Ulceration colitis (UC) is a chronic and recurrent inflammatory disorder in the gastro-intestinal tract. The purpose of our study is to explore the potential mechanisms of ginsenoside Rg1 (GS Rg1) on dextran sulfate sodium (DSS)-induced colitis in mice and lipopolysaccharide (LPS)-induced RAW 264.7 cells. Acute colitis was induced in male C57BL/6 mice. In vitro model of LPS-induced RAW 264.7 cells to simulate enteritis model. The disease activity index (DAI), colon length, body weight and histopathological analysis were performed in vivo. Pro-inflammatory cytokines and markers for oxidative and anti-oxidative stress, MPO level were measured in vivo and in vitro. Nuclear erythroid 2-related factor 2 (Nrf2) and NF-?B p65 protein levels were analyzed using western blotting. Our results indicated that the UC models were established successfully by drinking DSS water. GS Rg1 significantly attenuated UC-related symptoms, including preventing weight loss, decreasing DAI scores, and increasing colon length. GS Rg1 ameliorated the DSS-induced oxidative stress. IL-1beta, IL-6, and TNF-alpha levels were significantly increased in serum and cell supernatant effectively, while treatment with the GS Rg1 significantly reduced these factors. GS Rg1 reduced MPO content in the colon. GS Rg1 treatment increased SOD and decreased MDA levels in the serum, colon, and cell supernatant. GS Rg1 restored the Nrf-2/HO-1/NF-?B pathway in RAW 264.7 cells and UC mice, and these changes were blocked by Nrf-2 siRNA. Overall, GS Rg1 ameliorated inflammation and oxidative stress in colitis via Nrf-2/HO-1/NF-kappaB pathway. Thus, GS Rg1 could serve as a potential therapeutic agent for the treatment of UC.
- MeSH
- dextrany metabolismus farmakologie terapeutické užití MeSH
- ginsenosidy * MeSH
- kolitida * chemicky indukované MeSH
- kolon metabolismus MeSH
- lipopolysacharidy metabolismus MeSH
- modely nemocí na zvířatech MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- NF-kappa B metabolismus MeSH
- síran dextranu toxicita metabolismus MeSH
- sírany * MeSH
- ulcerózní kolitida * chemicky indukované farmakoterapie metabolismus MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Introduction As a commonly used chemotherapeutic agent, fluorouracil (5-FU) has serious dose-limiting side effects. In this study, we evaluated the synergy between red American ginseng (RAG) and 5-FU on human colorectal cancer cells, and explored the potential mechanisms. Methods Ginsenoside contents of white American ginseng (WAG) and RAG were determined by HPLC. Cell proliferation was evaluated by MTS assay. Combination Index (CI) analysis was executed using CompuSyn software. Paraptotic events were observed after crystal violet staining. Cell cycle distribution, cyclin A expression and apoptotic induction were analyzed using flow cytometry. Results We observed the heat treatment remarkably increased levels of ginsenoside Rg3, 20R-Rg3, Rk1 and Rg5. When the combinations of 5-FU and RAG were applied, cell proliferation inhibition rates were notably increased, indicating that RAG significantly enhanced 5-FU’s effect. Additionally, CI analysis suggested that there was a synergistic action of 5-FU and RAG when combined. The cell cycle data indicated 5-FU induced S phase arrest, and the combination of 5-FU and RAG increased G1 phase. Further, the RAG’s ability to enhance the anti-cancer effects of 5-FU was linked to both paraptosis and apoptosis inductions.
- MeSH
- apoptóza účinky léků MeSH
- fluoruracil aplikace a dávkování farmakologie MeSH
- ginsenosidy aplikace a dávkování farmakologie MeSH
- kolorektální nádory farmakoterapie MeSH
- kombinovaná farmakoterapie MeSH
- nádorové buňky kultivované účinky léků MeSH
- screeningové testy protinádorových léčiv MeSH
- synergismus léků MeSH
- techniky in vitro MeSH
- ženšen chemie MeSH
- Publikační typ
- práce podpořená grantem MeSH
Ginsenoside has been reported to have therapeutic effects for some types of cancer, but its effect on ovarian cancer cells has not been evaluated. In this study, we monitored the effects of ginsenoside-Rh2 (Rh2) on the inhibition of cell proliferation and the apoptotic process in the ovarian cancer cell line SKOV3 using an MTT assay and TUNEL assay. We found that Rh2 inhibited cell proliferation and significantly induced apoptosis. We confirmed the apoptotic effects of Rh2 using western blot analysis of apoptosis-related proteins. Specifically, the levels of cleaved poly ADP ribose polymerase (PARP) and cleaved caspase-3 significantly increased in SKOV3 cells treated with Rh2. Therefore, Rh2 clearly suppressed the growth of SKOV3 cells in vitro, which was associated with induction of the apoptosis pathway. Moreover, the migration assay showed that Rh2 inhibited the invasive ability of SKOV3 cells. Taken together, our results suggest that Rh2 has anticancer effects in SKOV3 cells through inhibition of cell proliferation and induction of apoptosis. Considering the therapeutic potential of Rh2, more studies should be carried out to facilitate the future application of this natural product as a potential anti-cancer agent.
