Background: Psychiatric patients appear to be at lower risk of cancer. Some antipsychotic drugs might have inhibitory effects on tumor growth, including penfluridol, a strong agent. To test this, we conducted a study to determine whether penfluridol exerts cytotoxic effects on tumor cells and, if so, to explore its anti-tumor mechanisms. Methods: Growth inhibition of mouse cancer cell lines by penfluridol was determined using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Cytotoxic activity was determined by clonogenic cell survival and trypan blue assays. Animal tumor models of these cancer cells were established and to evaluate penfluridol for its anti-tumor efficacy in vivo. Unesterified cholesterol in cancer cells was examined by filipin staining. Serum total cholesterol and tumor total cholesterol were detected using the cholesterol oxidase/p-aminophenazone (CHOD-PAP) method. Results: Penfluridol inhibited the proliferation of B16 melanoma (B16/F10), LL/2 lung carcinoma (LL/2), CT26 colon carcinoma (CT26) and 4T1 breast cancer (4T1) cells in vitro. In vivo penfluridol was particularly effective at inhibiting LL/2 lung tumor growth, and obviously prolonged the survival time of mice bearing LL/2 lung tumors implanted subcutaneously. Accumulated unesterified cholesterol was found in all of the cancer cells treated with penfluridol, and this effect was most evident in LL/2, 4T1 and CT26 cells. No significant difference in serum cholesterol levels was found between the normal saline-treated mice and the penfluridol-treated mice. However, a dose-dependent decrease of total cholesterol in tumor tissues was observed in penfluridol-treated mice, which was most evident in B16/F10-, LL/2-, and 4T1-tumor-bearing mice. Conclusion: Our results suggested that penfluridol is not only cytotoxic to cancer cells in vitro but can also inhibit tumor growth in vivo. Dysregulation of cholesterol homeostasis by penfluridol may be involved in its anti-tumor mechanisms.
Even though appropriate immune response is necessary for the survival of the individual, excessive or insufficient immune Response might cause autoimmune or allergic disease. So the immune response must be controlled to the degree that is beneficial for the well being of the individual. This study was undertaken to know the effects of Gunleetang Gagambang on the immune system of the mouse. Gunleetang Gagambang has been used for cure of tumor as a traditional medicine without any experimental evidence to support the rational basis for its clinical use. This study was carried out to evaluate the possible therapeutic or antitumoral effects of Gunleetang Gagambang extract against tumor, and to carry out some mechanisms responsible for its effect. Some kinds of tumor were induced by the typical application of 3-methylcholanthrene(MCA) or by the implantation(s.c) of malignant tumor cells such as leukemia cells(3LL cells) or sarcoma cells(S180 cells). Treatment of the Gunleetang Gagambang on water-extract(dailly 1mg/mouse, i. p.) was continued for 7 days prior to tumor induction and after that the treatment was lasted for 20 days. Against squamous cell carcinoma induced by MCA, Gunleetang Gagambang decreased not only the frequency of tumor production but also the number and the weight of tumors per tumor bearing mice(TBM). Gunleetang Gagambang on also significantly suppressed the development of 3LL cell and S180 cell-implanted tumors in occurrence-frequency and their size. and some developed tumors were regressed by the continuous treatment of Gunleetang Gagambang extract into TBM. In vitro, treatment of Gunleetang Gagambang extract had no effect on the growth of some kinds of cell line such as FsaII, A431 strain but significantly inhibited the proliferation of 3LL, S180 cells and augmented the DNA synthesis of mitogen-activated lymphocytes. Gunleetang Gagambang also stimulated the migrative ability of leukocyte, the MIF and IL-2 production of T lymphocytes, but not IL 6 production of B cells. Gunleetang Gagambang administration to mice enhanced NK cells activities. These results demonstrated that Gunleetang Gagambang extract exhibited a significant prophylactic benefits against tumors and its antitumor activity was manifested depending on the type of tumor cells. And these results also suggested that effect of Gunleetang Gagambang might be chiefly due to nonspecitie enhancement of NK cell activities and cell-mediated immune responses.
