| 摘要 |
In the present invention, an increase in SOCS3 effectively blocks signals from cytokines and cell growth factors, which cause inflammation in signaling. However, drugs for increasing the expression of SOCS3 and mechanisms thereof have not been known. Wogonin was first found as a drug for increasing SOCS3, and as a result of promoter analysis, it was verified that wogonin depends on the AP-1 sequence and two STAT3 response elements (TTACAAGAA and TTCCAGGAA). The expression of SOCS3, induced by wogonin, was blocked by PI3K, Akt, Raf, P38, JNK, MEK, and STAT3 inhibitors. However, the JAK2 inhibitor did not inhibit the expression of SOCS3 induced by wogonin. It can be seen from these results that the effect of wogonin of increasing SOCS3 is exhibited by the activation of MAPK signaling pathways (Akt, ERK1/2, P38, and JNK) mediated by PI3K. Therefore, wogonin and a derivative thereof, which increase SOCS3, can be drugs that effectively block cell transmission signals from the inflammatory cytokines and growth factors. The blocking of the signaling is applicable in various fields, and can be appropriately utilized for a cancer cell division inhibitor, and a therapeutic agent for chronic inflammatory diseases. |
