Ginsenoside Rk1 suppresses pro-inflammatory responses in lipopolysaccharide-stimulated RAW264.7 cells by inhibiting the Jak2/Stat3 pathway / 中国天然药物

The saponin ginsenoside Rk1 is a major compound isolated from ginseng. Ginsenoside Rk1 has been reported to have anti-inflammatory and anti-tumor properties and to be involved in the regulation of metabolism. However, the effect and mechanism of anti-inflammatory action of ginsenoside Rk1 has not been fully clarified. We investigated whether ginsenoside Rk1 could suppress the inflammatory response in lipopolysaccharide-stimulated RAW264.7 macrophages and to explore its mechanism of the action. RAW264.7 cells were treated with LPS (1 μg·mL) in the absence or the presence of Ginsenoside Rk1 (10, 20, and 40 μmol·L). Then the inflammatory factors were tested with Griess reagents, ELISA, and RT-PCR. The proteins were analyzed by Western blotting. Ginsenoside Rk1 inhibited lipopolysaccharide-induced expression of nitric oxide (NO), interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, and monocyte chemotactic protein (MCP)-1. Ginsenoside Rk1 inhibited the lipopolysaccharide-stimulated phosphorylation of NF-κB and janus kinase (Jak)2 and signal transducer and activator of transcription (Stat)3 at Ser727 and Tyr705. These data suggested that ginsenoside Rk1 could inhibit expression of inflammatory mediators and suppress inflammation further by blocking activation of NF-κB and the Jak2/Stat3 pathway in LPS-stimulated RAW264.7 cells.

A new triterpene natural product from stems and leaves of Panax ginseng / 中草药

Objective: To study the chemical constituents of saponins in the stems and leaves of Panax ginseng. Methods: The chemical constituents were isolated and purified by various chromatographic methods, and their structures were identified by NMR and MS data analysis. Results: Nine compounds were isolated and identified as 3β,6α,12β,25-tetrahydroxy-dammar-E-20(22)-ene-6-O-α-L-rhamnopyranosyl-(1→2)-β-D-glucopyranoside (1), sanchinoside B1 (2), 3β,6α,12β-dammar-E-20(22)-ene-3,6,12,25-tetraol (3), ginsenoside Rk3 (4), ginsenoside Rh4 (5), notoginsenoside T2 (6), 3β,6α,12β-dammar-20(21),24-diene-3,6,12-triol (7), ginsenoside Rk1 (8), and ginsenoside Rg5 (9). Conclusion: Compound 1 is a new natural product and the other eight compounds are all isolated from the stems and leaves of P. ginseng for the first time.

The effect of ginsenoside Rk1 in junctional protein of severe preeclamptic placenta / 대한산부인과학회지

OBJECTIVE: To investigate the differential expression of junctional proteins in the normal and preeclamptic human placenta and the effect of ginsenoside Rk1 in junctional proteins. METHODS: Placental tissues from 10 women with severe preeclampsia and 5 normal women were collected at the time of their cesarean section. Five of 10 preeclamptic women were complicated with intrauterine growth restriction (IUGR). Immunohistochemistry and Western blotting was employed to localize junctional proteins (zo-1, occludin and plakoglobin) positive cells. The placental explant culture was performed to investigate if Rk1 can attenuate the expression of junctional proteins (zo-1, occluding and plakoglobin) induced by deferoxamine-induced hypoxia. Rk1 was treated at the day 3 and Western blot analysis was performed for protein quantification. RESULTS: There was no different expression of zo-1 and plakoglobin among all the study groups. Occludin showed negative at the endothelial cells of the terminal villi in both normal and preeclampsia groups. At the endothelial cells of the stem villi, occludin was detected in both normal and severe preeclamptic placenta with normal fetal growth. However, severe preeclampsia with IUGR were decreased expression of occludin at the endothelial cells of the stem villi. When we administered Rk1 to the placenta treated with DFO, expression of occludin was not different. CONCLUSION: The placental expression of zo-1 and plakoglobin were not different among the study groups, while that of occludin was significantly decreased at the endothelium of stem villi in severe preeclampsia with IUGR. Rk-1 showed no effect on the placental junctional proteins. These results suggest that occludin may play a role in pathophysiology of fetal growth restriction in utero.