Bujeonghangamtang(扶正抗癌湯) has been used for cure of tumor as a traditional medicine without any experimental evidence to support the rational basis for its clinical use. This study was carroed out to evaluate the possible therapeutic or antitumoral effects of Bujeonghangamtang extract against tumor, and to carry out some mechanisms responsible for its effect. Some kinds of tumor were induced by .the typical application of 3-methylcholanthrene (MCA) or by the implantation(s.c) of malignant tumor cells such as leukemia cells(3LL cells) or sarcoma cells(Sl80 cells). Treatment of the Bujeonghangamtang water-extract (dailly 1mg/mouse, i. p.) was continued for 7 days prior to tumor induction and after that the treatment was lasted for 20 days. Against squamous cell carcinoma induced by MCA, Bujeonghangamtang decreased not only the frequency of tumor production but also the number and the weight of tumors per tumor bearing mice (TBM). Bujeongmngamtang also significantly suppressed the development of 3LL cell and S180 cell-implanted tumors in occurence-frequency and their size, and some developed tumors were regressed by the continuous treatment of Bujeonghangamtang extract into TBM. In vitro, treatment of Bujeonghangamtang extract had no effect on the growth of some kinds of cell line such as FsaII, A431 strain but significantly inhibited the proliferation of 3LL, S180 cells and augmented the DNA synthesis of mitogen-activated lymphocytes. Bujeonghangamtang also stimulated the migrative ability of leukocyte, the MIF and IL-2 production of T lymphocytes, but not IL 6 production of B cells. Bujeonghangamtang-administration to mice enhanced NK cells attivities. These results demonstrated that Bujeonghangamtang extract exhibited a significant prophylactic benefits against tumors and its antitumor activity was manifested depending on the type of tumor cells. And these results also suggested that effect of Bujeonghangamtang might be chiefly due to nonspecific enhancement of NK cell activities and cell-mediated immune responses.
The solvent extracts from Aloe arborescens and Aloe vera were randomly screened for inhibitory effects on the growth of tumor cell lines. In case of Aloe vera extracts, butyl alcohol extract and ethyl alcohol extract showed antitumor activity at $100\;{\mu}g/ml$ on lung cell lines(A427, Sk-mes-1, Calu-3 and 3LL). In Aloe arborescens extracts, butyl alcohol extract and ethyl alcohol extract exerted high activity at $100\;{\mu}g/ml$ on breast cell line(Hs-578T) and lung cell line(Sk-mes-1), respectively. The solvent extracts from Aloe vera exerted antitumor activity broadly on various tumor cell lines. In contract, the solvent extracts from Aloe arborescens exerted specific antitumoricity on a few tumor cell lines.
The purpose of this study was to find out effects of treatment of ginsenoside Re, Rc and EGCG on mRNA expressions of leptin, hormone sensitive lipase (HSL) and resistin in 3T3-L1 adipocytes. The concentrations of EGCG were treated with $0.01{\times}10^{-7},\;0.1{\times}10^{-7},\;1{\times}10^{-7}\;and\;1{\times}10^{-6}\;or\;100{\mu}g/ml$ ginsenoside Re, Rc in culture cell for 13 days. mRNA expression of leptin wasn't expressed in preadipocyte but according to differentiation of adipocyte, the that of mRNA expression was decreased at gensenosids or EGCG treated cells compared with non treated adipocyte. Expression of HSL mRNA was increased in G-Re, G-Rc and EGCG treated cells compared with non treated cells. The resistin level was significantly decreased in adipocytes treated with G-Re, G-Rc and EGCG. These pattern was similar to leptin expression. These results support that treatment of gensenosides or EGCG in 3T3-L1 adipocyte resulted to affect of leptin and resistin as well as HSL mRNA levels, accordingly, levels of leptin and HSL will be acted by signalling body fat stores to the hypothalamus which in turn regulates food intake andenergy expenditure to maintain body weight homeostasis. And also regulation of resistin mRNA will prevent to diabetics attacked with obesity. In conclusion, we suggest that consumption of ginseng saponine or EGCG might prevent human diabetics or/and obesity.
