本文選題：硼替佐米 + C2C12　； 參考：《蘇州大學(xué)》2015年碩士論文

【摘要】：目的:旨在探討硼替佐米對小鼠成肌細(xì)胞系C2C12的生長和分化的影響并探索影響過程中參與的信號轉(zhuǎn)導(dǎo)通路。方法:(1)利用低濃度馬血清(2%)體外誘導(dǎo)細(xì)胞分化,吉姆薩染色后顯微鏡觀察;(2)吉姆薩染色觀察硼替佐米對C2C12細(xì)胞分化的影響;(3)MTT法檢測硼替佐米對C2C12細(xì)胞增殖的影響;(4)利用流式細(xì)胞術(shù)檢測硼替佐米對C2C12細(xì)胞凋亡、周期的影響;(5)利用免疫印跡法和免疫熒光法檢測硼替佐米對C2C12細(xì)胞分化、周期及凋亡影響的作用機(jī)制。結(jié)果:硼替佐米能抑制多核肌管的形成并伴隨著Myogenin的低表達(dá)。用不同濃度的硼替佐米處理C2C12細(xì)胞,能引起C2C12細(xì)胞增殖能力濃度依賴性的降低。Annexin V/PI染色分析顯示用硼替佐米處理C2C12細(xì)胞24h后能導(dǎo)致細(xì)胞顯著性的凋亡,Cleaved caspas-3的檢測也更加證實(shí)了這一點(diǎn)。硼替佐米引起的細(xì)胞凋亡和p-ERK蛋白表達(dá)降低有關(guān)。細(xì)胞周期結(jié)果顯示用硼替佐米孵育24h會引起G2/M的累積。結(jié)論:結(jié)果表明醫(yī)用硼替佐米濃度能抑制C2C12細(xì)胞的分化,抑制C2C12細(xì)胞的增殖,誘導(dǎo)C2C12細(xì)胞凋亡,引起C2C12細(xì)胞G2/M期的累積。細(xì)胞水平上的研究不支持硼替佐米臨床上用于骨骼肌萎縮的治療。
[Abstract]:Aim: to investigate the effects of bortezomil on the growth and differentiation of mouse myoblast cell line C2C12 and to explore the signal transduction pathway involved in the process. Methods the cell differentiation was induced in vitro by using low concentration equine serums. The effect of bortezomil on the differentiation of C2C12 cells was observed by Giemsa staining. The effect of bortezomil on the proliferation of C2C12 cells was detected by MTT method. Flow cytometry was used to detect the apoptosis of C2C12 cells by bortezomil. The effect of bortezomib on the differentiation, cell cycle and apoptosis of C2C12 cells was studied by Western blot and immunofluorescence. Results: bortezomib inhibited the formation of polynuclear myotube and associated with the low expression of Myogenin. C2C12 cells were treated with bortezomil at different concentrations. The results of Annexin V/PI staining showed that bortezomib could induce the apoptosis of C2C12 cells after 24 hours. The results showed that the apoptosis of C2C12 cells was more obvious after treated with bortezomib for 24 hours. The results showed that the apoptosis of C2C12 cells was also confirmed by the assay of Cleaved caspas-3 after treatment with bortezomib for 24 hours. The apoptosis induced by bortezomib is related to the decrease of p-ERK protein expression. Cell cycle results showed that the accumulation of G _ 2 / M was induced by bortezomib for 24 hours. Conclusion: the results showed that the concentration of bortezomil could inhibit the differentiation of C2C12 cells, inhibit the proliferation of C2C12 cells, induce apoptosis of C2C12 cells, and induce the accumulation of G2 / M phase in C2C12 cells. Studies at the cell level do not support the clinical use of bortezomie in the treatment of skeletal muscle atrophy.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：R685

【參考文獻(xiàn)】

相關(guān)期刊論文 前1條

1 李強(qiáng);羅卓荊;朱錦宇;畢龍;呂榮;孟浩;耿丹;;蛋白酶體抑制劑MG-132對大鼠失神經(jīng)肌萎縮的防治作用[J];第四軍醫(yī)大學(xué)學(xué)報(bào);2007年07期

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本文編號：1981988