- MeSH
- aktivace enzymů účinky léků MeSH
- apoptóza účinky léků MeSH
- epitelo-mezenchymální tranzice účinky léků MeSH
- ginsenosidy farmakologie MeSH
- hojení ran účinky léků MeSH
- kaspasa 3 účinky léků metabolismus MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- nádory vaječníků metabolismus MeSH
- proliferace buněk účinky léků MeSH
- protoonkogenní proteiny c-bcl-2 účinky léků metabolismus MeSH
- signální transdukce účinky léků MeSH
- Check Tag
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
Generation of reactive oxygen species significantly contributes to the pathogenesis of acute renal failure (ARF) induced by myoglobin release. Ginsenosides (GS), the principal active ingredients of ginseng, is considered as an extremely good antioxidative composition of Chinese traditional and herbal drugs. The purpose of the present study was to investigate the protective effect of ginsenoside in rats with ARF on the changes of cholinergic nervous system in the kidney as well as on the involvement of mitogen-activated protein kinases (MAPK) in the hypothalamic paraventricular nuclei (PVN). In our assay, glycerol-induced acute renal failure in rats was employed to study the protective effects of ginsenoside. Our results indicated that the treatment of ARF rats with ginsenosides for 48 h significantly reduced lipid peroxidation, restored the superoxide dismutase (SOD) level. Meanwhile, the obvious increase of choline acetyltransferase-immunoreactivity (ChAT-IR) in the proximal convoluted tubular cells (PCT) was observed by immunohistochemistry in ARF+GS group. The same effect was also observed in the changes of p-ERK1/2-IR in the hypothalamic paraventricular nuclei. Our results suggest that ginsenoside administered orally may have a strong renal protective effect against glycerol-induced ARF, reduce the renal oxidative stress, and ginsenoside can also activate the cholinergic system in PCT, simultaneously MAPK signal pathway in the PVN was also activated.
- MeSH
- akutní poškození ledvin chemicky indukované enzymologie patologie prevence a kontrola MeSH
- antioxidancia aplikace a dávkování farmakologie MeSH
- aplikace orální MeSH
- časové faktory MeSH
- cholin-O-acetyltransferasa metabolismus MeSH
- cytoprotekce MeSH
- fosforylace MeSH
- ginsenosidy aplikace a dávkování farmakologie MeSH
- glycerol MeSH
- malondialdehyd metabolismus MeSH
- mitogenem aktivovaná proteinkinasa 1 metabolismus MeSH
- mitogenem aktivovaná proteinkinasa 3 metabolismus MeSH
- modely nemocí na zvířatech MeSH
- nucleus paraventricularis hypothalami účinky léků enzymologie MeSH
- oxidační stres účinky léků MeSH
- peroxidace lipidů účinky léků MeSH
- potkani Sprague-Dawley MeSH
- proximální tubuly ledvin účinky léků enzymologie patologie MeSH
- signální transdukce účinky léků MeSH
- superoxiddismutasa metabolismus MeSH
- upregulace MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Acute renal failure (ARF) is mainly characterized by acute tubular necrosis. No significant change was found for mortality rates over the past few decades despite significant advances in supportive care. In recent years, great effort has been focused on traditional and herbal medicine, which is much less toxic than those agents conventionally used and which is nowadays considered as a novel therapeutic agent for ARF. However, the effect of ginsenosides (GS) administered orally on ARF has not been reported yet and little is known about its cellular and molecular mechanism. The purpose of the study is to investigate the protective effect of ginsenoside in rats with ARF on the changes of tyrosine hydroxylase immunoreactivity (TH-IR) as well as on the involvement of mitogen-activated protein kinases (MAPK) in the locus coeruleus. In our assay, glycerol-induced acute renal failure in rats was employed to study the protective effects of ginsenoside. Our results indicated that the treatment of ARF rats with ginsenosides for 48 h significantly reduced the serum blood urea nitrogen, creatinine level, and lipid peroxidation, restored the GSH level and the normal renal morphology. Immunohistochemistry showed that an obvious increase of TH-IR was further enhanced in ARF+GS group. The same effect was also observed in the changes of p-ERK1/2-IR in the locus coeruleus. Our results suggest that ginsenoside administered orally may have a strong renal protective effect against glycerol-induced ARF, and ginsenoside can also activate the brain catecholaminergic neurons in the locus coeruleus. Our future attention will be focused to the question whether there is a correlation between the renal protective effect of ginsenosides against acute renal failure and the activation of tyrosine hydroxylase in the locus coeruleus.
