨勢(shì)曲線則發(fā)現(xiàn)在正常對(duì)照組中,小膠質(zhì)細(xì)胞分泌的IL-1β和TNF-α在共培養(yǎng)后3h至24h時(shí)間段內(nèi)基本保持穩(wěn)定且較低的水平。而相反的,與光損傷661W共培養(yǎng)的小膠質(zhì)細(xì)胞分泌的IL-1β蛋白量則隨著時(shí)間進(jìn)展逐步升高,在共培養(yǎng)后24h達(dá)到最高峰；同樣,其所分泌的TNF-α蛋白量也隨著時(shí)間上調(diào),在共培養(yǎng)后12h達(dá)到最高峰,之后到24h時(shí)間段內(nèi)略微下降。另一方面,正常對(duì)照組中的Muller細(xì)胞分泌的BDNF、CNTF蛋白量-時(shí)間曲線顯示BDNF蛋白量隨時(shí)間呈現(xiàn)逐漸衰減的趨勢(shì),而CNTF則相對(duì)保持穩(wěn)定。然而與光損傷661W共培養(yǎng)的Muller細(xì)胞分泌的BDNF蛋白量迅速上調(diào),在共培養(yǎng)后的6h達(dá)到最高峰,之后略有下降；其所分泌的CNTF則逐步平穩(wěn)上升。LDH、TUNEL等實(shí)驗(yàn)結(jié)果顯示相較單獨(dú)培養(yǎng)的光損傷661W細(xì)胞,與小膠質(zhì)細(xì)胞共培養(yǎng)的光損傷661W細(xì)胞的壞死率隨著時(shí)間進(jìn)展顯著上升；而與Muller細(xì)胞共培養(yǎng)的光損傷661W細(xì)胞的壞死率則明顯減低。 本部分的實(shí)驗(yàn)研究發(fā)現(xiàn)光損傷誘導(dǎo)的感光細(xì)胞凋亡引發(fā)了小膠質(zhì)細(xì)胞的激活和Muller細(xì)胞的反應(yīng)性膠質(zhì)化,并伴隨著小膠質(zhì)細(xì)胞分泌的促炎因子IL-1β和TNF-α和Muller細(xì)胞分泌的神經(jīng)營(yíng)養(yǎng)因子BDNF、CNTF的上調(diào),并且小膠質(zhì)細(xì)胞的激活加重了661W細(xì)胞的損傷,而Muller細(xì)胞的反應(yīng)性膠質(zhì)化則減輕了661W細(xì)胞的凋亡,表明了膠質(zhì)細(xì)胞活性改變?cè)诠鈸p傷誘導(dǎo)感光細(xì)胞變性過程起著重要的作用。 第三部分：電刺激干預(yù)光損傷感光細(xì)胞凋亡誘導(dǎo)的膠質(zhì)細(xì)胞激活的作用 將1h雙相方波、直流電刺激(3ms,20Hz,300～1600μA)預(yù)先作用于光損傷661W和小膠質(zhì)細(xì)胞或Muller細(xì)胞共培養(yǎng)體系,視為干預(yù)組；將未接受電刺激的此共培養(yǎng)體系視為未干預(yù)對(duì)照組；正常661W細(xì)胞和小膠質(zhì)細(xì)胞或Muller細(xì)胞共培養(yǎng)體系視為正常對(duì)照組。采用免疫熒光染色在共培養(yǎng)24h后觀察各組小膠質(zhì)細(xì)胞及Muller細(xì)胞形態(tài)學(xué)、數(shù)量的差異；利用Real-time PCR和Western blot法在共培養(yǎng)后3h,6h,12h,24h對(duì)各組小膠質(zhì)細(xì)胞所分泌的促炎因子IL-1β、TNF-α以及Muller細(xì)胞所分泌的神經(jīng)營(yíng)養(yǎng)因子BDNF、CNTF的基因表達(dá)量和蛋白分泌量?jī)山M差異以及時(shí)間趨勢(shì)變化進(jìn)行定量分析。 結(jié)果顯示：免疫學(xué)熒光染色顯示的未干預(yù)對(duì)照組和正常對(duì)照組間的小膠質(zhì)細(xì)胞和Muller細(xì)胞形態(tài)學(xué)差別如第一部分所述,電刺激干預(yù)組的小膠質(zhì)細(xì)胞的阿米巴樣的活化數(shù)量則較干預(yù)組明顯減少,并且一部分細(xì)胞雖然沒有出現(xiàn)像靜息狀態(tài)時(shí)的明顯的分支狀,但胞體呈扁平狀態(tài),我們將其視作“中間狀態(tài)”；而電刺激干預(yù)組的Muller細(xì)胞則較未干預(yù)對(duì)照組和正常對(duì)照組的Muller細(xì)胞顯得胞體更大,胞體內(nèi)纖維組織更豐富,且細(xì)胞數(shù)量也明顯增多。