Effect Of Panax Notoginseng Saponins On Increased Proliferation Of Cultured Aortic Smooth Musclec Cells Stimulated By Hypercholesterolemic

Author

Lin Shu-Guang, Zheng Xi-Long, Chen Qi-Yun, Sun Jia-Jun, Division of Pharmacology, Guangdong Cardiovascular Institute, Guangzhou 510100, China: Department of Pharmacology, SUN Yat-Sen University of Medical Sciences, Guangzhou 510100, China.

Proceeding

Trends in Traditional Medicine Research, Proceedings of the International Conference on the Use of Traditional Medicine & Other Natural Products in Health Care

Date

8/6/1993

Keyword

ginseng; saponins; cultured cells; thoracic aorta; vascular smooth muscle; cell count; hypercholesterolemia; thymidine.

Abstract

Panax notoginseng saponins (PNS) was extracted from a Chinese herb medicine. After preparation of cultured aortic smooth muscle cell (SMC) from primary aortic explants, the cytotoxicity of hypercholesterolemic serum (HCS) for cultured cells was determined by trypan blue exclusion test, and [3H] thymidine incorporation and cell numbers were counted at the same time. The results showed that HCS (0.5 mg cholesterol, ml-1) increased the incorporation of [3H] thymidine into cultured cells (3722±440 vs 1655 + 288 dpm/µg cell protein, P<0.01). stimulated the proliferation of SMC [(6.5+1.5) X 105 vs (4.3 +1.2) X 105 cells/plate, P<0.01], and that high concentration HCS (final cholesterol concentration 2 mg. ml-1) was cytotoxic to the cultured cells. PNS (100 and 400 µg. ml-1) decreased the incorporation of [3H] thymidine into SMC in culture with or without HCS (1292 + 260 and 982 + 314 or 4111 + 886 and 2361 +751 dpm/µg cell protein) and inhibited the proliferation of the cultured cells [(3.3 ±0.7) X 105 and (2.9±0.7) X 105 or (4.7± 1.4) X 105 and (4.1 +1.2) X 105 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 prevent atherosclerosis and inhibit progression of the atherosclerotic lesions by interfering with the proliferation of arterial SMC.