本文選題：百草枯　切入點(diǎn)：肺纖維化　出處：《環(huán)境與職業(yè)醫(yī)學(xué)》2017年08期

【摘要】：近年來,除草劑在農(nóng)業(yè)生產(chǎn)中廣泛使用,中毒事件時(shí)有發(fā)生,其中以百草枯中毒多見,死亡率較高。百草枯中毒的主要靶器官是肺臟,其病理改變主要為早期的肺泡炎、肺水腫及晚期的肺纖維化。百草枯中毒致肺纖維化的機(jī)制復(fù)雜,新近研究發(fā)現(xiàn)多種細(xì)胞因子及其介導(dǎo)的信號(hào)通路是百草枯致肺纖維化形成過程中的關(guān)鍵環(huán)節(jié)。本文對(duì)轉(zhuǎn)化生長(zhǎng)因子-β1(TGF-β1)及其介導(dǎo)的主要細(xì)胞信號(hào)通路(Smads、MAPK、Wnt)在百草枯致肺上皮間質(zhì)轉(zhuǎn)化中的作用進(jìn)行綜述。
[Abstract]:In recent years, herbicides are widely used in agricultural production, and poisoning events occur frequently, among which paraquat poisoning is more common and mortality is higher. The main target organ of paraquat poisoning is lung, and its pathological changes are mainly early alveolitis. Pulmonary edema and late pulmonary fibrosis. The mechanism of pulmonary fibrosis caused by paraquat poisoning is complicated. Recent studies have found that many cytokines and their mediated signaling pathways are the key link in the process of pulmonary fibrosis induced by paraquat. In this paper, we studied the expression of transforming growth factor-尾 1 (TGF- 尾 1) and its main cell signaling pathway, SmadsMAPKwnt, in paraquat induced by paraquat. The role of interstitial transformation in pulmonary epithelium was reviewed.
【作者單位】： 濟(jì)南大學(xué)山東省醫(yī)學(xué)科學(xué)院醫(yī)學(xué)與生命科學(xué)學(xué)院;山東省醫(yī)學(xué)科學(xué)院山東省職業(yè)衛(wèi)生與職業(yè)病防治研究院;山東大學(xué)附屬省立醫(yī)院中毒與職業(yè)病科;
【基金】：山東省中醫(yī)藥科技發(fā)展計(jì)劃(編號(hào):2015-328) 山東省自然科學(xué)基金(編號(hào):ZR2015YL046)
【分類號(hào)】：R595.4

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