【摘要】：目的觀察Bevacizumab(貝伐單抗)對轉(zhuǎn)化生長因子(transforming growth factor,TGF)-β2誘導(dǎo)下的人Tenon囊成纖維細(xì)胞轉(zhuǎn)分化的抑制作用,探討抗新生血管藥物抑制青光眼術(shù)后濾過泡瘢痕化的機(jī)制。方法用含體積分?jǐn)?shù)10%胎牛血清的DMEM高糖型培養(yǎng)基對人Tenon囊成纖維細(xì)胞株進(jìn)行體外常規(guī)培養(yǎng)和傳代。實驗分為空白對照組、TGF-β2處理組(加入終濃度為10μg·L-1的TGF-β2DMEM完全培養(yǎng)基)及Bevacizumab干預(yù)組(加入10μg·L-1的TGF-β2和1.0 g·L-1的Bevacizumab DMEM完全培養(yǎng)基),置于37℃、體積分?jǐn)?shù)5%二氧化碳培養(yǎng)箱中培養(yǎng)48 h,并分別應(yīng)用細(xì)胞免疫熒光染色技術(shù)和Western Blot實驗檢測Bevacizumab對TGF-β2刺激下人Tenon囊成纖維細(xì)胞α-平滑肌肌動蛋白(α-smooth muscle actin,α-SMA)表達(dá)的影響。結(jié)果α-SMA蛋白主要表達(dá)在細(xì)胞質(zhì)中,免疫熒光染色結(jié)果顯示TGF-β2處理組可以見到α-SMA的熒光表達(dá),而Bevacizumab干預(yù)組α-SMA蛋白表達(dá)受到抑制。Western Blot結(jié)果顯示空白對照組、TGF-β2處理組及Bevacizumab干預(yù)組α-SMA蛋白相對表達(dá)量分別為0.630±0.038、1.130±0.071和0.340±0.033,Bevacizumab干預(yù)組α-SMA蛋白相對表達(dá)量低于空白對照組和TGF-β2處理組(均為P0.05)。結(jié)論 Bevacizumab可明顯抑制TGF-β2誘導(dǎo)下人Tenon囊成纖維細(xì)胞α-SMA蛋白的表達(dá),抑制成纖維細(xì)胞表型轉(zhuǎn)化。
[Abstract]:Objective to observe the inhibitory effect of Bevacizumab (bevacizumab) on the transdifferentiation of human Tenon capsule fibroblasts induced by transforming growth factor (transforming growth factor,TGF-尾 2, and to explore the mechanism of anti-angiogenic drugs inhibiting bleb scarring after glaucoma surgery. Methods Human Tenon capsule fibroblasts were cultured and subcultured in vitro on DMEM medium containing 10% fetal bovine serum. The experiment was divided into blank control group, TGF- 尾 2 treatment group (adding 10 渭 g L -1 TGF- 尾 2DMEM complete medium) and Bevacizumab intervention group (10 渭 g L -1 TGF- 尾 2 and 1.0 g L -1 Bevacizumab DMEM complete medium) at 37 鈩，

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