本文選題：對(duì)乙酰氨基酚 + 線粒體��； 參考：《中國(guó)藥理學(xué)與毒理學(xué)雜志》2017年02期

【摘要】：目的探討對(duì)乙酰氨基酚(APAP)對(duì)HepaRG細(xì)胞過(guò)氧化物酶體增殖物激活受體γ共激活因子1α(PGC-1α)信號(hào)通路介導(dǎo)的線粒體新生的影響。方法接種HepaRG細(xì)胞并給予生長(zhǎng)培養(yǎng)基,待細(xì)胞長(zhǎng)滿后,替換為分化培養(yǎng)基進(jìn)行誘導(dǎo)分化,每天觀察細(xì)胞形態(tài)并拍照。APAP(0.125,0.25,0.5,1,2,4,8和12 mmol·L~(-1))處理誘導(dǎo)分化后的HepaRG細(xì)胞24和48 h,MTT法測(cè)定細(xì)胞存活率。Western蛋白印跡法檢測(cè)細(xì)胞線粒體新生相關(guān)蛋白PGC-1α、核呼吸因子2(NRF-2)和線粒體轉(zhuǎn)錄因子A(TFAM),以及線粒體構(gòu)成蛋白NADH脫氫酶亞基1(ND-1)的表達(dá)。結(jié)果誘導(dǎo)分化后顯微鏡下可見(jiàn)肝細(xì)胞樣和膽管細(xì)胞樣2種形態(tài)的細(xì)胞。與正常對(duì)照組相比,APAP作用24和48 h后,隨APAP濃度的增加,細(xì)胞存活率不斷降低,其IC_(50)分別5.64和2.65 mmol·L~(-1)。與正常對(duì)照組相比,APAP作用24 h,0.5,1,2和4 mmol·L~(-1)組PGC-1α表達(dá)水平顯著增加(P0.01),8 mmol·L~(-1)組顯著降低(P0.01);0.5 mmol·L~(-1)組NRF-2表達(dá)水平顯著增加(P0.05),2,4和8 mmol·L~(-1)組顯著降低(P0.01);1 mmol·L~(-1)組TFAM表達(dá)水平顯著增加(P0.05),4和8 mmol·L~(-1)組顯著降低(P0.01);0.5,1,2和4 mmol·L~(-1)組ND-1表達(dá)水平顯著增加(P0.01),8 mmol·L~(-1)組顯著降低(P0.01)。結(jié)論 APAP可誘導(dǎo)或抑制HepaRG細(xì)胞的線粒體新生,其機(jī)制可能與PGC-1α通路蛋白表達(dá)有關(guān)。
[Abstract]:Objective to investigate the effect of paracetamol (AP) on mitochondrial neogenesis mediated by peroxisome proliferator activated receptor 緯 -coactivator 1 偽 -PGC-1 偽 signal pathway in HepaRG cells. Methods HepaRG cells were inoculated and the growth medium was given. When the cells were full, the cells were replaced with the differentiation medium to induce differentiation. Observation of cell morphology and photo taking of .APAPN 0.125 ~ 0.25 ~ (0.25) and 12 mmol / L ~ (-1) treatment of differentiated HepaRG cells for 24 and 48 h MTT assay for cell viability. Western blot assay for the detection of mitochondrial neo-associated protein PGC-1 偽, nuclear respiratory factor 2NRF-2) and mitochondrial transcription. The expression of TFAM and NADH dehydrogenase subunit 1 ND-1. Results Hepatocyte-like cells and cholangiobiliary cell-like cells were observed under microscope after induced differentiation. Compared with the normal control group, the cell survival rate decreased with the increase of APAP concentration at 24 and 48 h after treatment with APAP, and its ICD 50 was 5.64 and 2.65 mmol / L ~ (-1), respectively. Compared with the normal control group, the expression of PGC-1 偽 increased significantly in the 24 h and 4 mmol groups (P 0.01 and 8 mmol / L).) the NRF-2 expression level in the P0.01 + 0. 05 mmol / L + 1) group was significantly lower than that in the control group. (2) the expression of NRF-2 in the P0. 055 and 8 mmol / L ~ (1) groups was significantly lower than that in the control group. (2) the expression level of TFAM in the P0. 01 + 1 mmol group was significantly higher than that in the control group. (0. 051 and 8 mmol / L ~-1) groups were significantly lower than those in the control group. The expression of ND-1 was significantly increased in the group of P0.01P0. 01 and 4 mmol. The expression of ND-1 was significantly increased in the group of P0. 01 and P0. 01 mmol. (1) the expression level of P0. 01 was significantly decreased in the group of P0. 01 and P0. 01 of P0. 01. Conclusion APAP can induce or inhibit mitochondrial neogenesis in HepaRG cells, and its mechanism may be related to the expression of PGC-1 偽 pathway protein.
【作者單位】： 軍事醫(yī)學(xué)科學(xué)院疾病預(yù)防控制所毒理學(xué)評(píng)價(jià)研究中心;
【基金】：國(guó)家自然科學(xué)基金青年科學(xué)基金(81302864) 聯(lián)合利華國(guó)際合作項(xiàng)目(CH-2011-1318)~~
【分類(lèi)號(hào)】：R96

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