本文選題：Src激酶　切入點(diǎn)：神經(jīng)炎癥　出處：《中國(guó)醫(yī)學(xué)科學(xué)院學(xué)報(bào)》2017年04期 　論文類型：期刊論文

【摘要】：目的研究小膠質(zhì)細(xì)胞上非受體型酪氨酸激酶Src通過第10號(hào)染色體缺失的磷酸酶張力蛋白同源物基因(PTEN)編碼的PTEN蛋白調(diào)節(jié)細(xì)菌脂多糖(LPS)誘導(dǎo)神經(jīng)炎癥反應(yīng)的分子機(jī)制。方法采用LPS誘導(dǎo)小膠質(zhì)細(xì)胞系BV2,Western blot法檢測(cè)蛋白激酶B(Akt)磷酸化水平評(píng)價(jià)PTEN活性,酶聯(lián)免疫吸附法測(cè)定腫瘤壞死因子-α含量評(píng)價(jià)神經(jīng)炎癥反應(yīng);加入PTEN抑制劑以及Src的小干擾RNA后,觀察神經(jīng)炎癥反應(yīng)的變化,研究Src調(diào)控神經(jīng)炎癥機(jī)制。結(jié)果 LPS誘導(dǎo)BV2細(xì)胞激活后,Akt磷酸化水平顯著升高(P0.001),腫瘤壞死因子-α釋放量顯著增多(P0.001),即引起明顯的神經(jīng)炎癥反應(yīng)。而抑制PTEN蛋白活性后,LPS誘導(dǎo)的Akt磷酸化水平進(jìn)一步升高(P0.05),炎癥因子釋放量進(jìn)一步增多(P0.001);干擾Src基因后,Src蛋白表達(dá)量明顯下降(P0.001),同時(shí)LPS誘導(dǎo)的炎癥因子釋放量與未干擾Src組相比明顯減少,炎癥反應(yīng)減輕(P0.001);PTEN和Akt磷酸化水平也明顯下降(P0.001)。結(jié)論在小膠質(zhì)細(xì)胞上Src激酶可能通過調(diào)節(jié)PTEN蛋白活性調(diào)控神經(jīng)炎癥反應(yīng)。
[Abstract]:Objective to study the molecular mechanism by which non-recipient tyrosine kinase (Src) regulates bacterial lipopolysaccharide (LPS) -induced neuritis induced by PTEN protein encoded by PTEN, a homologue of phosphatase (PTEN) homologue absent on chromosome 10, in microglial cells. Methods LPS-induced microglial cell line BV2-blot was used to detect the phosphorylation level of protein kinase BU-Akt and to evaluate the activity of PTEN. The level of tumor necrosis factor- 偽 was measured by enzyme-linked immunosorbent assay (Elisa) to evaluate the neuroinflammatory response, and the changes of neuroinflammatory response were observed after the addition of PTEN inhibitor and small interfering RNA of Src. Results after the activation of BV2 cells induced by LPS, the phosphorylation level of BV2 cells increased significantly, and the release of tumor necrosis factor- 偽 increased significantly (P0.001), which resulted in an obvious neuroinflammatory response, and inhibited the activity of PTEN protein. LPS-induced phosphorylation level of Akt increased further, the release of inflammatory factors increased, and the expression of SRC protein decreased significantly after interfering with Src gene, and the release of inflammatory factors induced by LPS was significantly decreased compared with that of undisturbed Src group. The levels of PTEN and Akt phosphorylation were also significantly decreased in microglial cells. Conclusion Src kinase may regulate the neuroinflammatory response by regulating the activity of PTEN protein in microglia.
【作者單位】： 中國(guó)醫(yī)學(xué)科學(xué)院北京協(xié)和醫(yī)學(xué)院藥物研究所天然藥物活性物質(zhì)與功能國(guó)家重點(diǎn)實(shí)驗(yàn)室;
【分類號(hào)】：R741

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