• Korean Journal of Pharmacognosy
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• v.23 no.3
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• pp.158-170
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• 1992

The studies were conducted to investigate the combined effects of several combined preparation of crude drugs and mitomycin C(MMC). The combined effects on the proliferation of Molt-4 cells and activation of human lymphocytes were estimated by MTT colorimetric assays. The drugs itself enhanced the proliferation of Molt-4, but the inhibitory action of MMC was not affected by the combined treatment of the drugs and MMC. Among 9 kinds of the drugs, Sip Jeon Dae Bo Tang(SDT), Saeng Maek San(SMS) and Kwi Bi Tang(KBT) did not inhibit the action of MMC, but activated lymphocytes. When the mice were treated by MMC, the number of leukocytes was decreased significantly at the 1st day, but recovered at the 7th day. In the groups of MMC treated with SDT or KBT, the number of leukocytes was increased significantly than the group of MMC treated only at the 3rd day. The combined treatment of SDT, SMS and MMC retained the body weight of mice at the level of normal mice. The SDT, SMS and KBT did not change the number of plaque forming cells(PFC) and the proliferation of T cells. The combined treatment of SDT and MMC increased the number of PFC significantly than the MMC treated group. The combined treatment of SDT, SMS, KBT and MMC increased the T cell proliferation significantly than the MMC treated group. In conclusion, it is suggested that SDT, SMS and KBT can recover the side effects of MMC, such as weight loss, leukopenia and immunosuppression, without any intercalating the anti-proliferative action of MMC in vivo.

• Journal of Life Science
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• v.16 no.7 s.80
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• pp.1235-1242
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• 2006

Sulforaphane, an isothiocyanate derived from hydrolysis of glucoraphanin in broccoli and other cruciferous vegetables, was shown to induce phase II detoxification enzymes and inhibit chemically induced mammary tumors in rodents. Recently, sulforaphane is known to induce cell cycle arrest and apoptosis in human canter cells, however its molecular mechanisms are poorly understood. In tile present study, we demonstrated that sulforaphane acted to inhibit proliferation and induce morphological changes of human hepatocarcinoma HepG2 cells. Treatment of HepG2 cells with $10{\mu}M\;or\;15{\mu}M$ sulforaphane resulted in significant G2/M cell cycle arrest as determined by DNA flow cytometry. Moreover, $20{\mu}M$ sulforaphane significantly induced the population of sub-G1 cells suggesting that sulforaphane induced apoptosis. This anti-proliferative effect of sulforaphane was accompanied by a marked inhibition of ryclin A, cyclin 31 and Cdc2 protein. However, the levels of tumor suppressor p53 and Cdk inhibitor p21 mRNA and protein expression were significantly increased by sulforaphane treatment in a concentration-dependent manner. Although further studies are needed, the present work suggests that sulforaphane may be a potential rhemoprevetiveichemotherapeucc agent for the treatment of human cancer cells.

• Tuberculosis and Respiratory Diseases
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• v.66 no.4
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• pp.274-279
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• 2009

Background: Uteroglobin (UG) is a secretary protein that has strong immunomodulatory properties, and which is synthesized in most epithelia including lung tissue. Overexpression of UG is associated with decreased expression of cyclooxygenase (COX)-2 and suppression of cancer cell growth. Indoleamine 2,3-dioxygenase (IDO) catalyzes tryptophan along the kynurenine pathway, and both the reduction in local tryptophan and the production of tryptophan metabolites contribute to the immunosuppressive effects of IDO. Methods: In this study, we investigated the pattern of expression of COX-2 and IDO, and the effect of UG transduction in the expression of COX-2 and IDO in several non-small cell lung cancer cell lines, especially A549. Results: Both COX-2 and IDO were constitutionally expressed in A549 and H460 cells, and was reduced by UG transduction. In A549 cells, the slightly increased expression of COX-2 and IDO with the instillation of interferon-gamma (IFN-$\gamma$) was reduced by UG transduction. However, the reduced expression of COX-2 and IDO by UG transduction was not increased with IFN-$\gamma$ instillation in A549 cells. In both the A549 COX-2 sense and the A549 COX-2 anti-sense small interfering RNA (siRNA)-transfected cells, IDO was expressed; expression was reduced by UG transduction, irrespective of the expression of COX-2. Conclusion: The results suggest that the anti-proliferative function of UG may be associated with the immune tolerance pathway of IDO, which is independent of the COX-2 pathway.

