Se Hoon Kim

Effect of Korea red ginseng on the blood pressure in conscious hypertensive rats.

The change of blood pressure and heart rate after intravenous injection of Korea red ginseng (KRG) were studied in the conscious normotensive and one-kidney, one-clip Goldblatt hypertensive (1K, 1C-GBH) rats. Crude saponin (CS) of KRG (50, 100 mg/kg i.v.) induced a hypotensive effect and bradycardia in a dose-dependent manner in the anesthetized rats. On the other hand, CS of KRG (100 mg/kg) induced a hypotensive effect and reflex tachycardia in the conscious rats. Saponin-free fraction (SFF) of KRG did not affect them in the anesthetized normotensive rats (P>.05). The maximal hypotensive effect by CS of KRG in the conscious 1K, 1C-GBH hypertensive rats and L-nitroarginine methyl ester (L-NAME, 40 mg/kg)-treated conscious hypertensive rats was not different from that of conscious normotensive rats (Delta 31.6+/-6.3, Delta 27.5+/-5.8 vs. Delta 26.7+/-4.3 mmHg, P>.05). However, pretreatment of L-NAME significantly inhibited the reflex tachycardia by CS of KRG (70.8+/-7.0 vs. 30.6+/-15.0 bpm, P<.05). Hemolysate-sensitive nitric oxide (NO) current by the CS of KRG was greater than that of the SFF of KRG (651.9+/-128.2 pA for CS and 164.9+/-92.5 pA for SFF, P<.001). These findings suggest that KRG has a hypotensive effect and its effect may be due to saponin fraction of KRG in the conscious rats. The releasing effect of NO of KRG, like NO donor, may be partly contributed to the hypotensive effect of KRG.

Korean Red Ginseng Extract inhibits Tumor Necrosis Factor-alpha-induced Monocyte Adhesion in the Human Endothelial Cells

Vascular inflammation is an important step in the development of cardiovascular disorder. Since it has not been known whether Korean red ginseng has a role to play on the vascular inflammation, we investigated the effects of Korean red ginseng extract (KRGE) on monocyte adhesion and its underlying signaling mechanism. Monocyte adhesion assay and Western blot were conducted on the human umbilical vein endothelial cells to study monocyte adhesion and the expression of adhesion molecules. Intracellular calcium was measured with Fura-2 fluorescent staining, and superoxide production was measured with lucigenin chemiluminescence in the endothelial cells. KRGE inhibits tumor necrosis factor (TNF)-alpha-induced monocyte adhesion on the endothelial cells at the range of 0.03~1 ㎎/㎖. TNF-alpha-induced vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 expression were inhibited by the pretreatment of KRGE in the endothelial cells. KRGE also inhibits TNF-alpha-induced intracellular calcium and the superoxide production in the endothelial cells. This study first demonstrated that KRGE inhibits TNF-alpha-induced monocyte adhesion by inhibiting the adhesion molecule expression, intracellular calcium and superoxide production in the endothelial cells. Therefore, the anti-inflammatory function of KRGE may be contributed to protecting the endothelial dysfunction in the vascular inflammatory disorders.

Vasorelaxing Mechanism of Crude Saponin of Korea Red Ginseng in the Resistance-sized Mesenteric Artery of Rat

It has been well known that Korea red ginseng has an antihypertensive effect. The antihypertensive effect may be due to its ability to change the peripheral resistance. Change of vascular tone in the resistance-sized artery contribute to the peripheral resistance, thereby regulate the blood pressure. Therefore, we investigated to clarify the vasorelaxing mechanism induced by crude saponin of Korea red ginseng in the resistance-sized mesenteric artery of rats. The resistance-sized mesenteric artery was isolated and cut into a ring. The ring segment was immersed in HEPES-buffered solution and its isometric tension was measured using myograph force-displacement transducer. Crude saponin of ginseng relaxed the mesenmetric arterial rings precontracted with norepinephrine (3M) in dose-dependent manner (0.01 mg/㎖ -1 mg/㎖. The relaxation by crude saponin was smaller in endothelium-intact preparation than that in endothelium-denuded preparation. The contraction induced by A23187 or phorbol 12,13-dibutyrate was not affected by crude saponin of ginseng. The vasorelaxing effect of crude saponin of ginseng was significantly attenuated by the increase of the extracellular K+/ concentration. Crude saponin-induced vasorelaxation was not affected by tetraethylammonium (1 mM), glybenclamide (10M), and 4-aminopyridine (0.1 mM) in these preparations. Ba2+/(10M ∼100M) markedly reduced the crude saponin-induced vasorelakation dose-dependently. From the above results, we suggest that crude saponin of ginseng may stimulate K+/ efflux and hyperpolarize the membrane, thereby cause the vasorelaxation in the resistance-sized mesenteric artery of rats.

Effects of gonadal steroid hormones on amylase secretion in pancreatic lobules of rats.

Objectives: Because functional changes of the pancreas during the ovarian cycle are not fully understood, effects of gonadal steroid hormones on pancreatic amylase content and secretion were investigated. Methods: The estrus cycle of female rats was confirmed by vaginal smear. To mimic the estrus or the diestrus, estradiol 17&bgr; (25 &mgr;g/kg) or progesterone (50 mg/kg) was subcutaneously injected to ovariectomized rats once daily for 2 days. Amylase secretion of pancreatic lobules (˜6 mg wet weight) was induced by acetylcholine (10−8˜10−4 M). Results: In normal rats, pancreatic amylase content was not altered during the estrus cycle, whereas spontaneous amylase secretion of pancreatic lobules at the diestrus was significantly higher than that at the estrus. In ovariectomized rat, pancreatic amylase content was markedly reduced, which was restored by either estradiol 17&bgr; or progesterone. Pancreatic lobules of ovariectomized rats spontaneously secreted amylase at the level identical to that at the estrus, which was elevated to the level at the diestrus by progesterone, but not affected by estradiol 17&bgr;. In normal rats, acetylcholine induced amylase secretion much higher at the diestrus than at the estrus. In ovariectomized rats, the acetylcholine-induced amylase secretion was similar to that at the estrus, which was elevated by progesterone, but not affected by estradiol 17&bgr;. Conclusion: We conclude from the above results that both estradiol 17&bgr; and progesterone are necessary to maintain amylase content in the rat pancreas, but only progesterone exerts a stimulatory effect on spontaneous and stimulated amylase secretion in pancreatic lobules of rats.