1.石家庄市人民医院药剂科,石家庄 050000
2.石家庄市人民医院骨科,石家庄 050000
刘晓珂,女,37岁,大学本科,主管药师。研究方向:中药药剂学基础研究。
喻伟光,E-mail:nhpvn7@163.com
收稿:2025-02-13,
纸质出版:2026-03-25
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刘晓珂,周芸,张勇,等.积雪草苷脂质体凝胶通过调控Nrf2/HO-1通路促进糖尿病足溃疡大鼠创面愈合的研究[J].北京中医药,2026,45(3):373-378.
LIU Xiaoke,ZHOU Yun,ZHANG Yong,et al.Asiaticoside liposome gel promotes wound healing of diabetic foot ulcer rats by regulating Nrf2/HO-1 signaling pathway[J]. Beijing Journal of Traditional Chinese Medicine,2026,45(03):373-378.
刘晓珂,周芸,张勇,等.积雪草苷脂质体凝胶通过调控Nrf2/HO-1通路促进糖尿病足溃疡大鼠创面愈合的研究[J].北京中医药,2026,45(3):373-378. DOI: 10.16025/j.1674-1307.2026.03.015.
LIU Xiaoke,ZHOU Yun,ZHANG Yong,et al.Asiaticoside liposome gel promotes wound healing of diabetic foot ulcer rats by regulating Nrf2/HO-1 signaling pathway[J]. Beijing Journal of Traditional Chinese Medicine,2026,45(03):373-378. DOI: 10.16025/j.1674-1307.2026.03.015.
目的
2
探讨积雪草苷(AS)脂质体凝胶通过调控核因子E2相关因子(Nrf)2/血红素加氧酶(HO)-1通路对糖尿病足溃疡(DFU)大鼠创面愈合的影响。
方法
2
随机取15只大鼠构建DFU模型,将构建成功的DFU大鼠按照随机数字表法分为DFU组、AS脂质体凝胶治疗组(ALG组)、AS脂质体凝胶治疗+Nrf2抑制剂ML385组(ALG+ML385组),各5只。另取5只健康大鼠作为NC组。NC组、DFU组在创面敷含生理盐水纱布,同时腹腔注射与ML385溶液等量的生理盐水;ALG组在创面敷含AS脂质体凝胶纱布,同时腹腔注射与ML385溶液等量的生理盐水;ALG+ML385组在创面敷含AS脂质体凝胶纱布,同时腹腔注射30 mg/kg ML385溶液。隔日换药1次,均持续干预14 d。干预第1、7、14天观察大鼠创面;干预第14天,检测血清氧化应激指标超氧化物歧化酶(SOD)、丙二醛(MDA);HE染色观察大鼠创面组织病理变化;免疫荧光染色法检测大鼠创面组织微血管内皮细胞CD34表达;Western Blotting法检测大鼠创面组织中Nrf2、HO-1蛋白表达。
结果
2
与NC组比较,DFU组创面愈合慢,组织形态损伤重,CD34、SOD水平及Nrf2、HO-1蛋白表达低,MDA水平高(
P
<
0.05);与DFU组比较,ALG组大鼠创面愈合快,组织形态损伤轻,CD34、SOD水平及Nrf2、HO-1蛋白表达高,MDA水平低(
P
<
0.05);与ALG组比较,ALG+ML385组大鼠创面愈合慢,组织形态损伤重,CD34、SOD水平及Nrf2、HO-1蛋白表达低,MDA水平高(
P
<
0.05)。
结论
2
AS脂质体凝胶可能通过激活Nrf2/HO-1通路减轻氧化应激反应,促进血管新生及DFU的愈合。
Objective
2
To investigate the effects of asiaticoside (AS) liposome gel (ALG) on wound healing in diabetic foot ulcer (DFU) rats by regulating the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway.
Methods
2
Fifteen rats were randomly selected to establish a DFU model. The successfully modeled rats were randomly divided into three groups using a random number table method: DFU group, ALG treatment group (ALG group), and ALG plus Nrf2 inhibitor ML385 group (ALG + ML385 group), with 5 rats in each group. In addition, 5 healthy rats were assigned to the normal control (NC) group. The NC group and DFU group received saline-soaked gauze applied to the wound, and intraperitoneal injection of an equal volume of saline corresponding to ML385 solution. The ALG group received ALG-soaked gauze applied to the wound, along with intraperitoneal injection of an equal volume of saline corresponding to ML385 solution. The ALG + ML385 group received ALG-soaked gauze applied to the wound, together with intraperitoneal injection of ML385 solution (30 mg/kg). Dressings were changed once every 2 days, and all interventions were continued for 14 days. Wound conditions were observed on days 1, 7, and 14 of intervention. On day 14, serum oxidative stress indicators including superoxide dismutase (SOD) and malondialdehyde (MDA) were measured. Hematoxylin-eosin (HE) staining was used to observe histopathological changes in wound tissue. Immunofluorescence staining was used to detect CD34 expression in microvascular endothelial cells of wound tissue. Western blot was used to determine the expression of Nrf2 and HO-1 proteins in wound tissue.
Results
2
Compared with the NC group, the DFU group showed delayed wound healing, more severe tissue morphological damage, decreased levels of CD34 and SOD, reduced Nrf2 and HO-1 protein expression, and increased MDA levels (P < 0.05). Compared with the DFU group, the ALG group showed accelerated wound healing, alleviated tissue damage, increased CD34 and SOD levels, upregulated Nrf2 and HO-1 protein expression, and decreased MDA levels (P < 0.05). Compared with the ALG group, the ALG + ML385 group showed delayed wound healing, aggravated tissue damage, decreased CD34 and SOD levels, downregulated Nrf2 and HO-1 protein expression, and increased MDA levels (P < 0.05).
Conclusion
2
ALG may alleviate oxidative stress, promote angiogenesis, and enhance wound healing in DFU rats by activating the Nrf2/HO-1 signaling pathway.
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