摘要：目的分析湿润烧伤膏(MEBO)对创面组织自噬信号因子Beclin1、LC3、p62的调控作用及其促进创面愈合的机制。方法选取SPF级Wistar雄性大鼠250只,随机分为空白组、对照组、模型组、康复新组、MEBO组各50只。对照组建立常规创面模型,模型组、康复新组、MEBO组建立糖尿病创面模型,对照组、模型组大鼠创面予生理盐水外敷治疗,康复新组、MEBO组分别予康复新和MEBO外敷治疗。分别于干预第1、5、11、18、25天观察创面愈合情况、苏木素-伊红(HE)染色病理及自噬体的变化;免疫荧光法及Western印迹检测创面组织Beclin1、LC3、p62的变化;qRT-PCR分析Beclin1、LC3、p62 mRNA的表达。结果治疗过程中,对照组愈合最快,模型组愈合最慢,早期各组创面愈合率无显著差异(P>0.05),晚期各组创面愈合率:对照组>MEBO组>康复新组>模型组(P<0.05)。对照组、康复新组、MEBO组创面组织病理形态改善优于模型组。对照组、模型组、康复新组、MEBO组创面组织中Beclin1、LC3平均光密度(OD)值上升后下降,p62 OD值下降后上升;细胞内自噬体数目升高后下降;创面组织Beclin1、p-Beclin1表达量及LC3Ⅱ/LC3Ⅰ比值上升后下降,p62表达下降后上升;Beclin1、LC3 mRNA表达上升后下降,p62表达下降后上升差异均有统计学意义(均P<0.05)。结论 MEBT/MEBO可有效促进糖尿病创面愈合,细胞自噬激活可能是其作用机制之一。

摘要：目的:探讨湿润烧伤膏(MEBO)干预糖尿病性溃疡创面组织超微结构及细胞间粘附分子-1(ICAM-1)、血管细胞粘附分子-1(VCAM-1)表达的作用机制。方法:于2015年6月选取145只雄性健康SPF级SD大鼠,35只为空白组,110只采用腹腔注射链脲佐菌素(STZ)法制备糖尿病模型,8周后选取糖尿病成模大鼠90只采用随机数字表分为模型组、MEBO组及贝复济组,每组30只,和空白组30只一起制备溃疡创面模型,成功后空白及模型组予0.9%氯化钠溶液纱条、MEBO组予MEBO纱条、贝复济组予贝复济溶液纱条局部换药处理,1次/d。各组分别于创面干预后第3、6、12天每次随机选10只大鼠,取相同位点创面组织,应用荧光PCR技术检测ICAM-1、VCAM-1mRNA表达,电镜观察创面组织超微病理结构。结果:空白组、模型组、MEBO组和贝复济组第3、6、12天创面组织ICAM-1、VCAM-1 mRNA表达比较,差异均有统计学意义(P<0.05);其中第3天时,模型组创面组织ICAM-1、VCAM-1 mRNA表达均低于空白组,MEBO组创面组织ICAM-1、VCAM-1 mRNA表达均高于... 更多 还原 __vpn_eval__((function(){ AbstractFilter('ChDivSummary', 'ChDivSummaryMore', 'ChDivSummaryReset'); }).toString().slice(12, -2))

摘要：目的 探讨湿润烧伤膏(MEBO)治疗大鼠糖尿病性创面的作用及部分作用机制。方法 采用高脂饲料喂养及腹腔注射链脲佐菌素(STZ)构建糖尿病大鼠模型，成模后将糖尿病大鼠随机分为模型组、MEBO组及重组牛碱性成纤维细胞生长因子外用液(贝复济)组，与空白组同时制备创面模型后，分别予以相应药物干预治疗，MEBO组予以MEBO创面外敷，贝复济组予以贝复济创面外敷，空白组与模型组予以凡士林无菌纱布创面外敷。各组于干预治疗后第4、6、12天观察创面情况计算创面愈合率，分别取相同位点创面组织采用实时荧光定量-聚合酶链反应(RT-qPCR)法检测miRNA-21和转化生长因子(TGF)-β1 mRNA表达，应用Western印迹检测创面组织中TGF-β1、P-Smad2、P-Smad3和Smad7蛋白表达。结果 与空白组比较，模型组第4、6、12天创面愈合率、创面组织中miRNA-21、TGF-β1 mRNA及TGF-β1、P-Smad2、P-Smad3蛋白表达显著降低，Smad7蛋白表达显著升高(均P<0.05);与模型组比较，MEBO组干预第6、12天创面愈合率、创面组织中miRNA-21、TGF-β1 mRNA表达及TGF-β1、P-Smad2、P-Smad3蛋白表达显著升高，Smad7蛋白表达显著降低(均P<0.05)。结论 MEBO可能通过miRNA-21调控TGF-β1/Smads信号通路促进成纤维细胞迁移、增殖，促进糖尿病性创面修复。

摘要：Burn therapy (MEBT)/moist exposed burn ointment (MEBO) is an effective traditional Chinese medicine method to treat diabetic wound, but the mechanism is unclear. Autophagy has been proved to be closely related with wound healing, so MEBO/MEBT is hypothesized to promote diabetic wound healing by regulating autophagy. To explore the mechanism of moist exposed MEBT/MEBO promoting diabetic wound repair. Eighty male Wistar rats were randomly assigned to control (n = 20) and diabetic group induced by intraperitoneal injection of STZ (n = 60), which were further randomly assigned to MEBO, Kangfuxin and model groups (n = 20 each). All rats underwent full-thickness skin resection in the back. Wound healing was dynamically observed and wound tissues were collected at five time points for pathological examination, autophagosome and the expression of PI3K, Akt and mTOR. The healing time in the control group was the shortest, no statistically significant difference was found between the MEBO and the Kangfuxin group (p = 0.76). The morphology of autophagosomes ranged large to small, which was the most obvious in the MEBO group. The mRNA and protein expression of PI3K, Akt and mTOR in each group reached the peak on Day 5, the levels in the MEBO group were the highest (F = 18.43, 19.97, 15.36, p < 0.05). On Day 11, the expression levels in each group began to decline. In this study, we discussed the molecular mechanism of MEBT/MEBO promoting the repair of diabetic ulcer wounds through autophagy and PI3K-Akt-mTOR signalling pathway, which provides a new way for drug design in the future.