Arsenic exposure is associated with several human diseases, including cancers, atherosclerosis, hypertension, and cerebrovascular diseases. In cultured cells, arsenite, an inorganic arsenic com-pound, was demonstrated to interfere with many physiological functions, such as enhancement of oxidative stress, delay of cell cycle progression, and induction of structural and numerical changes of chromosomes. The objective of this study is to investigate the effects of arsenic exposure on gene expression profiles by colorimetric cDNA microarray technique. HFW (normal human diploid skin fibroblasts), CL3 (human lung adenocarcinoma cell line), and HaCaT (immortalized human keratinocyte cell line) were treated with 5 $\mu\textrm{M}$ or 10 $\mu\textrm{M}$ sodium arsenite for 6 or 16 h, respectively. By a dual-color detection system, the expression profile of arsenite-treated cultures was compared to that of control cultures. Several genes expressed differentially were identified on the microarray membranes. For example, MDM2, SWI/SNF, ubiquitin specific protease 4, MAP3K11, RecQ protein-like 5, and Ribosomal protein Ll0a were consistently induced in all three cell types by arsenite, whereas prohibitin, cyclin D1, nucleolar protein 1, PCNA, Nm23, and immediate early protein (ETR101) were apparently inhibited. The present results suggest that arsenite insults altered the expression of several genes participating in cellular responses to DNA damage, stress, transcription, and cell cycle arrest.
No, Hun-Jeong;Jeon, Byeong-Hun;Mun, Gu;Mun, Seok-Jae
THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
/
v.2
no.1
/
pp.75-90
/
1996
This experiment was designed to study the antitumor effects and Activity of Natural Killer Cell of semen Tiglii plus Rhizoma Rhei. The cytotoxic and antitumor effects were evaluated on human cell lines(A549, Caki-1, LL2, Sarcoma 180, NIH/3T3) after exposure to prebrewed Semen Tiglii plus Rhizoma Rhei water extract 0.1, 0.2, 0.4, 0.8, 1.6mg/ml using in MTT assay, LDH, colony forming efficency and SRB assay which were regarded as a valuable method for cytotoxic and antitumor effects of unknown compound on tumor cell lines. The results obtained in this studies were as follows. 1. From the result of MTT assay, the cytotoxicity of ST(生巴豆霜), ST+RR(生巴豆霜加大黃) were concentration-dependently increased in both group of the ST and ST+RR, the cytotoxicity of ST+RR(生巴豆霜加大黃) was similar to that of ST(生巴豆霜). 2. From the result of LDH, the cytotoxicity of ST, ST +RR were concentrati -on-dependently increased in both group of the ST and ST+RR, the cytotoxicity of ST+RR was similar to that of ST. 3. The antitumor effect on A549 tumor cell from the result of colony forming efficiency showed the inhibitory effect on the growth in both group of the ST and ST+RR, the inhibitory effect on growth was low slightly in the ST+RR. 4. From the result of SRB assay, the antitumor effect on caki-1 tumor cell of ST, ST+RR showed the inhibitory effect on the growth in both group of the ST and ST+RR, the antitumor effect of ST+RR was similar to that of ST. 5. Median survival time and increased life span were increased slightly in both group of the ST and ST+RR. 6. The inhibitory effect on the growth of Sarcoma 180 and Lewis lung carcinoma tumor cell were increased slightly in both group of the ST and ST+RR. 7. The activity of NK cell was increased in the ST+RR.
The inhibitory effects of adipogenesis in 3T3-L1 adipocytes with water and ethanol extracts of Curdrania tricuspidata leaves were investigated. The lipid accumulation of ethanol extract from Curdrania tricuspidata leaves at a concentration of 5 mg/mL was reduced by 50% compared with control cells, whereas water extracts reduced by 86%. The survival rate of cell viability test showed 80% in the growth of cells at concentrations of 0.5-5 mg/mL. The contents of DNJ(1-deoxynojirimycin) and rutin were higher in leaves than those of stem. Moreover, DNJ contents were detected in large amounts in ethanol extract ($3921.3{\mu}g/g$) compared with water extract ($2906.3{\mu}g/g$). On the contrary, the rutin contents was detected in large amounts in water extracts compared with ethanol extract. These results indicate that Curdrania tricuspidata leaves extract is potential sources of natural antiobesity agent.
