银屑病中核因子NF-kB的调控机制研究

We separated and cultured the lymphocytes from lesion and PBMC of patients with psoriasis, established the psoriasis cell model, then assayed the alive cells quantity in the supernatant of mixture culture by MTT method and detected IL-2, IL-4 and IFN-γ. The results showed, compared with the normal controls, the lymphocytes from psoriasis patients could stimulate keratinocytes proliferation significantly, especially the lymphocytes from lesion. In the supernatant of the psoriasis cell model, the concentrations of IL-2 and IFN-γwere higher markedly than thoses in controls, while IL-4 was lower than that in controls. There were no significant difference between the group treated with tripterygium glycosides and the normal controls. It suggested that Lymphocytes in psoriasis patients(Th1 cells) played important roles in KC proliferation and tripterygium glycosides can inhibit the promotion of proliferation of KC by psoriasis lymphocytes. Then we analyzed the cytokines mRNA by semi-quantative PCR and evaluated NF-κB activity in psoriasis cell model by EMSA(electrophoresis mobility shift assay). It showed the cytokines mRNA increased and NF-κB activity reinforced in psoriasis cell model, TPCK and tripterygium glycosides pretreatment could inhibit cytokines production and NF-κB activation, suggesting NF-κB activation is one of the important factors in psoriasis pathogenesis and inhition of NF-κB activation is helpful for improving patient's condition. Finaly we detected IκB-α mRNA level by semi-quantative RT-PCR and assay TNFR1 and TRAF-2. The results showed IκB-α mRNA level arrived at the highest point after 30min mixed cultures, TPCK pretreatment could inhibit IκB-α degradation, TNFR1 appeared at 20, 30 min after mixed cultures and TRAF appeared at 30min after mixed cultures. In general, NF-κB was receptor-independent activated by TNF-α pathway, involving TRADD-TRAF-2 interaction, therefore, inflammation reaction could be inhibited by blocking NF-κB pathway, then to improve psoriasis patients' condition.

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