[關(guān)鍵詞]
[摘要]
目的 考察王不留行黃酮苷促創(chuàng)傷愈合作用,并探討其作用機制。方法 構(gòu)建SD大鼠皮膚開放性創(chuàng)傷模型,創(chuàng)傷部位分別涂抹0.02 g空白軟膏劑基質(zhì)(模型組)、0.02 g含0.1%王不留行黃酮苷的軟膏劑(王不留行黃酮苷組)、0.02 g美寶潤濕燒傷膏(陽性藥)。觀察創(chuàng)傷愈合速率,并取創(chuàng)傷部位皮膚制作石蠟切片,通過HE染色進行組織病理學(xué)評估,通過免疫組化染色觀察增殖細(xì)胞核抗原(PCNA)、p-堿性成纖維細(xì)胞生長因子受體(p-bFGFR)、p-血管內(nèi)皮細(xì)胞生長因子受體(p-VEGFR)、CD31、p-Akt、p-Erk表達,Western blotting法分析Erk和Akt蛋白的磷酸化水平、bFGFR磷酸化水平。結(jié)果 與模型組比較,創(chuàng)傷后3、6、9 d,王不留行黃酮苷組顯著促進開放性創(chuàng)傷愈合(P<0.05、0.01);隨著時間的延長,與模型組比較,王不留行黃酮苷組中成纖維細(xì)胞和內(nèi)皮細(xì)胞大量增殖,炎癥細(xì)胞增殖減少,微血管密度顯著增加(P<0.01);免疫組化及Western blotting結(jié)果顯示,與模型組比較,王不留行黃酮苷組內(nèi)皮細(xì)胞膜受體中bFGFR的磷酸化程度明顯升高(P<0.05、0.01),p-VEGFR磷酸化程度無明顯變化,PI3K/Akt與MAPK/Erk信號通路的節(jié)點蛋白Akt和Erk磷酸化程度均明顯升高(P<0.05)。結(jié)論 王不留行黃酮苷促進開放性創(chuàng)傷愈合,機制可能與激活bFGFR及其下游MAPK/Erk和PI3K/Akt信號通路相關(guān)。
[Key word]
[Abstract]
Objective To investigate the effect of vaccarin on wound healing and to explore the mechanism of vaccarin promoting wound healing. Methods The open wound model of SD rat skin was constructed, and the wound sites were smeared with 0.02 g blank cream matrix (model group), 0.02 g containing 0.1% vaccarin (vaccarin group) or 0.02 g MEBO wetting burn ointment (positive drug). The rate of wound healing was observed and paraffin sections were made from the skin of the wound. Histopathological evaluation was performed by HE staining. Proliferating cell nuclear antigen (PCNA), p-Akt, p-Erk P-basic fibroblast growth factor receptor (p-bFGFR), p-vascular endothelial cell growth factor receptor (p-VEGFR), and CD31 were observed by immunohistochemical staining. Western blotting method were used to analyze the phosphorylation level of Erk, Akt, and bFGFR protein. Results Compared with model group, 3, 6, and 9 d after trauma, vaccarin significantly promoted the healing of open wound healing (P<0.05, 0.01). Compared with model group, the fibroblasts and endothelial cells in vaccarin group were proliferating, the proliferation of the inflammatory cells decreased and the microvessel density increased significantly (P<0.01); The results of immunohistochemistry and Western blotting showed that the degree of phosphorylation of bFGFR in the endothelial cell membrane receptor of vaccarin group was significantly higher than that in model group (P<0.05, 0.01), and the degree of p-VEGFR phosphorylation was not significantly changed, and the degree of Akt and Erk phosphorylation of PI3K/Akt and MAPK/Erk signaling pathway were significantly increased (P<0.05). Conclusion Vaccarin could promote open wound healing, and may be related to activation of bFGFR and its downstream MAPK/Erk and PI3K/Akt signaling pathways.
[中圖分類號]
[基金項目]
中央高?;究蒲袠I(yè)務(wù)費專項(JUSRP51412B)