Background
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.
Conclusion
These results suggest that PSORI-CM02 treats psoriasis by inducing autophagy via inhibition of the PI3K/Akt/mTOR pathway.
Methods
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.
Results
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.