伴隨著形態(tài)學(xué)的改變,Real-time PCR和Western blot結(jié)果顯示電刺激干預(yù)組中的小膠質(zhì)細(xì)胞IL-1β和TNF-α的基因和蛋白表達(dá)量較未干預(yù)組顯著降低,Muller細(xì)胞BDNF和CNTF的基因和蛋白表達(dá)量較未干預(yù)組進(jìn)一步升高；蛋白量-時(shí)間趨勢(shì)曲線則顯示電刺激干預(yù)抑制了未十預(yù)組中小膠質(zhì)細(xì)胞IL-1β和TNF-α持續(xù)升高,分別在共培養(yǎng)后24h和12h降至最低最低點(diǎn)；而電刺激干預(yù)組中Muller細(xì)胞分泌的BDNF蛋白量較未干預(yù)組隨時(shí)間上升幅度進(jìn)一步加大；CNTF的分泌高峰則被提前至共培養(yǎng)后6h,上升幅度增大并保持至共培養(yǎng)后24h。 這部分實(shí)驗(yàn)結(jié)果表明：電刺激能夠有效抑制由光損傷感光細(xì)胞誘導(dǎo)的小膠質(zhì)細(xì)胞激活,也能夠顯著提升Muller細(xì)胞反應(yīng)性膠質(zhì)化,從而減輕小膠質(zhì)細(xì)胞的毒性作用,促進(jìn)Muller細(xì)胞的神經(jīng)保護(hù)作用,證明了電刺激保護(hù)光損傷感光細(xì)胞是通過調(diào)控膠質(zhì)活性這一機(jī)理,使得電刺激作為一種促進(jìn)感光細(xì)胞存活的治療方法效果更為確切。
[Abstract]:Part I: neuroprotective effects of electrical stimulation on photoreceptor survival
The photoreceptor cell line (661W) was cultured in vitro. After inoculation on the six hole plate wall, a broad spectrum blue light irradiation with the intensity of 4-6h light intensity of 150001ux was received in a light irradiation incubator. The LDH cell necrosis was measured by 24h after light irradiation. The apoptosis and morphological changes of 661W were observed by TUNEL apoptosis and immunofluorescence staining. The results showed: light After the LDH experiment, the LDH experiment showed that 59.7% + 2.7% of 661W cell necrosis, and 70% of the positive staining was apoptosis, while the immunofluorescence staining found that the normal 661W was flat and the cells were closely connected. But after the light damage, the 661W synapses became elongated, the cells lost the flat shape, and the space between the cells became significantly larger, indicating that light damage induced the photoreceptor cells. The apoptosis model was successfully established.
