HSP22過(guò)表達(dá)介導(dǎo)線粒體未折蛋白反應(yīng)對(duì)PD轉(zhuǎn)基因果蠅的影響
發(fā)布時(shí)間:2018-11-24 19:36
【摘要】:目的:探討HSP22過(guò)表達(dá)介導(dǎo)線粒體未折疊蛋白反應(yīng)對(duì)PD轉(zhuǎn)基因果蠅的影響,為進(jìn)一步研究PD的致病機(jī)制提供依據(jù)。方法:采用HSP22 OE、GCN2RNAi和平衡系HSP22 OE;GCN2 RNAi基因干預(yù)PD轉(zhuǎn)基因果蠅,通過(guò)飛行試驗(yàn)觀察對(duì)果蠅表型的影響,蛋白免疫印跡檢測(cè)P-AMPK、P-e IF2α表達(dá)水平。結(jié)果:GCN2 RNAi能明顯降低PD轉(zhuǎn)基因果蠅異翅率(P0.005),輕微提高果蠅的跳躍或者飛行能力(P0.05),使PD轉(zhuǎn)基因果蠅的P-AMPK和P-e IF2α表達(dá)水平均下調(diào);HSP22 OE使PD轉(zhuǎn)基因果蠅的異翅率顯著降低(P0.001),伴隨著跳躍或者飛行能力顯著提高(P0.001),P-AMPK和P-e IF2α表達(dá)水平均顯著下調(diào);平衡系HSP22OE;GCN2 RNAi明顯降低PD轉(zhuǎn)基因果蠅異翅率(P0.005),輕微提高跳躍或者飛行能力(P0.05),反而使PD轉(zhuǎn)基因果蠅的P-AMPK和P-e IF2α表達(dá)水平上調(diào)。結(jié)論:(1)UPRmt過(guò)度應(yīng)激水平是PD轉(zhuǎn)基因果蠅的致病機(jī)制之一。(2)HSP22對(duì)PD轉(zhuǎn)基因果蠅具有保護(hù)作用,其保護(hù)機(jī)制可能與UPRmt應(yīng)激水平存在負(fù)相關(guān)性。
[Abstract]:Aim: to investigate the effect of HSP22 overexpression mediated mitochondrial unfolded protein reaction on PD transgenic Drosophila melanogaster, and to provide evidence for further study on the pathogenesis of PD. Methods: HSP22 OE,GCN2RNAi and balance line HSP22 OE;GCN2 RNAi gene were used to interfere with PD transgenic Drosophila. The phenotype of Drosophila melanogaster was observed by flight test. The expression of P-AMPKG P-e IF2 偽 was detected by Western blot. Results: GCN2 RNAi could significantly decrease the abnormal wing rate of PD transgenic Drosophila (P0.005), slightly improve the jumping or flying ability of Drosophila melanogaster (P0.05), and down-regulate the expression of P-AMPK and P-e IF2 偽 in PD transgenic Drosophila (P0.05). HSP22 OE significantly decreased the heteropterygoid rate of PD transgenic Drosophila (P0. 001), accompanied by jumping or flight ability (P0. 001), and decreased the expression of P-AMPK and P-e IF2 偽. GCN2 RNAi significantly decreased the abnormal wing rate of PD transgenic Drosophila (P0.005), slightly improved the jumping or flying ability (P0.05), but increased the expression of P-AMPK and P-e IF2 偽 in PD transgenic Drosophila (P0.05). Conclusion: (1) the level of UPRmt overstress is one of the pathogenetic mechanisms of PD transgenic Drosophila. (2) HSP22 has protective effect on PD transgenic Drosophila, and its protective mechanism may have a negative correlation with UPRmt stress level.
【學(xué)位授予單位】:桂林醫(yī)學(xué)院
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2016
【分類(lèi)號(hào)】:R741
本文編號(hào):2354788
[Abstract]:Aim: to investigate the effect of HSP22 overexpression mediated mitochondrial unfolded protein reaction on PD transgenic Drosophila melanogaster, and to provide evidence for further study on the pathogenesis of PD. Methods: HSP22 OE,GCN2RNAi and balance line HSP22 OE;GCN2 RNAi gene were used to interfere with PD transgenic Drosophila. The phenotype of Drosophila melanogaster was observed by flight test. The expression of P-AMPKG P-e IF2 偽 was detected by Western blot. Results: GCN2 RNAi could significantly decrease the abnormal wing rate of PD transgenic Drosophila (P0.005), slightly improve the jumping or flying ability of Drosophila melanogaster (P0.05), and down-regulate the expression of P-AMPK and P-e IF2 偽 in PD transgenic Drosophila (P0.05). HSP22 OE significantly decreased the heteropterygoid rate of PD transgenic Drosophila (P0. 001), accompanied by jumping or flight ability (P0. 001), and decreased the expression of P-AMPK and P-e IF2 偽. GCN2 RNAi significantly decreased the abnormal wing rate of PD transgenic Drosophila (P0.005), slightly improved the jumping or flying ability (P0.05), but increased the expression of P-AMPK and P-e IF2 偽 in PD transgenic Drosophila (P0.05). Conclusion: (1) the level of UPRmt overstress is one of the pathogenetic mechanisms of PD transgenic Drosophila. (2) HSP22 has protective effect on PD transgenic Drosophila, and its protective mechanism may have a negative correlation with UPRmt stress level.
【學(xué)位授予單位】:桂林醫(yī)學(xué)院
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2016
【分類(lèi)號(hào)】:R741
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