| 谢瑞敏,李 想,李强强,魏建仝,王勇平.HMGB1对大鼠糖尿病足溃疡炎症的影响及机制分析[J].,2020,(13):2430-2434 |
| HMGB1对大鼠糖尿病足溃疡炎症的影响及机制分析 |
| Effect and Mechanism of HMGB1 on the Inflammation of Diabetic Foot Ulcer in Rats |
| 投稿时间：2020-02-23 修订日期：2020-03-18 |
| DOI：10.13241/j.cnki.pmb.2020.13.006 |
| 中文关键词: 高迁移率族蛋白B1 糖尿病足 炎症 微血管密度 |
| 英文关键词: HMGB1 Diabetic foot Inflammation Microvascular density |
| 基金项目:甘肃省卫生行业科研计划项目(GSWSKY-2015-53)；甘肃省科技厅创新基地和人才计划项目(18JR3RG211)；兰州大学第一临床医学院卓越计划想项目(20180060130) |
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| 中文摘要: |
| 摘要 目的：分析高迁移率族蛋白1(High mobility group protein 1，HMGB1)对大鼠糖尿病足溃疡炎症的影响及机制。方法：经腹腔注射链脲佐菌素建立糖尿病大鼠模型，并在大鼠的双后足背部做一3 mm×7 mm的全层矩形皮肤缺损，接种质控菌株。将建模成功的大鼠随机分成：模型组(等量生理盐水)、低剂量组(12.5 μg?kg-1?d-1)、中剂量组(25 μg?kg-1?d-1)和高剂量组(50 μg?kg-1?d-1)，每组6只，每天单次腹腔注射，连续给药14 d。另取6只大鼠作为空白组(等量生理盐水)。于规定时间对各组大鼠创面愈合率、微血管密度(Microvascular density，MVD)、组织中血管内皮生长因子(Vascular endothelial growth factor，VEGF)、CD45、Toll 样受体4(Toll like receptor 4，TLR4)、核因子κB (Nuclear factor kappa-B，NF-κB)、白介素-1β(Interleukin-1β，IL-1β)、白介素-6(Interleukin-6，IL-6)、IL-8(Interleukin-8，IL-8)和肿瘤坏死因子-α(Tumor necrosis factor-α，TNF-α)mRNA或蛋白表达量进行检测。结果：与对照组相比，模型组大鼠创面治愈率和微血管密度均较低，VEGF、CD45、TLR4、NF-κB、IL-1β、IL-6、IL-8和TNF-α mRNA或蛋白表达量均较高(P＜0.05)。与模型组相比，三个剂量组大鼠创面治愈率和微血管密度均明显降低(P＜0.05)，VEGF、CD45、TLR4、NF-κB、IL-1β、IL-6、IL-8和TNF-α mRNA或蛋白表达量均较高(P＜0.05)。且随着HMGB1注射剂量增大，创面愈合率、血管生成明显减少(P＜0.05)，炎症因子表达量显著升高(P＜0.05)。结论：HMGB1对大鼠糖尿病足溃疡炎症有促进作用，机制可能与HMGB1/TLR4/NF-κB信号通路相关。 |
| 英文摘要: |
| ABSTRACT Objective: To analyze the effect and mechanism of High mobility group protein 1(HMGB1) on the inflammation of diabetic foot ulcer in rats. Methods: The diabetic rat model was established by intraperitoneal injection of streptozotocin, and a full-thickness rectangular skin defect of 3 mm×7 mm was made on the back of two hind feet of the rat, and inoculation of quality control strains as successful model of foot ulcer. The rats were randomly divided into three groups: the model group (equal amount of normal saline), the low dose group (12.5 μg?kg-1?d-1), the medium dose group (25 μg?kg-1?d-1) and the high dose group (50 μg?kg-1?d-1). Each group consisted of six rats, which were injected intraperitoneally once a day for 14 days. Another 6 rats were taken as the blank group. The wound healing rate, microvascular density (MVD), vascular endothelial growth factor (VEGF), CD45, toll like receptor 4 (TLR4), nuclear factor kappa B (NF-κB), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8(IL-8) and tumor necrosis factor-α(TNF-α) mRNA or protein expression were detected. Results: Compared with the control group, the wound healing rate and microvessel density of the model group were lower, the expression of VEGF, CD45, TLR4, NF-κB, IL-1 β, IL-6, IL-8 and TNF-α mRNA or protein were higher (P<0.05). Compared with the model group, the wound healing rate and MVD of the three dose groups were lower, the expression of VEGF, CD45, TLR4, NF-κB, IL-1 β, IL-6, IL-8 and TNF-α mRNA or protein were higher (P<0.05). Compared with the model group, the wound healing rate and MVD of the three dose groups were significantly reduced (P<0.05), the expression levels of VEGF, CD45, TLR4, NF-κB, IL-1β, IL-6, IL-8 and TNF-α mRNA or protein were higher (P<0.05). With the increase of HMGB1 injection dose, the wound healing rate and angiogenesis decreased significantly (P<0.05), and the expression of inflammatory factors increased significantly (P<0.05). Conclusion: HMGB1 could promote the inflammation of diabetic foot ulcer in rats, and the mechanism may be related to HMGB1/TLR4/ NF-κB signal pathway. |
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