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芦荟提取物通过在脂多糖诱导的RAW264.7巨噬细胞模型中调节NF-κB、ERK和JNK信号通路来抑制皮肤炎症反应。

Aloe Extracts Inhibit Skin Inflammatory Responses by Regulating NF-κB, ERK, and JNK Signaling Pathways in an LPS-Induced RAW264.7 Macrophages Model.

作者信息

Wang Fei, Liu Jitao, An Quan, Wang Yiming, Yang Yang, Huo Tong, Yang Simin, Ju Ruijun, Quan Qianghua

机构信息

Research and Development Department, Yunnan Baiyao Group Health Products Co., Ltd., Kunming, People's Republic of China.

East Asia Skin Health Research Center, Beijing, People's Republic of China.

出版信息

Clin Cosmet Investig Dermatol. 2023 Jan 28;16:267-278. doi: 10.2147/CCID.S391741. eCollection 2023.

DOI:10.2147/CCID.S391741
PMID:36742263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9891070/
Abstract

INTRODUCTION

Inflammation generally refers to the body's defensive response to stimuli, and skin inflammation is still one of the major problems that affect human physical and mental health. While current pharmacological treatments are reported to have cytotoxicity and various side effects, herbal medicines with few side effects and low cytotoxicity are considered as alternative therapeutic approaches.

METHODS

In order to investigate anti-inflammatory effects and mechanisms of ALOE, the potential cytotoxicity of extracts (ALOE) was determined in vitro at first. The production of the pro-inflammatory proteins (ie, IL-6, TNF-α) in lipopolysaccharides (LPS) and ultraviolet A (UVA)-stimulated HaCaT and RAW264.7 cells were then treated with ALOE to test its inhibitory effects using enzyme-linked immunosorbent assay (ELISA). To further explore the anti-inflammatory mechanisms of ALOE, quantitative Polymerase Chain Reaction (qPCR) was used to analyze the mRNA expression of inflammatory genes and NO production. For NF-κB and MAPK signaling pathways analysis, Western blotting and nuclear fluorescence staining were used to evaluate the expression of key factors.

RESULTS

ALOE did not exhibit obvious cytotoxicity (0-3 mg/mL) in vitro. ALOE was able to inhibit the expression of pro-inflammatory cytokines IL-6, TNF-α and functioned more prominently in LPS-induced model. ALOE could also suppress the mRNA expression of LPS-induced and and further down-regulate NO level. Furthermore, ALOE reduced the protein expression of P65 in NF-κB signaling pathway and suppressed LPS-induced activation of ERK and JNK, instead of p38 MAPK pathway.

CONCLUSION

Taken together, these results demonstrated that ALOE is a potential treatment in suppressing LPS-stimulated inflammation reactions targeting NF-κB, JNK and ERK signaling pathways. The anti-inflammatory effects of ALOE indicated that it has the potential to become an effective cosmetic ingredient.

摘要

引言

炎症通常指机体对刺激的防御反应,皮肤炎症仍是影响人类身心健康的主要问题之一。虽然据报道目前的药物治疗具有细胞毒性和各种副作用,但副作用少且细胞毒性低的草药被视为替代治疗方法。

方法

为了研究芦荟的抗炎作用及其机制,首先在体外测定了芦荟提取物(ALOE)的潜在细胞毒性。然后用芦荟处理脂多糖(LPS)和紫外线A(UVA)刺激的HaCaT和RAW264.7细胞中促炎蛋白(即IL-6、TNF-α)的产生,使用酶联免疫吸附测定(ELISA)来测试其抑制作用。为了进一步探究芦荟的抗炎机制,采用定量聚合酶链反应(qPCR)分析炎症基因的mRNA表达和一氧化氮(NO)的产生。对于核因子κB(NF-κB)和丝裂原活化蛋白激酶(MAPK)信号通路分析,采用蛋白质免疫印迹法和细胞核荧光染色来评估关键因子的表达。

结果

芦荟在体外(0 - 3 mg/mL)未表现出明显的细胞毒性。芦荟能够抑制促炎细胞因子IL-6、TNF-α的表达,并且在LPS诱导的模型中作用更为显著。芦荟还可以抑制LPS诱导的 和 的mRNA表达,并进一步下调NO水平。此外,芦荟降低了NF-κB信号通路中P65的蛋白表达,抑制了LPS诱导的细胞外信号调节激酶(ERK)和应激活化蛋白激酶(JNK)的活化,而非p38 MAPK通路。

结论

综上所述,这些结果表明芦荟是一种潜在的治疗方法,可通过靶向NF-κB、JNK和ERK信号通路抑制LPS刺激的炎症反应。芦荟的抗炎作用表明它有潜力成为一种有效的化妆品成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/4110b435b363/CCID-16-267-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/088725f18132/CCID-16-267-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/7b70f91fcb03/CCID-16-267-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/b1ebf6fb8ac5/CCID-16-267-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/64b3d0762f65/CCID-16-267-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/60879bf205c3/CCID-16-267-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/4110b435b363/CCID-16-267-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/088725f18132/CCID-16-267-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/7b70f91fcb03/CCID-16-267-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/b1ebf6fb8ac5/CCID-16-267-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/64b3d0762f65/CCID-16-267-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/60879bf205c3/CCID-16-267-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc23/9891070/4110b435b363/CCID-16-267-g0006.jpg

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