Using 1H biphasic square wave, direct current stimulation (3MS, 20Hz, 300~1600 u A) pre acted on the co culture system of light damaged 661W and microglia or Muller cells, and regarded it as an intervention group. The co culture system without electrical stimulation was considered as a non intervention control group; the co culture system of normal 661W cells and microglia or Muller cells was used as a co culture system. As a normal control group, LDH experiments were carried out after co culture of 3H, 6h, 12h, 24h, and TUNEL apoptosis staining and immunofluorescence staining were carried out after co culture of 24h. The results were as follows: the apoptosis time curve of LDH showed that the 1000 micron electrical stimulation was preacted on the co culture of 661W and microglia in the light damage of 661W and microglia. The cell mortality of the cell was significantly reduced from 12h to 661W after co culture, and remained relatively constant until the co culture of 24h. Similarly, after the 1600M electrical stimulation was pre acted on the co culture group of 661W and Muller cells, the death rate of 661W from the co culture of 3H was significantly reduced and the decrease was gradually increased. After co culture, 24h. TUNEL staining showed 24h after co culture. The ratio of TUNEL staining positive cells in the electrical stimulation intervention group decreased significantly than that in the non intervention group. The immunofluorescence staining also indicated that the 661W of the light injured 661W cells and the microglia intervention group was lighter than that in the non intervention group, and the cell space was smaller. We also used electrical stimulation to stimulate the 661W cells that were cultured separately after light damage, and performed LDH, TUNEL and immunofluorescence staining at the same time nodes, but the results were different from the electrical stimulation that acted on the co culture system. The intervention of electrical stimulation did not reduce the apoptosis of 661W cells.
The experimental results in this part show that electrical stimulation can reduce the apoptosis and degeneration of photoreceptor cells caused by strong light irradiation, but the photoreceptor cells themselves do not respond to the electrical stimulation. Electrical stimulation may change the activity of glial cells, and the changes in the activity of glial cells affect the survival of the photoreceptor.
The second part: light induced photoreceptor degeneration can activate retinal glial cells and activate glial cells, thereby affecting the apoptosis of photoreceptor cells.
After successful establishment of a model of photoreceptor degeneration induced by light damage, we further explore the number of microglia and Muller cells affected by photoreceptor cells, morphologic changes and the changes associated with the associated function, and explore parallel, using the co culture system of glial cells and light damaged photoreceptor cells. Changes in the survival state of 661W cells. Normal 661W cells and microglia or Muller cell co culture group were considered as normal controls. After co culture of 24h, the number and morphology of two groups of microglia and Muller cells were observed by immunofluorescence staining, while Real-time PCR and Western blot were used in the co culture of 3H, 6h, 12h, and 24. H was used to quantitatively analyze the difference in the two groups of gene expression and protein secretion of CNTF secreted by two groups of microglia secreted by two microglia cells, the two groups of neurotrophic factor BDNF, the two groups of gene expression and protein secretion and the change of the time trend. And the individual cultured 661W cells were cultured by LDH, TUNEL and immunofluorescence staining. The difference in necrosis and apoptosis rate between 661W cells co cultured with microglia or Muller cells was observed.
The results showed that the immunocytochemical experiments found that the microglia co cultured with normal 661W cells were in a state of rest, with a branched form, a long synapse and a smaller cell body. The microglia co cultured with light damaged 661W cells was activated by a form of amoeba like or round shape, short synapses and large bodies, and the number was increased in number than that of a normal control group. There was no significant difference in the form of Muller cells in the two groups. In addition, the 24h, Real time PCR and Western blot after co culture showed that the gene and protein expression of IL-1 beta and TNF- a in the microglia co cultured with light damaged 661W was significantly higher than that in the normal control group. The expression of IL-1 beta and TNF- alpha secreted by microglia in the normal control group was basically stable and low in the time period of 3H to 24h in the normal control group. On the contrary, the amount of IL-1 beta protein secreted by the microglia cultured with light damaged 661W was the amount of IL-1 beta protein As time progresses gradually, 24h reaches the highest peak after co culture. Similarly, the amount of TNF- alpha protein secreted by the 12h is up to the highest peak after co culture, and then slightly decreases in the 24h time period. On the other hand, the BDNF of Muller cells in the normal control group and the CNTF protein quantity time curve show BDNF protein. While the amount of CNTF was gradually declining with time, while the amount of BDNF protein secreted by Muller cells co cultured with light damage 661W increased rapidly, and the 6h reached the highest peak after co culture, and then decreased slightly, and the CNTF secreted by the co culture was gradually increased by.LDH, TUNEL and other experimental results showed that it was compared to the individual culture. Light damage of 661W cells and light injury co cultured with microglia cells, the necrosis rate of 661W cells increased significantly with time, while the necrosis rate of 661W cells co cultured with Muller cells decreased significantly.
