Possible mechanism of growth inhibition by Scutellaria baicalensis in an estrogen-responsive mouse tumor cell line.

Abstract:

:We have studied the effects of Saiboku-to, a traditional Chinese medicine having suppressive activities for leukotriene production and release, on the proliferation of the estrogen-responsive mouse Leydig tumor cell line B-1F. In our previous reports, it is shown that Saiboku-to promotes, but Scutellaria baicalensis, one of the components (herbs) of Saiboku-to, significantly inhibits the proliferation of B-1F cells in vitro and in vivo, and induces DNA fragmentation and morphological changes such as nuclear aggregation and fragmentation. In this study, we examined telomerase activity, cell cycle, polyunsaturated fatty acid metabolism and expression of nuclear factor κB (NF-κB) in order to determine the mechanism of growth inhibition in B-1F cells treated with Scutellaria baicalensis. Telomerase activity was decreased in a dose-dependent manner in treated B-1F cells. Cellular populations in the sub-G0/G1 and G2/M phases were increased, but those in M phase had no change. Although cyclin D1 mRNA was highly expressed in the presence of estradiol (E2), cyclin A and E mRNA levels did not significantly change. When B-1F cells were treated with Scutellaria baicalensis, expression of cyclin D1 was suppressed and that of p21 was inversely increased. Moreover, Scutellaria baicalensis influenced arachidonic and linoleic acid metabolism, and increased production of 13(S)-HODE. In the presence of E2 Scutellaria baicalensis decreased expression of NF-κB p65 to 0.71-fold in B-1F cells. These results show that Scutellaria baicalensis might induce cell cycle arrest at G1 phase and apoptosis via inhibition of telomerase activity, changes of enzymatic activities in polyunsaturated fatty acid metabolism and suppression of NF-κB.

journal_name

Oncol Rep

journal_title

Oncology reports

authors

Murashima T,Katayama H,Shojiro K,Nishizawa Y

doi

10.3892/or.2011.1196

subject

Has Abstract

pub_date

2011-05-01 00:00:00

pages

1431-8

issue

5

eissn

1021-335X

issn

1791-2431

journal_volume

25

pub_type

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