Scutellaria barbata D. Don (Lamiaceae; SB) inhibited the growth of uterine leiomyomal (LM) cells with unknown actions. The expression patterns of beta-adrenergic receptors (beta-ARs) in human uterine LM cells and functional coupling to gene expression have also been investigated. Northern blot analysis showed that beta-AR subtypes are expressed at different levels in the uterine LM cells and myometrial smooth muscle cells (SMCs). beta1-AR expression was to be found approximately at the same level in the two cell types. beta2-ARs were expressed at higher levels in uterine LM cells than that in myometrial SMCs. beta3-AR expression was not found in both the cells. c-fos gene expression was induced by SB in uterine LM cells via increases in adenosine-3',5', cyclic monophosphate (cAMP), which in turn activated the cAMP/protein kinase A (PKA) pathway. The PKA inhibitor, H89, inhibited c-fos gene expression induced by SB. It seems that the mechanism of proto-oncogenes c-fos different leiomyoma from other myometrial cancer. Further studies are necessary to elucidate whether c-fos induction by SB in uterine LM cells influences a regression of leiomyoma or induces other differentiation.

Human myometrial smooth muscle cells (MSMC) showed high protein kinase C (PKC) activity when a maximal dose of PKC-activating phorbol ester was used, while uterine leiomyomal cells (ULMC) showed only 6-12% of PKC activity. MSMC exhibited a low proliferation rate, whereas ULMC exhibited a high proliferation rate. These different cell types of MSMC and ULMC responded to 10 U/mL thrombin, with a twofold stimulation of PKC activity. Downregulation of PKC activity was found when MSMC were treated with phorbol ester or with transforming growth factor-beta2. We concluded that differences in PKC activity exist between MSMC and ULMC, which may be related to their different proliferative activity. ULMC treated with Euonymus alatus (Thunb.) Sieb (EA), known as "gui-jun woo" in Korea, which is used for leiomyomal tumors, exhibited a much lower proliferation rate than untreated cells, suggesting that EA inhibited the cellular proliferation of ULMC. The PKC activity of MSMC by EA treatment (50 microg/mL) changed little. ULMC showed increased PKC activity by addition of EA, indicating that PKC is activated by EA. The EA-treated ULMC were differentiated into phenotypes characteristic for normal untransformed cells, since the EA-treated cells possess higher PKC activity than untreated cells.