This experiment was designed to study the change of cytotoxic and antitumor effects according to the prebrewed method of Semen Tiglii and Rhizoma Coptidis. The cytotoxic and antitumor effects were evaluated on human cell lines(A 549, Caki-1, LL2, Sarcoma 180, NIH/3T3) after exposure to prebrewed Semen Tiglii and Rhizoma Coptidis water extract 0.1, 0.2, 0.4, 0.8, 1.6 mg/ml using in MTT assay, LDH, colony forming efficency and SRB assay which were regarded as a valuable method for cytotoxic and antitumor effects of unknown compound on tumor cell lines. The results obtained in this studies were as follows. 1. The cytotoxicity from the result of MTT assay was low slightly in the ST II(炒巴豆霜), high in the ST III(醋炒巴豆). The cytotoxicity of ST I + RC(生巴豆霜加黃連) was similar to that of STI(生巴豆霜). 2. The cytotoxicity from the result of LDH was low slightly in the ST Ⅱ (炒巴豆霜), high in the ST III(醋炒巴豆). The cytotoxicity of ST I + RC(生巴豆霜加黃連) was similar to that of ST I(生巴豆霜). 3. The antitumor affect on A 549 tumor cell from the result of colony forming efficiency was low slightly in the ST II (炒巴豆霜) and ST I + RC(生巴豆霜加黃連). 4. The antitumor effect on Caki-1 tumor cell from the result of SRB assay was low slightly in the ST II (炒巴豆霜). 5. Median survival time and Increased life span increased slightly in the ST I RC(生巴豆霜加黃連) and ST II (炒巴豆霜). 6. The inhibitory effect on the growth of Sarcoma 180 and Lewis lung carcinoma tumor cell increased slightly in the ST I + RC(生巴豆霜加黃連) and ST II (炒巴豆霜).
Journal of the Korean Society of Food Science and Nutrition
/
v.34
no.1
/
pp.13-20
/
2005
The effects of pectin on obesity was studied using 3T3-L1 pre-adipocytes and rats fed 20% high fat diets. The concentration of leptin released from 3T3-L1 adipocytes in the presence of pectin was significantly decreased by 85% compared to that of the control (p<0.05), however, glycerol concentration was not changed. These data indicate that pectin seems to inhibit lipids accumulation in the adipocytes rather than enhance the lipolytic activity. Forty Sprague Dawley rats were fed 20% high fat diet for 8 weeks to induce obesity and then divided equally into four groups. Experimental groups were normal diet group (ND), high fat diet group (HFD), HDF with 10% pectin group (HFP10), and HDF with 20% pectin group (HFP20). Diet for the each group was prepared to be iso-caloric following AIN-76 guideline. After obesity was induced, rats were placed on an restricted diet for 9 weeks. The body weight of HFD increased 50% (p<0.05) compared to the ND, while it was decreased by 12% and 16% for HFP10 and HFP20, respectively (p<0.05). The relative amount of visceral fats for HFDl0 and HFD20 were decreased by 45% and 59% compared to that of HDF (130%), respectively (p<0.05). Pectin seems to have a greater effect on reducing visceral fats accumulation than weight reduction. Significantly increased level of triglyceride, total cholesterol or LDL-cholesterol in the plasma of HFD was returned to the normal or even below the normal by pectin diet, while the level of HDL-cholesterol increased. Lipid lowering effect was also observed in the liver and heart. These effects of pectin were dosedependent. In conclusion, the beneficial effect of pectin on the obesity was observed from cell culture experiment and animal study in terms of inhibiting the accumulation of lipids in the adipocytes.
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