富血小板血漿促糖尿病創(chuàng)面愈合機制的初步研究
發(fā)布時間：2018-10-31 14:00
【摘要】：目的探討富血小板血漿(PRP)促進糖尿病創(chuàng)面愈合與核苷酸結(jié)合寡聚化結(jié)構(gòu)域樣受體蛋白(NLRP3)炎性反應(yīng)復(fù)合物/IL-1β信號通路的關(guān)系。方法共收集25份組織標本,5份取自5例糖尿病截肢患者截下肢體的遠端壞死交界區(qū)(DMD組),5份取自前述5例糖尿病截肢患者截下肢體的近端創(chuàng)面(DMP組),5份取自5例非糖尿病截肢患者截下肢體的近端創(chuàng)面(NDM組),5份取自5例糖尿病足潰瘍保肢治療患者的潰瘍創(chuàng)面使用PRP治療前行清創(chuàng)時去除的組織(NPRP組),5份取自前述5例糖尿病足潰瘍保肢治療患者的潰瘍創(chuàng)面使用PRP治療后首次行清創(chuàng)時去除的組織(PRP組)。分別采用Western印跡法檢測NIRP3蛋白表達,ELISA檢測IL-1β蛋白表達,實時熒光定量PCR檢測NLRP3基因和IL-1β基因表達。結(jié)果 DMD組和DMP組的IL廣1β和NLRP3蛋白相對表達量和基因相對表達量均顯著高于NDM組(P值均0.05),DMP組的IL-1β和NIRP3蛋白相對表達量和基因表達量均顯著高于DMD組(P值均0.05)。NPRP組的IL-1β和NLRP3蛋白相對表達量和基因相對表達量均顯著高于PRP組(P值均0.05)。結(jié)論 NLRP3炎性反應(yīng)復(fù)合物/IL-1β信號通路上調(diào)可阻礙糖尿病創(chuàng)面的愈合。PRP通過抑制NLRP3炎性反應(yīng)復(fù)合物/IL-1β信號通路,加快糖尿病創(chuàng)面愈合進程,是其促進糖尿病創(chuàng)面愈合的機制之一。
[Abstract]:Objective to investigate the relationship between platelet rich plasma (PRP) and nucleotide binding oligodeoxyribonucleotide domain like receptor protein (NLRP3) inflammatory response complex / IL-1 尾 signaling pathway in diabetic wound healing. Methods A total of 25 tissue specimens were collected from the distal necrotic junction region (DMD group) of 5 patients with diabetic amputation (DMD group) and from the proximal wound surface (DMP group) of 5 patients with diabetic amputation (DMP group). Five cases were taken from the proximal wound of limb amputation in 5 cases of non-diabetic amputation (NDM group), and 5 cases were taken from the ulcer wounds of 5 cases of diabetic foot ulcer treated with limb salvage (NPRP group), and 5 cases were treated with PRP before debridement (NPRP group). Five patients with diabetic foot ulcer treated with limb salvage therapy were treated with PRP for the first time after debridement (PRP group). NIRP3 protein expression was detected by Western blot, IL-1 尾 protein was detected by ELISA, NLRP3 gene and IL-1 尾 gene expression were detected by real-time fluorescence quantitative PCR. Results the relative expression of IL 1 尾 and NLRP3 protein in DMD group and DMP group was significantly higher than that in NDM group (P < 0. 05). The relative expression and gene expression of IL-1 尾 and NIRP3 protein in DMP group were significantly higher than those in DMD group (P < 0. 05). The relative expression of IL-1 尾 and NLRP3 protein and gene expression in). NPRP group were significantly higher than those in PRP group (P < 0. 05). Conclusion the upregulation of NLRP3 inflammatory response complex / IL-1 尾 signaling pathway may inhibit the healing of diabetic wounds. PRP can accelerate the healing process of diabetic wounds by inhibiting the NLRP3 inflammatory response complex / IL-1 尾 signaling pathway. It is one of the mechanisms of promoting wound healing of diabetes mellitus.
【作者單位】： 上海交通大學(xué)附屬第一人民醫(yī)院骨科;上海交通大學(xué)附屬第六人民醫(yī)院骨科;
【分類號】：R587.2
本文編號：2302450
[Abstract]:Objective to investigate the relationship between platelet rich plasma (PRP) and nucleotide binding oligodeoxyribonucleotide domain like receptor protein (NLRP3) inflammatory response complex / IL-1 尾 signaling pathway in diabetic wound healing. Methods A total of 25 tissue specimens were collected from the distal necrotic junction region (DMD group) of 5 patients with diabetic amputation (DMD group) and from the proximal wound surface (DMP group) of 5 patients with diabetic amputation (DMP group). Five cases were taken from the proximal wound of limb amputation in 5 cases of non-diabetic amputation (NDM group), and 5 cases were taken from the ulcer wounds of 5 cases of diabetic foot ulcer treated with limb salvage (NPRP group), and 5 cases were treated with PRP before debridement (NPRP group). Five patients with diabetic foot ulcer treated with limb salvage therapy were treated with PRP for the first time after debridement (PRP group). NIRP3 protein expression was detected by Western blot, IL-1 尾 protein was detected by ELISA, NLRP3 gene and IL-1 尾 gene expression were detected by real-time fluorescence quantitative PCR. Results the relative expression of IL 1 尾 and NLRP3 protein in DMD group and DMP group was significantly higher than that in NDM group (P < 0. 05). The relative expression and gene expression of IL-1 尾 and NIRP3 protein in DMP group were significantly higher than those in DMD group (P < 0. 05). The relative expression of IL-1 尾 and NLRP3 protein and gene expression in). NPRP group were significantly higher than those in PRP group (P < 0. 05). Conclusion the upregulation of NLRP3 inflammatory response complex / IL-1 尾 signaling pathway may inhibit the healing of diabetic wounds. PRP can accelerate the healing process of diabetic wounds by inhibiting the NLRP3 inflammatory response complex / IL-1 尾 signaling pathway. It is one of the mechanisms of promoting wound healing of diabetes mellitus.
【作者單位】： 上海交通大學(xué)附屬第一人民醫(yī)院骨科;上海交通大學(xué)附屬第六人民醫(yī)院骨科;
【分類號】：R587.2
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1 嚴姍姍;PRP對RA-FLS細胞遷移和侵襲的影響[D];揚州大學(xué);2015年
2 劉宸;富血小板血漿對糖尿病大鼠創(chuàng)面巨噬細胞浸潤變化的影響[D];南京醫(yī)科大學(xué);2014年
，本文編號：2302450
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