目的 研究過氧化氫對(duì) A549 細(xì)胞表達(dá)轉(zhuǎn)化生長(zhǎng)因子 β1 （ TGF-β1 ）和 Smad3 磷酸化的影響。方法 用過氧化氫建立體外A549細(xì)胞損傷模型，MTT法檢測(cè)過氧化氫對(duì)A549細(xì)胞增殖活性的影響，免疫印跡法（Western Blotting）觀察過氧化氫作用不同時(shí)間后A549細(xì)胞TGF-β1和Smad 3磷酸化的表達(dá)。結(jié)果 過氧化氫明顯抑制A549細(xì)胞的增殖，濃度為1.0 mmol/L時(shí)，其對(duì)A549細(xì)胞增殖的抑制率為46.34%；A549細(xì)胞在過氧化氫（1.0 mmol/L）的刺激下，TGF-β1和Smad3磷酸化的表達(dá)量逐漸升高，24 h時(shí)達(dá)到高峰, 48 h下降。結(jié)論 氧化損傷早期，A549細(xì)胞表達(dá)TGF-β1和Smad3磷酸化增加,這可能與肺損傷后依賴Smad3的組織修復(fù)有關(guān)。
引用本文： 楊冬梅 ,丁宇,應(yīng)斌武,蔣飛,徐丹,美朗曲措,范紅. 過氧化氫對(duì)A549細(xì)胞轉(zhuǎn)化生長(zhǎng)因子β1和Smad3表達(dá)的影響. 中國(guó)呼吸與危重監(jiān)護(hù)雜志, 2008, 08(1): 43-46. doi: 復(fù)制
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- 1. Matthay MA, Geiser T, Matalon S,et al.Oxidant-mediated lung injury in the acute respiratory distress syndrome. Crit Care Med, 1999,27:2028-2030.
- 2. Chabot F, Mitchell JA, Gutteridge JM, et al. Reactive oxygen species in acute lung injury. Eur Respir J, 1998,11:745-757.
- 3. Waxman AB, Mahboubi K, Knickelbein RG,et al. Interleukin-11 and interleukin-6 protect cultured human endothelial cells from H2O2-induced cell death. Am J Respir Cell Mol Biol, 2003,29:513-522.
- 4. Bellingan GJ.The pulmonary physician in critical care 6: The pathogenesis of ALI/ARDS.Thorax,2002,57:540-546.
- 5. 陳謙.二喹啉甲酸（BCA）檢測(cè)法.見：汪家政，范明，主編.蛋白質(zhì)技術(shù)手冊(cè)．北京：科學(xué)出版社，2001，51-54．.
- 6. Fehrenbach H. Alveolar epithelial type II cell: defender of the alveolus revisited. Respir Res,2001,2:33-46.
- 7. 張靜，吳瑜.N-乙酰-L-半胱氨酸對(duì)H2O2引起的血管內(nèi)皮細(xì)胞損傷的拮抗效應(yīng).中國(guó)呼吸與危重監(jiān)護(hù)雜志，2003，2：91-94.
- 8. Derynck R, Zhang YE. Smad-dependent and Smad-independent pathways in TGF-beta family signalling. Nature,2003,425:577-584.
- 9. Ebner R, Chen RH, Lawler S, et al . Determination of type I receptor specificity by the type II receptors for TGF-beta or activin.Science,1993,262:900-902.
- 10. Verrecchia F, Chu ML, Mauviel A.Identification of novel TGF-beta /Smad gene targets in dermal fibroblasts using a combined cDNA microarray/promoter transactivation approach.J Biol Chem,2001,276:17058-17062.
- 11. Muthukrishnan L, Warder E, McNeil PL.Basic fibroblast growth factor is efficiently released from a cytolsolic storage site through plasma membrane disruptions of endothelial cells. J Cell Physiol,1991,148:1-16.