EFFECT OF PANAX-NOTOGINSENG SAPONINS ON INCREASED PROLIFERATION OF CULTURED AORTIC SMOOTH-MUSCLE CELLS STIMULATED BY HYPERCHOLESTEROLEMIC SERUM

Citation
Sg. Lin et al., EFFECT OF PANAX-NOTOGINSENG SAPONINS ON INCREASED PROLIFERATION OF CULTURED AORTIC SMOOTH-MUSCLE CELLS STIMULATED BY HYPERCHOLESTEROLEMIC SERUM, Zhongguo yaoli xuebao, 14(4), 1993, pp. 314-316
Citations number
9
Categorie Soggetti
Pharmacology & Pharmacy",Chemistry
Journal title
ISSN journal
02539756
Volume
14
Issue
4
Year of publication
1993
Pages
314 - 316
Database
ISI
SICI code
0253-9756(1993)14:4<314:EOPSOI>2.0.ZU;2-K
Abstract
Panax notoginseng saponins (PNS) was extracted from a Chinese herb med icine. After preparation of cultured aortic smooth muscle cell (SMC) f rom primary aortic explants , the cytotoxicity of hypercholesterolemic serum (HCS) for cultured cells was determined by trypan blue exclusio n test, and [H-3] thymidine incorporation and cell numbers were counte d at the same time. The results showed that HCS (0.5 mg cholesterol.ml -1) increased the incorporation of [H-3] thymidine into cultured cells (3722 +/- 440 vs 1655 +/- 288 dpm/mug cell protein, P<0.01), stimulat ed the proliferation of SMC [(6.5 +/- 1.5) X 10(50 vs (4.3 +/- 1.2) X 10(5) cells/plate, P<0.01], and that high concentration HCS (final cho lesterol concentration 2 mg . ml-1) was cytotoxic to the cultured cell s. PNS (100 and 400 mug-ml-1) decreased the incorporation of [H-3]thym idine into SMC in culture with or without HCS (1292 +/- 260 and 982 +/ - 314 or 4111 +/- 886 and 2361 +/- 751 dpm/mug cell protein), and inhi bited the proliferation of the cultured cells [(3.3 +/- 0.7) X 10(5) a nd (2.9 +/- 0.7) X 10(5) or (4.7 +/- 1.4) X 10(5) and (4.1 +/- 1.2) X 10(5) cells/plate). We conclude that PNS can inhibit the proliferation of aortic SMC stimulated by HCS. These results also suggest that HCS may play an atherogenic role in the arterial wall and that PNS may pre vent atherosclerosis and inhibit progression of the atherosclerotic le sions by interfering with the proliferation of arterial SMC.