Effects of aloe polysaccharide, a polysaccharide extracted from Aloe vera, on TNF-alpha-induced HaCaT cell proliferation and the underlying mechanism in psoriasis

摘要

Aloe vera is a traditional wound-healing medicine used for the treatment of skin disorders. Aloe polysaccharide (APS) is the main macromolecule of Aloe vera, which contributes to its function. Psoriasis is an immune-mediated chronic inflammatory disease, which affects 2-3% of the general population. The conventional remedies used to treat psoriasis demonstrate limited effects; therefore, natural products, including Aloe vera, are being taken into consideration. However, the effects of APS on the treatment of psoriasis and the underlying mechanisms remain to be elucidated. The human keratinocyte cell line HaCaT was used to determine the effects of APS on psoriasis. Cells were randomly divided into five groups: i) Negative control group; ii) tumor necrosis factor (TNF)-alpha stimulated psoriasis model group; and iii) APS (20, 40 and 80 mu g/ml) pretreated psoriasis groups. Cell viability and proliferation were investigated using the CCK-8 assay. ELISA and western blotting were applied to study the abundance of interleukin (IL)-8 and IL-12 in TNF-alpha-incubated culture medium and APS-treated HaCaT cells, respectively. In addition, the mRNA expression levels of p65, and the protein expression levels of nuclear factor (NF)-kappa B inhibitor-alpha (I kappa B alpha) and phosphorylated-p65, were detected by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. APS was revealed to significantly reduce TNF-alpha-stimulated elevation of HaCaT cell proliferation in a dose-dependent manner. The expression levels of inflammatory factors, including IL-8 and IL-12, were increased in response to TNF-alpha. In addition, the mRNA and protein expression levels of p65 were increased following treatment with TNF-alpha. Notably, treatment with APS was demonstrated to significantly attenuate the aforementioned effects in a dose-dependent manner. Furthermore, I kappa B alpha protein expression levels were significantly reduced following treatment with TNF-alpha, which was significantly reversed following treatment with APS. In conclusion, these results suggested that APS inhibited TNF-alpha-induced proliferation of keratinocytes and overactivation of the NF-kappa B signaling pathway.