• Food Science and Preservation
• /
• v.8 no.4
• /
• pp.481-487
• /
• 2001

Grifola umbellatus was extracted using methanol, and the extract was further fractionated by water and ethyl acetate. Assay of each fraction with MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium-bromide] revealed significant cytotoxicity effect of the methanol extract of Grifola umbellatus against human gastric cancer cell but not normal human lymphocytes. The methanol extract showed the highest antioxidant activity as well. Antimicrobial activity of Grifola umbellants against Helicobacter pylori was higher in method extract than in other fractions. Grifola umbellatus had a significant inhibitory effect on Helicobacter pylori reducing both its growth and urease activity. These results show that the methanol extract of Grifola umbellatus possesses therapeutic potential on gastric diseases.

• Food Science and Preservation
• /
• v.21 no.1
• /
• pp.114-120
• /
• 2014

Zizyphus jujube leaf fractions (ZLFs) showed no cytotoxic effects of up to $100{\mu}g/mL$, while the anti-inflammatory effects of ZLFs were analyzed by checking the productions of nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), cyclooxygenase-2 (COX-2), and inflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 in the lipopolysaccharide (LPS)-stimulated Raw264.7 macrophage up to the concentration of $100{\mu}g/mL$. ZLFs ($100{\mu}g/mL$) demonstrated a strong anti-inflammatory activity that reduced 61~85% of NO and 71~100% of $PGE_2$ production in the LPS-stimulated Raw264.7 macrophage. Even the low ZLFs concentration of $1{\mu}g/mL$ have reduced NO and $PGE_2$ production by 34~64%. Expressions of COX-2 protein were also effectively inhibited by the ZLFs. Furthermore, the TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 production were significantly suppressed through the treatment of ZLFs at concentrations of 1, 10, and $100{\mu}g/mL$. In the order of the Zizyphus jujube leaf water fraction (ZLWF) < buthanol fraction (ZLBF) < ethyl acetate fraction (ZLEF) showed anti-inflammatory activity. In particular, the ethyl acetate fraction ZLEF at $100{\mu}g/mL$ showed an excellent anti-inflammatory activity by reducing the production of NO, $PGE_2$, COX-2, and inflammatory cytokines (TNF-${\alpha}$, IL-$1{\beta}$, IL-6) in the level of Raw264.7 macrophage without LPS-stimulation or even better. The results of our study suggest the potential of ZLEF for use as an excellent ant-inflammatory inhibiting mediator and may be used as a therapeutic approach to various inflammatory diseases.

• Korean Journal of Plant Resources
• /
• v.31 no.2
• /
• pp.117-123
• /
• 2018

In this study, we evaluated anti-inflammatory effect of biji in LPS-stimulated RAW264.7 cells. Biji inhibited the generation of NO and $PGE_2$ through the suppression of iNOS and COX-2 expression. In addition, biji attenuated the expression of TNF-${\alpha}$ and IL-$1{\beta}$ induced by LPS. Biji blocked LPS-mediated $I{\kappa}B-{\alpha}$ degradation and subsequently inhibited p65 nucleus accumulation in RAW264.7 cells, which indicates that biji inhibits NF-${\kappa}B$ signaling. In addition, biji suppressed p38 phosphorylation induced by LPS. Our results suggests that biji may exert anti-inflammatory activity through blocking the generation of the inflammatory mediators such as NO, $PGE_2$, iNOS, COX-2, TNF-${\alpha}$ and IL-$1{\beta}$ via the inhibiting the activation of NF-${\kappa}B$ and p38. From these findings, biji has potential to be a candidate for the development of chemoprevention or therapeutic agents for inflammatory diseases.

