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三七介导的白细胞介素1β失活通过核因子κB途径缺陷加速伤口愈合。

Sanchi-mediated inactivation of IL1B accelerates wound healing through the NFκB pathway deficit.

作者信息

Li Xiaoling, Zhao Zhiwei, Cui Bo, Li Yanfeng

机构信息

Health Control Department, Luoyang Orthopedic Hospital of Henan Province (Orthopedic Hospital of Henan Province), Zhengzhou, 450016, Henan, PR China.

Department of Hand Surgery & Micro Orthopedics, Luoyang Orthopedic Hospital of Henan Province (Orthopedic Hospital of Henan Province), Zhengzhou, 450016, Henan, PR China.

出版信息

Heliyon. 2024 Feb 28;10(5):e26982. doi: 10.1016/j.heliyon.2024.e26982. eCollection 2024 Mar 15.

Abstract

CONTEXT

Sanchi promotes wound healing by repressing fibroblast proliferation.

OBJECTIVE

This study examined the effect of Sanchi on keratinocytes (KCs) and microvascular endothelial cells (MECs) and rats with skin injury.

MATERIALS & METHODS: Hydrogels containing different concentrations of Sanchi extract were prepared to observe wound closure over 10 days. SD rats were divided into the control, Hydrogel, 5% Hydrogel, 10% Hydrogel, 10% Hydrogel + Ad5-NC, and 10% Hydrogel + Ad5-IL1B groups. KCs and MECs were induced with HO for 24 h. Cell viability, apoptosis, and the levels of inflammation- and oxidative stress-related factors were examined. The effect of IL1B on wound healing was also evaluated.

RESULTS

Compared to the Control group (83% ± 7.4%) or Hydrogel without Sanchi extract (84% ± 8.5%), Hydrogel with 5% (95% closure ± 4.0%) or 10% Sanchi extract (98% ± 1.7%) accelerated wound healing in rats and attenuated inflammation and oxidative stress. Hydrogels containing Sanchi extract increased collagen deposition and CD31 expression in tissues. HO (100 μM) induced injury in KCs and MECs, whereas Sanchi rescued the viability of KCs and MECs. Sanchi inhibited cell inflammation and oxidative stress and decreased apoptosis. As Sanchi blocked the NFκB pathway IL1B, IL1B mitigated the therapeutic effect of Sanchi.

DISCUSSION AND CONCLUSION

Sanchi demonstrated therapeutic effects on wound healing in rats by promoting KCs and MECs activity. These findings provide valuable information for the clinical application of Sanchi, which needs to be validated in future clinical trials.

摘要

背景

三七通过抑制成纤维细胞增殖促进伤口愈合。

目的

本研究考察三七对角质形成细胞(KCs)、微血管内皮细胞(MECs)以及皮肤损伤大鼠的影响。

材料与方法

制备含不同浓度三七提取物的水凝胶,观察10天内伤口闭合情况。将SD大鼠分为对照组、水凝胶组、5%水凝胶组、10%水凝胶组、10%水凝胶+Ad5-NC组和10%水凝胶+Ad5-IL1B组。用HO诱导KCs和MECs 24小时。检测细胞活力、凋亡以及炎症和氧化应激相关因子水平。还评估了IL1B对伤口愈合的影响。

结果

与对照组(83%±7.4%)或不含三七提取物的水凝胶组(84%±8.5%)相比,含5%(伤口闭合率95%±4.0%)或10%三七提取物的水凝胶(98%±1.7%)加速了大鼠伤口愈合,减轻了炎症和氧化应激。含三七提取物的水凝胶增加了组织中的胶原蛋白沉积和CD31表达。HO(100μM)诱导KCs和MECs损伤,而三七挽救了KCs和MECs的活力。三七抑制细胞炎症和氧化应激并减少凋亡。由于三七阻断了IL1B的NFκB通路,IL1B减弱了三七的治疗效果。

讨论与结论

三七通过促进KCs和MECs活性对大鼠伤口愈合具有治疗作用。这些发现为三七的临床应用提供了有价值的信息,有待未来临床试验验证。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4984/10926082/b4a12437a456/gr1.jpg

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