The experimental study in this part found that photoreceptor apoptosis induced by light damage induces the activation of microglia and the reactive glia of Muller cells, and is accompanied by the increase of the neurotrophic factor BDNF, CNTF, secreted by microglia secreted by pro-inflammatory cytokines and TNF- A and Muller cells, and the activation of microglia is aggravated. The damage of 661W cells and the reactive glialization of Muller cells reduce the apoptosis of 661W cells, indicating that the change of glial cell activity plays an important role in the process of photoreceptor degeneration induced by light damage.
The third part: the effect of electrical stimulation on glial cell activation induced by photoreceptor apoptosis.
1H biphasic square wave, direct current stimulation (3MS, 20Hz, 300~1600 u A) were pre acted on the co culture system of light damage 661W and microglia or Muller cells, and the co culture system without electrical stimulation was considered as untreated control group; normal 661W cells and microglia or Muller cell co culture system were regarded as normal. In the control group, the morphologic and quantitative differences of microglia and Muller cells were observed by immunofluorescence staining after co culture of 24h, and 3h, 6h, 12h and 24h were used in the co culture of 3H, 6h, 12h, and 24h on the microglia and the secretion of neurotrophic factors secreted by Real-time PCR and Western blot. F, CNTF gene expression and protein secretion in two groups of differences and time trend changes were quantitatively analyzed.
The results showed that the morphological differences between the microglia and Muller cells between the non intervention control group and the normal control group showed that the number of amoeba like activation in the microglia in the electrical stimulation intervention group was significantly lower than that in the intervention group, and some of the cells did not appear to be resting like resting form in the electrical stimulation intervention group. The obvious branch of the state, but the cell body is flat, we regard it as the "middle state", and the Muller cells in the electrical stimulation intervention group are larger than the Muller cells in the control group and the normal control group, and the fibrous tissue in the cell is more abundant, and the number of cells is also significantly increased. With the morphological changes, Real- The results of time PCR and Western blot showed that the gene and protein expression of IL-1 beta and TNF- alpha in the microglia in the electrical stimulation intervention group was significantly lower than that in the non intervention group. The gene and protein expression of BDNF and CNTF in Muller cells was further higher than that in the unintervened group; the protein quantity time trend curve showed that the electrical stimulation intervention inhibited the pre ten preconditioning. The IL-1 beta and TNF- alpha of primary and middle glial cells in the group continued to rise, and 24h and 12h decreased to the lowest lowest point after co culture, and the amount of BDNF protein secreted by Muller cells in the electrical stimulation intervention group was further increased as compared with those in the non intervention group. The peak of CNTF secretion was advanced to the co culture of 6h, and the increase was increased and kept to the same level. 24h. after culture
The experimental results show that electrical stimulation can effectively inhibit the activation of microglia induced by light damaged photoreceptor cells, and can significantly enhance the reactive gliosis of Muller cells, thus mitigate the toxicity of microglia and promote the neuroprotective effect of Muller cells. It is proved that the electrical stimulation of light damaged photoreceptor cells can be used to protect the photoreceptor cells. Over regulation of glial activity makes electrical stimulation more effective as a therapeutic method to promote the survival of photoreceptors.

【學(xué)位授予單位】：復(fù)旦大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2012
【分類號(hào)】：R329

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