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地肤子通过激活pERK1/2/TLR4/NF-κB信号通路对过敏性接触性皮炎大鼠的抗炎作用

The Anti-Inflammatory Effect of Fructus Kochiae on Allergic Contact Dermatitis Rats via pERK1/2/TLR4/NF-B Pathway Activation.

作者信息

Xiao Zuoqi, Xiao Suxi, Zhang Yongning, Pan Tao, Ouyang Bo

机构信息

Hunan Provincial Maternal and Child Health Care Hospital, Changsha 410008, China.

College of Biomedical Engineering, South-Central University for Nationalities, Wuhan 430074, China.

出版信息

Evid Based Complement Alternat Med. 2018 Jan 4;2018:1096920. doi: 10.1155/2018/1096920. eCollection 2018.

Abstract

Allergic contact dermatitis (ACD) is a common irritability skin disease, which can be cured by using the Chinese patent medicine. To explore the pharmacological effect of total flavonoids of Fructus Kochiae (FK) on ACD, we used dinitrochlorobenzene- (DNCB-) induced ACD rats. Five groups were used in our experiments. The normal group and the DNCB group were treated with 0.5% CMC-Na; the DNCB + hFK group was treated with a high dose of total flavonoids of FK (200 mg/kg); the DNCB + lFK group was treated with a low dose of FK (100 mg/kg); the DNCB + Pre group was treated with prednisolone acetate (2.5 mg/kg). The results showed that FK treatment had significantly attenuated the inflammation induced by DNCB. The increased concentration of cytokines including IL-6, IL-18, and IFN- in ACD rats could be reversed by the FK administration, while IL-10 expressed the opposite result; the expression level of TLR4, pERK, and NF-B could be downregulated by the treatment with FK in the ACD rat. In a word, the total flavonoids of the FK had an anti-inflammatory effect on the DNCB-induced ACD rat; this regulatory mechanism was highly possible based on the pERK/TLR4-NF-B pathway activation.

摘要

过敏性接触性皮炎(ACD)是一种常见的刺激性皮肤病,可通过使用中成药治愈。为探讨地肤子总黄酮(FK)对ACD的药理作用,我们使用二硝基氯苯(DNCB)诱导的ACD大鼠。实验分为五组。正常组和DNCB组用0.5%羧甲基纤维素钠(CMC-Na)处理;DNCB + hFK组用高剂量地肤子总黄酮(200mg/kg)处理;DNCB + lFK组用低剂量地肤子(100mg/kg)处理;DNCB + Pre组用醋酸泼尼松龙(2.5mg/kg)处理。结果表明,FK治疗显著减轻了DNCB诱导的炎症。给予FK可逆转ACD大鼠中包括IL-6、IL-18和IFN-在内的细胞因子浓度升高,而IL-10则呈现相反结果;在ACD大鼠中,FK处理可下调TLR4、pERK和NF-κB的表达水平。总之,地肤子总黄酮对DNCB诱导的ACD大鼠具有抗炎作用;这种调节机制很可能是基于pERK/TLR4-NF-κB途径的激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c02/5817368/7cf803ff9cda/ECAM2018-1096920.001.jpg

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