• Tuberculosis and Respiratory Diseases
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• v.54 no.4
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• pp.403-414
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• 2003

Background : Proteasome inhibitors can promote either cell survival or programmed cell death, depending on both the specific type and proliferative status of the cell. However, it is not well known whether inhibition of proteasome activity is related to apoptosis in lung cancer cells. In addition, the exact mechanisms responsible for apoptosis induced by proteasome inhibition are not well understood. In the present study, we have examined the effect of proteasome inhibition on lung cancer cells and tried to test the mechanisms that may be associated with the apoptosis of these cells. Methods : We examined the effect of proteasome inhibition with MG132 or PS-341 on cell survival in A549 and NCI-H157 lung cancer cells using MTT assay, and analyzed the cleavage of PARP by Western blot analysis to find evidence of apoptosis. Next, we evaluated the activation of caspase 3 by Western blot analysis and the activity of JNK by immunocomplex kinase assay. We also examined the changes in anti-apoptotic pathways like ERK and cIAP1 by Western blot analysis after inhibition of proteasome function. Results : We demonstrated that MG132 reduced cell survival by inducing apoptosis in A549 and NCI-H157 cells. Proteasome inhibition with MG132 or PS-341 was associated with activation of caspase 3 and JNK, reduced expression of activated ERK, and downregulation of cIAP1. Conclusion : Apoptosis induced by proteasome inhibition may be associated with the activation of pro-apoptotic pathways like caspase 3 and JNK and the inactivation of anti-apoptotic pathways in lung cancer cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.4
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• pp.395-401
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• 2006

In this study, we investigated anticarcinogenic effects of extracts from Gloiopeltis tenax (GT). GT was extracted with methanol (GTM), which was then further fractionated into four fractions by using solvent fractionation method, affording methanol (GTMM), hexane (GTMH), butanol (GTMB) and aqueous (GTMA) soluble fractions. We determined the cytotoxic effects of these fractions on cancer cells by MTT assay. Among various fractions of GT, the GTMM showed the strongest cytotoxic effect at concentration of $150{\mu}g/mL$, displaying 95.97% on HepG2 cell lines and 93.64% on HT-29 cell lines, respectively. And, the anti-proliferative effect of GT was accompanied by a marked in increase of levels of Bad, Bax, Bok and Bak protein and activation of caspase-3, caspase-7 and PARP protein. Also, we observed quinone reductase (QR) induced effects in all fraction layers of GT on HepG2 cells. The QR induced effects of the GTMM and GTMB on HepG2 cells at concentration of $60{\mu}g/mL$ showing inductive indexes of 2.86 and 2.04 compared to the control value of 1.0.

• Journal of Preventive Medicine and Public Health
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• v.27 no.1 s.45
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• pp.11-24
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• 1994

The studies reported here were undertaken to investigate the effects of mercury chloride on immune system of Balb/c mouse employing a flexible tier of in vitro and in vivo assays. Mercury chloride inhibited the proliferative responses of spleen cells to lipopolysaccharide, pokeweed mitogen, and phytohemagglutinin as a dose-dependent manner. This inhibitory effect was observed not only when $HgCl_2$ was added 2nd or 3rd day of 3 days culture period but also when spleen cells was pretreated with $HgCl_2$ for 2 hours. Mercury chloride, however, potentiated the production of IgM and IgG from spleen cells. During the $HgCl_2$ administration by drinking for 3 weeks, the weight gain of mice was significantly blunted than that o control group mice, while no overt signs related to mercury toxicity were noted in any mice of experimental group. There was no change in thymus and spleen weights, and in histological findings of kidney, bone marrow of femur, thymus, spleen, and popliteal lymph node after 3 weeks of mercury exposure. However, $HgCl_2$ induced a significant increase of total serum IgM, IgG including $IgG_1,\;IgG_{2a}\;and\;IgG_{2b}$, and IgE in Balb/c mice. Treatment in vivo with anti-IL-4 monoclonal antibody significantly abrogated the $HgCl_2$-induced increase in total serum IgG1 and IgE. Whereas $HgCl_2$ potentiated total serum IgM and IgG, there was no difference in total serum hemagglutinin to SRBC (Sheep Red Blood Cell) between experimental and control group mice when these mice were immunized with SRBC. All these findings observed in Balb/c mice suggest that mercury perturbates well-orchestrated regulation of immune responses before developing histopathological changes in lymphoid tissues.