Effects of matrine on inflammation,oxidative stress and wound healing in atopic dermatitis
- VernacularTitle:苦参碱对特应性皮炎炎症、氧化应激和伤口愈合的影响
- Author:
Bo WU
1
;
Zhuonong ZHU
;
Lijuan ZHENG
;
Junru CHEN
Author Information
- Keywords: matrine; dermatitis,atopic; inflammation; NF-kappa B; oxidative stress
- From: Tianjin Medical Journal 2024;52(6):566-571
- CountryChina
- Language:Chinese
- Abstract: Objective To evaluate the effects of matrine on the inflammatory,oxidative and migratory responses of HaCaT keratinocytes in an in vitro atopic dermatitis(AD)model.Methods HaCaT cells were divided into the control group(no treatment)and the model group(0.05,0.1 and 0.2 mmol/L).HaCaT cells in the model group were stimulated with 10 μg/L tumor necrosis factor-α(TNF-α)/interferon-γ(IFN-γ)for 24 h.Cells in the model group were pretreated with 0.05,0.1 and 0.2 mmol/L matrine for 1 h and then stimulated with 10 μg/L TNF-α/IFN-γ for 24 h.MTT assay was used to assess the cytotoxicity of matrine.Enzyme-linked immunosorbent(ELISA)assay was performed to determine levels of cytokines(IL-6,IL-8 and IL-1β)and chemokines(TARC,MDC and RANTES).mRNA expression levels of antioxidant genes were detected by real-time quantitative PCR(RT-qPCR).Cell migration was analyzed by scratch closure assay.Immunohistochemistry was commended to analyze the nuclear translocation of NF-κB p65.Western blot assay was used to detect the phosphorylation levels of p38,ERK and p65 proteins.Results Compared with the model group,matrine 0.1 and 0.2 mmol/L significantly decreased the expression levels of IL-6,IL-1β,IL-8 and chemokines,and matrine significantly enhanced the expression levels of superoxide dismutase-1(SOD1),SOD2,catalase(CAT)and glutathione peroxidase(GPx),and promoted scratch wound healing(P＜0.05).In addition,matrine 0.1 and 0.2 mmol/L inhibited the phosphorylation levels of p38,ERK and p65 proteins and the nuclear translocation of p65.Conclusion Matrine possesses anti-inflammatory and antioxidant properties,and stimulates wound closure in eratinocyte AD model,which may be related to the inhibition of the activation of MAPK and NF-κB pathways.
