目的 觀察骨碎補(bǔ)總黃酮對(duì)大鼠誘導(dǎo)膜中血管內(nèi)皮生長(zhǎng)因子（VEGF）、骨形態(tài)發(fā)生蛋白-2（BMP-2）表達(dá)的影響。方法 60只3月齡SD大鼠，隨機(jī)分為3組：模型組、填充組和填充+TFDR組，每組20只，建立大鼠長(zhǎng)段骨缺損模型，模型組骨缺損處僅克氏針固定，填充組及填充+TFDR組骨缺損處用抗生素骨水泥填充，并用克氏針固定；填充+TFDR組ig給予TFDR （67.5 mg/kg），模型組及填充組ig等量生理鹽水，每天給藥1次，連續(xù)6周。給藥結(jié)束后，處死大鼠，切取骨水泥周?chē)@的白色膜狀物，模型組切取對(duì)應(yīng)階段的瘢痕組織，Elisa定量及免疫組化法觀察誘導(dǎo)膜中BMP-2、VEGF表達(dá)變化。結(jié)果 填充組BMP-2、VEGF表達(dá)水平顯著高于模型組，填充+TFDR組BMP-2、VEGF表達(dá)水平均顯著高于填充組和模型組，各組間差異均有統(tǒng)計(jì)學(xué)意義（P<0.05）；免疫組化檢測(cè)結(jié)果顯示相同趨勢(shì)。結(jié)論 TFDR促進(jìn)Masquelet技術(shù)誘導(dǎo)膜中BMP-2和VEGF表達(dá)。

Objective To observe the effects of total flavonoids of Drynariae Rhizoma (TFDR) on the expression of vascular endothelial growth factor (VEGF) and bone morphogenetic protein (BMP-2) in rat Masquelet-induced membrane.Methods Sixty SD rats aged 3 months were randomly divided into three groups:model group, filling group, and filling + TFDR group with 20 rats in each group. Rat long segment bone defect model was established. The bone defects in model group were fixed only by Kirschner wire, and were filled with antibiotic bone cement in filling group and filling + TFDR group. Rats in filling + TFDR group were ig given TFDR (67.5 mg/kg), the model group and the filling group were treated with equivalent saline, once a day for six weeks. The rats were sacrificed after administration, and bone cement and scar tissue in model group were removed. The expression of BMP-2 and VEGF in the induced membrane was observed by immuno-histochemical analysis of the filling tissue and the induced membrane.Results The positive expression of BMP-2 and VEGF in filling group were higher than model group by Elisa quantitative detection, which of the filling + TFDR group were significantly higher than model group and filling group, the difference was statistically significant by statistical analysis (P < 0.05). Immuno-histochemical analysis showed the same trend.Conclusion TFDR can promote the expression of BMP-2 and VEGF in Masquelet-induced membrane.

河南省中醫(yī)藥科學(xué)研究專(zhuān)項(xiàng)課題資助項(xiàng)目（2015ZY02062）