PI3K/AKT/mTOR通路
自噬
哈卡特
蛋白激酶B
银屑病
RPTOR公司
活力测定
细胞凋亡
污渍
化学
癌症研究
膜联蛋白
细胞生物学
医学
生物
体外
免疫学
生物化学
基因
作者
Yue Lu,Ailin Wang,Zhang Jinwei,Li Leng,Jianan Wei,Li Li,Haiming Chen,Ling Han,Chuanjian Lu
出处
期刊:Phytomedicine
[Elsevier]
日期:2019-11-01
卷期号:64: 153054-153054
被引量:38
标识
DOI:10.1016/j.phymed.2019.153054
摘要
Psoriasis is an inflammatory skin disease that affects an estimated 3% of the world's population. PSORI-CM02 is an empirically developed Chinese medicine formula optimised from Yin Xie Ling, summarised by national medical master Guo-Wei Xuan, that has been used for decades to treat psoriasis in the Guangdong Provincial Hospital of Chinese Medicine. However, its anti-psoriatic mechanisms are still poorly understood. In this study, we explored the effects of PSORI-CM02 on autophagy and the underlying mechanisms in TNF-α–stimulated HaCaT cells and in a mouse model of imiquimod-induced psoriasis. Cell viability was assessed by MTT assay. Apoptosis was detected by annexin V–FITC/PI double-staining and caspase-3 assays. Autophagy was detected by electron microscopy, RT-PCR and western blotting. The PI3K/Akt/mTOR pathway was analysed by western blotting and immunochemical analysis. PSORI-CM02 induced autophagy and thus inhibited the proliferation of HaCaT cells via suppression of the PI3K/Akt/mTOR pathway. In mice with IMQ-induced psoriasis, PSORI-CM02 relieved psoriasis symptoms, induced autophagy and inhibited the phosphorylation of the PI3K/AKT/mTOR pathway in the skin. These results suggest that PSORI-CM02 treats psoriasis by inducing autophagy via inhibition of the PI3K/Akt/mTOR pathway.
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