• Archives of Pharmacal Research
• /
• v.25 no.5
• /
• pp.685-690
• /
• 2002

The mitogen-stimulated serine/threonine kinase $p70^{S6k}$ plays an important role in the progression of cells from $G_0/G$_1$$ to S phase of the cell cycle by translational up-regulation of a family of mRNA transcripts family of mRNA transcripts which contain polypyrimidine tract at their 5 transcriptional start site. Here, we report that $p70^{S6k}$ was constitutively phosphorylated and activated to various degrees in serum-deprived AGS, A2058, HT-1376, MG63, MCF7, MDA-MB-435S, MDA-MB-231 and MB-157. Rapamycin treatment induced a significant dephosphorylation and inactivation of $p70^{S6k}$ in all cancer cell lines, while wortmannin, a specific inhibitor of PI3-K, caused a mild dephosphorylation of $p70^{S6k}$ in AGS, MDA-MB-435S and MB-157. In addition, SQ20006, methylxanthine phosphodiesterase inhibitor, reduced the phosphorylation of $p70^{S6k}$ in all cancer cells tested. Consistent with inhibitory effect of rapamycin on $p70^{S6k}$ activity, rapamycin inhibited [$^3H$]-thymidine incorporation and increased the number of cells at $G_{0}G_{1}$ phase. Furthermore, these inhibitory effects were accompanied by the decrease in growth of cancer cells. Taken together, the results indicate that the antiproliferative activity of rapamycin might be attributed to cell cycle arrest at $G_{0}G_{1}$ phase in human cancer cells through the inhibition of constitutively activated $p70^{S6k}$ of cancer cells and suggest $p70^{S6k}$ as a potential target for therapeutic strategies aimed at preventing or inhibiting tumor growth.

• Journal of Ginseng Research
• /
• v.44 no.4
• /
• pp.664-671
• /
• 2020

Background: Ginsenoside compound-Mc1 (Mc1) is a member of the deglycosylated ginsenosides obtained from ginseng extract. Although several ginsenosides have a cardioprotective effect, this has not been demonstrated in ginsenoside Mc1. Methods: We treated H9c2 cells with hydrogen peroxide (H₂O₂) and ginsenoside Mc1 to evaluate the antioxidant effects of Mc1. The levels of antioxidant molecules, catalase, and superoxide dismutase 2 (SOD2) were measured, and cell viability was determined using the Bcl2-associated X protein (Bax):B-cell lymphoma-extra large ratio, a cytotoxicity assay, and flow cytometry. We generated mice with high-fat diet (HFD)-induced obesity using ginsenoside Mc1 and assessed their heart tissues to evaluate the antioxidant effect and the fibrosis-reducing capability of ginsenoside Mc1. Results: Ginsenoside Mc1 significantly increased the level of phosphorylated AMP-activated protein kinase (AMPK) in the H9c2 cells. The expression levels of catalase and SOD2 increased significantly after treatment with ginsenoside Mc1, resulting in a decrease in the production of H₂O₂-mediated reactive oxygen species. Treatment with ginsenoside Mc1 also significantly reduced the H₂O₂-mediated elevation of the Bax:Bcl2 ratio and the number of DNA-damaged cells, which was significantly attenuated by treatment with an AMPK inhibitor. Consistent with the in vitro data, ginsenoside Mc1 upregulated the levels of catalase and SOD2 and decreased the Bax:B-cell lymphoma-extra large ratio and caspase-3 activity in the heart tissues of HFD-induced obese mice, resulting in reduced collagen deposition. Conclusion: Ginsenoside Mc1 decreases oxidative stress and increases cell viability in H9c2 cells and the heart tissue isolated from HFD-fed mice via an AMPK-dependent mechanism, suggesting its potential as a novel therapeutic agent for oxidative stress-related cardiac diseases.

• Journal of Veterinary Clinics
• /
• v.28 no.3
• /
• pp.314-317
• /
• 2011

A 16-year-old, spayed female, Maltese dog weighing 4.3 kg was presented with a 2-week history of yellowish nose-and oral-discharge, anorexia and lethargy. In physical examination, indefinite ulcerative mass about $3{\times}3$ cm in size in the left sublingual region, severe gingivoperiodontitis, halitosis, moderate dental calculus, fever and swelling of mandible soft tissue were noted. In radiographic view, periodontitis and bone lysis findings on the left rostral part of maxilla and mandible were observed. In complete blood count and blood chemistry test, thrombocytosis, increased levels of serum $NH_3$, AST and ALP were obtained. Urinalysis revealed hematuria and proteinuria. In histological examination, squamous cell carcinoma was diagnosed. No surgery was performed, but combined treatment with carboplatin and piroxicam was initiated. Five days after initiation of medication, because of insistent vomiting, piroxicam was substituted to meloxicam. Although the therapeutic efficacy of meloxicam could not be known; administration of meloxicam might be less potential to gastrointestinal side-effects than piroxicam. The dog totally received 3 times of carboplatin infusion. Five days after third infusion of carboplatin, the dog was hospitalized with severe lethargy, vomiting and bloody diarrhea. In examination, severe renal failure signs were noted, and the dog was euthanized.

