Fuzhenghefuzhiyang Formula (FZHFZY) Improves Epidermal Differentiation via Suppression of the Akt/mTORC1/S6K1 Signalling Pathway in Psoriatic Models.

Fuzhenghefuzhiyang Formula (FZHFZY) Improves Epidermal Differentiation via Suppression of the Akt/mTORC1/S6K1 Signalling Pathway in Psoriatic Models.
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扶正和扶直阳方通过抑制银屑病模型中Akt/mTORC1/S6K1信号通路改善表皮分化

DOI:
10.3389/fphar.2021.650816
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发表时间:
2021
影响因子:
5.6
通讯作者:
Lu C
Lu C
中科院分区:
医学2区
文献类型:
--
作者:
Lu Y;Chen H;Zhang J;Tang B;Zhang H;Ma C;Tang X;Li L;Wu J;Wei J;Li S;Yang L;Han L;Lu C

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银屑病是一种慢性增生性皮肤病,其特征是表皮分化异常。由皮肤科中医大师卢传健创立的扶正和肤止痒方(FZHFZY)已在广东省中医院外用治疗银屑病,但其作用机制仍知之甚少。本研究旨在探讨扶正化瘀方对白细胞介素(IL)-17 A/IL-22/干扰素(IFN)-γ/肿瘤坏死因子(TNF)-α刺激的HaCaT细胞和咪喹莫特(IMQ)诱导的银屑病小鼠模型表皮分化的影响及其机制。MTT法检测细胞活力。逆转录聚合酶链反应和免疫印迹法检测表皮分化。通过苏木精和伊红染色进行皮肤组织的组织学评价,并通过蛋白质印迹法分析Akt/mTORC 1/S6 K1通路。FZHFZY抑制IL-17 A/IL-22/IFN-γ/TNF-α诱导的HaCaT细胞增殖并促进其表皮分化。FZHFZY改善银屑病症状,调节表皮分化,抑制Akt/mTORC 1/S6 K1通路的磷酸化。我们的研究结果表明,FZHFZY可能通过抑制Akt/mTORC 1/S6 K1通路调节表皮分化对银屑病表现出治疗作用。
Psoriasis is a chronic proliferative skin disorder characterised by abnormal epidermal differentiation. The Fuzhenghefuzhiyang (FZHFZY) formula created by Chuanjian Lu, a master of Chinese medicine in dermatology, has been external used in the Guangdong Provincial Hospital of Chinese Medicine for the treatment of psoriasis, but its mechanisms of action against psoriasis remain poorly understood. This study involved an exploration of the effects of FZHFZY on epidermal differentiation and its underlying mechanisms in interleukin (IL)-17A/IL-22/interferon (IFN)-γ/tumour necrosis factor (TNF)-α–stimulated HaCaT cells and in a mouse model of imiquimod (IMQ)-induced psoriasis. Cell viability was assessed by MTT assay. Epidermal differentiation was detected by reverse-transcription polymerase chain reaction and western blotting. Histological evaluation of the skin tissue was performed via haematoxylin and eosin staining, and the Akt/mTORC1/S6K1 pathway was analysed by western blotting. FZHFZY inhibited proliferation and improved epidermal differentiation in IL-17A/IL-22/IFN-γ/TNF-α–induced HaCaT cells. FZHFZY ameliorated symptoms of psoriasis, regulated epidermal differentiation and inhibited phosphorylation of the Akt/mTORC1/S6K1 pathway in the skin of mice with imiquimod-induced psoriasis. Our results suggest that FZHFZY may exhibit therapeutic action against psoriasis by regulating epidermal differentiation via inhibition of the Akt/mTORC1/S6K1 pathway.
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