- MeSH
- akutní poškození ledvin MeSH
- aplikace orální MeSH
- biologické markery krev MeSH
- časové faktory MeSH
- deprivace z nedostatku vody MeSH
- dusík močoviny v krvi MeSH
- financování organizované MeSH
- fosforylace MeSH
- ginsenosidy aplikace a dávkování farmakologie MeSH
- glutathion metabolismus MeSH
- glycerol MeSH
- imunohistochemie MeSH
- kreatinin krev MeSH
- krysa rodu rattus MeSH
- ledviny MeSH
- locus coeruleus enzymologie účinky léků MeSH
- malondialdehyd metabolismus MeSH
- mitogenem aktivovaná proteinkinasa 1 metabolismus MeSH
- mitogenem aktivovaná proteinkinasa 3 metabolismus MeSH
- modely nemocí na zvířatech MeSH
- ochranné látky aplikace a dávkování farmakologie MeSH
- peroxidace lipidů účinky léků MeSH
- potkani Sprague-Dawley MeSH
- tyrosin-3-monooxygenasa metabolismus MeSH
- upregulace MeSH
- zvířata MeSH
- Check Tag
- krysa rodu rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
Článek uvádí jednotlivé případy zaznamenaných interakcí u přípravků s obsahem Panax ginseng s ostatními léčivy za období 1997–2001. Jedná se zejména o interakce s heparinem, warfarinem, nesteroidními antiflogistiky, psychofarmaky.
- MeSH
- antiflogistika nesteroidní klasifikace metabolismus terapeutické užití MeSH
- financování organizované MeSH
- ginsenosidy metabolismus terapeutické užití MeSH
- heparin metabolismus terapeutické užití MeSH
- interakce bylin a léků MeSH
- lidé MeSH
- psychotropní léky klasifikace metabolismus terapeutické užití MeSH
- warfarin metabolismus terapeutické užití MeSH
- ženšen metabolismus MeSH
- Check Tag
- lidé MeSH
- MeSH
- alkaloidy farmakologie terapeutické užití MeSH
- apoptóza účinky záření MeSH
- fenoly farmakologie terapeutické užití MeSH
- finanční podpora výzkumu jako téma MeSH
- flavonoidy farmakologie terapeutické užití MeSH
- ginsenosidy farmakologie terapeutické užití MeSH
- kaspasy MeSH
- nádorová transformace buněk účinky léků MeSH
- nádorové buňky kultivované účinky léků MeSH
- nekróza MeSH
- MeSH
- antihypertenziva terapeutické užití MeSH
- diabetes mellitus farmakoterapie prevence a kontrola MeSH
- ginsenosidy farmakokinetika farmakologie toxicita MeSH
- Gynostemma chemie MeSH
- hypolipidemika terapeutické užití MeSH
- imunitní systém * účinky léků MeSH
- inhibitory agregace trombocytů terapeutické užití MeSH
- kardiotonika terapeutické užití MeSH
- kardiovaskulární nemoci * farmakoterapie prevence a kontrola MeSH
- lidé MeSH
- nemoci jater farmakoterapie prevence a kontrola MeSH
- sapogeniny farmakokinetika farmakologie toxicita MeSH
- saponiny * farmakokinetika farmakologie toxicita MeSH
- ženšen chemie MeSH
- Check Tag
- lidé MeSH