• Journal of Life Science
• /
• v.23 no.4
• /
• pp.510-517
• /
• 2013

This study was performed to evaluate the antiobesity effect of supercritical fluid extracts (SFC) and marc methanol extracts (SFM) from Cinnamomum verum in 3T3-L1 preadipocytes. In inducing the differentiation of 3T3-L1 preadipocytes in the presence of an adipogenic cocktail, iso-butylmethylanthine (IBMX), dexamathasone, and insulin, treatment with fraction residue SFC and SFM. SFC significantly reduced the mRNA expression of the transcription factor peroxisome proliferator-activate-dreceptor-${\gamma}$ ($PPAR{\gamma}$), the sterol regulatory-element-binding protein-1c (SREBP1c), and the CCAAT enhancer-binding-protein ${\alpha}$ ($C/EBP{\alpha}$) in a concentration-dependent manner. Moreover, SFC markedly down-regulated acyl-CoA synthetase-1 (ASC1), fatty acid synthesis (FAS), fatty acid transport-1 (FATP1), fatty acid binding protein 4 (FABP4), and perilipin. These findings suggest that SFC may be a potential therapeutic adjunct for obesity by targeting the differentiation of preadipocytes, as well as their functions.

• Journal of Life Science
• /
• v.23 no.3
• /
• pp.462-469
• /
• 2013

Withaferin A is a steroidal lactone purified from the Indian medicinal plant Withania somnifera. It exhibits a wide variety of activities, including anti-tumor, anti-inflammation, and immunomodulation properties. In this review, we focused on the anti-cancer effects of withaferin A. Withaferin A inhibits cell proliferation, metastasis, invasion, and angiogenesis in cancer cells. Furthermore, it sensitized irradiation, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-, and doxorubicin-mediated apoptosis. The results showed that multiple mechanisms were involved in withaferin A-mediated anti-cancer effects. First, withaferin A increased intracellular reactive oxygen species (ROS) production and induced ER stress- and mitochondria-mediated apoptosis. Second, withaferin A inhibited the signaling pathways (Jak/STAT, Akt, Notch, and c-Met), which are important in cell survival, proliferation, and metastasis. Third, it induced apoptosis and inhibited cancer cell migration through the up-regulation of prostate apoptosis protein-4 (Par-4). Finally, withaferin A up-regulated pro-apoptotic protein expression levels through the inhibition of proteasome activity. Our findings suggested that withaferin A is a potential, potent therapeutic agent.

• Journal of Life Science
• /
• v.26 no.10
• /
• pp.1130-1136
• /
• 2016

The purpose of this study was to investigate the anti-proliferative and apoptotic effects of acid extract of Gracilaria verrucosa (AEG) on RC-58T/h/SA#4 primary human prostate cancer cells. AEG significantly decreased the cell viability of prostate cancer cells in a dose-dependent manner. AEG also showed relatively low cytotoxicity on normal cell (RWPE-1). The morphology of prostate cancer cells treated with AEG was distorted to shrunken cell masses. In addition, it was revealed that AEG induced cell death as evidenced by increased formation of apoptotic body and nuclear condensation. Furthermore, AEG clearly modulated the down regulation of Bcl-2 (anti-apoptotic)/Bax (pro-apoptotic) family and activated caspase-3 as an effector caspase in a dose-dependent manner. AEG inhibited cell proliferation induced by environmental hormones as a bisphenol A in a dose-dependent manner. These results indicate that AEG act as anti-proliferative effects as a potential therapeutic agent on primary human prostate cancer cells.

• Molecules and Cells
• /
• v.20 no.3
• /
• pp.401-408
• /
• 2005

Reactive oxygen species (ROS) contribute to the development of various human diseases. Cu,Zn-superoxide dismutase (SOD) is one of the major means by which cells counteract the deleterious effects of ROS. SOD activity is dependent upon bound copper ions supplied by its partner metallochaperone protein, copper chaperone for SOD (CCS). In the present study, we investigated the protective effects of PEP-1-CCS against neuronal cell death and ischemic insults. When PEP-1-CCS was added to the culture medium of neuronal cells, it rapidly entered the cells and protected them against paraquat-induced cell death. Moreover, transduced PEP-1-CCS markedly increased endogenous SOD activity in the cells. Immunohistochemical analysis revealed that it prevented neuronal cell death in the hippocampus in response to transient forebrain ischemia. These results suggest that CCS is essential to activate SOD, and that transduction of PEP-1-CCS provides a potential strategy for therapeutic delivery in various human diseases including stroke related to SOD or ROS.