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gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1599 8114&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSu m Mycelia from Antrodia camphorata in Submerged culture induce apoptosis of human hepatoma HepG2 cells possibly through regulation of Fas pathway. Song TY, Hsu SL, Yeh CT, Yen GC. Department of Food Science, National Chung Hsing University, 250 Kuokuang Road, Taichung 40227, Taiwan. The objective of this study was to investigate the antiproliferative effect and the mechanism of the methanol extracts of mycelia (MEM) form Antrodia camphorata in submerged culture toward HepG2 cells. The results showed that MEM-induced cell apoptosis involved up-regulation of Fas and down-regulation of Bcl-2, DR3, DR4, TNFRI, and TNFRII in HepG2 cells, while no changes on the levels of Bax, Bid, Bad, and Bak protein were observed. On the basis of these results, the involvement of the Fas/Fas ligand (FasL) death-receptor pathway, in MEM-induced apoptosis in HepG2 cells, was investigated. The apoptosis inducing activity was significantly enhanced by a Fas activator and inhibited by a Fas antagonist. To know about the effect of MEM on the activation of the apoptotic pathway, the adenovirus transfected with Bcl-2 was infected on HepG2 cells. The data showed that the percentage of apoptotic cells induced by MEM in Bcl-2-infected HepG2 (Bcl-2 overexpression) was not significantly different from that of uninfected HepG2. These results demonstrate that MEM induces HepG2 apoptosis through inhibition of cell growth and up-regulation of Fas/FasL to activate the pathway of caspase-3 and -8 cascades. PMID: 15998114 [PubMed - indexed for MEDLINE] 2: J Ethnopharmacol. 2005 Aug 22;100(1-2):158-67. Induction of apoptosis in human hepatoma cells by mycelia of Antrodia camphorata in submerged culture. Song TY, Hsu SL, Yen GC. Department of Food Science, National Chung Hsing University, 250 Kuokuang Road, Taichung 40227, Taiwan. The effect of methanolic extracts of mycelia (MEM) from Antrodia camphorata (Polyporaceac, Aphyllophorales) of submerged culture (ACSC) on the inhibition of cell viability and the mechanism of MEM-induced cytotoxic in hepatoma cells were investigated. The IC(50) of MEM on the cytotoxicity of HepG2 (wild type p53) and Hep3B (delete p53) were 49.5 and 62.7 microg/ml, respectively, on 48 h incubation. There is no observable cytotoxicity of MEM in Chang liver cells and rat primary hepatocytes at the concentration of 100 microg/ml. Cell cycle analysis revealed that MEM induced apoptosis on HepG2 via G0/G1 cell cycle arrest. MEM (100 microg/ml) treated HepG2 and Hep3B for 72 h, the apoptotic cells were 98.3 and 39.5%, respectively. The activities of caspase-3, -8 and -9 in HepG2 induced by MEM (50 microg/ml) were increased 5.3, 6.7 and 2.2-fold, respectively. MEM-induced apoptotic cell death was accompanied by up-regulation of caspase-3 and -8 in HepG2 cells. Combined treatment with MEM and caspase-3, -8 and -9 inhibitors, the caspase-3 and -8 inhibitors were accounting for 63 and 47% inhibition in MEM-induced apoptosis, respectively; however, caspase-9 inhibitor exhibited no obvious inhibition effect on the apoptosis percentage (p>0.05). The results indicated that MEM induced HepG2 apoptosis through activation of caspase-3 and -8 cascades and regulation of the cell cycle progression to inhibit hepatoma cells proliferation.
it could inhibit the proliferation of U937 cells via activation of mononuclear cells (MNCs). The in vitro antitumor activity was substantiated by the in vivo therapeutical study of AC-PS in sarcoma 180-bearing mice. In addition. Lin WS. Huang TS. In vivo studies also showed that several immunoparameters. ROC. the cytolytic activity of spleen 2 . 2004 Dec 1. Furthermore. there is little information available about its action. EAC also initiated mitochondrial apoptotic pathway through regulation of Bcl-2 family proteins expression.221(1):77-89. Publication Types: Research Support. EAC therefore decreased the cell growth and induced apoptosis both in Hep G2 and PLC/PRF/5 cells.indexed for MEDLINE] 3: Cancer Lett. Lin CC. camphorata mycelia (AC-PS) and found that it has pronounced anti-tumor effects on both in vitro and in vivo model. 100 and 200 mg/kg significantly suppressed the tumor growth with the inhibition rate of 69. Taiwan. Our results showed that AC-PS alone did not show any direct cytotoxic effect to human leukemic U937 cells. Kaohsiung Medical University. Hsu ML. and activation of caspase-9 both in Hep G2 and PLC/PRF/5 cells. Intraperitoneal and oral administration of AC-PS. The fruiting body of Antrodia camphorata is well known in Taiwan as a traditional medicine for treating cancer and inflammation. Chang WH.indexed for MEDLINE] 4: Toxicol Appl Pharmacol. Gov't PMID: 15797630 [PubMed . Furthermore.201(2):186-93. Apoptotic effects of extract from Antrodia camphorata fruiting bodies in human hepatocellular carcinoma cell lines. The purpose of this study was to evaluate the apoptotic effects of ethylacetate extract from A. Ng LT.S. College of Medicine. and subsequently attenuated the expression of Bcl-X(L) in Hep G2 and PLC/PRF/5 cells. Non-U. in a p53-indenpendent manner. However. Kuo PL. we purified a unique polysaccharide component from A.S. Hep G2 and PLC/PRF/5. camphorata (EAC) fruiting bodies in two human liver cancer cell lines. after AC-PS administration. Taipei. National Taiwan University. Kuo YC. Gov't PMID: 15949907 [PubMed . membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL). Treatment with EAC decreased the cell growth of Hep G2 and PLC/PRF/5 cells in a dose dependent manner. Antrodia camphorata is a popular folk medicine that has attracted great attention due to its fame for antitumor activity against cancer.Publication Types: Research Support. Chen CC. Lu FJ. 100 Shin-Chuan 1st Road. Kaohsiung 807. Taiwan.3% growth inhibition rate. Liu JJ. In the present study. No. EAC also inhibited the cell survival signaling by enhancing the amount of IkappaBalpha in cytoplasm and reducing the level and activity of NF-kappaB in the nucleus. even at high concentration (200 microg/ml). Graduate Institute of Natural Products. Kuo YH. were two-fold higher than in control mice. EAC increased the expression level of Fas/APO-1 and its two forms of ligands. Non-U. such as the spontaneous proliferation of spleen cells. Graduate Institute of Biochemistry and Molecular Biology. respectively. In Fas/APO-1 positive-Hep G2 cells. However. Treatment of U937 cells with AC-PS-stimulated-MNC-CM could significantly inhibit its proliferation with 55.1% and 58. Antitumor effects of the partially purified polysaccharides from Antrodia camphorata and the mechanism of its action. 2005 Apr 18. release of cytochrome c. College of Pharmacy. Hsu YL.8%.
7 microg/mL. Wu LY.51(11):3302-8. National Chung Hsing University. Non-U. When HepG2 cells were pretreated with DMF at the concentration of 0.20 in the absorbance of DPPH was about 31 +/. camphorata extract dose-dependently (250-1250 mg/kg) ameliorated the increase in plasma aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) levels caused by chronic repeated CCl(4) intoxication in mice.2 +/. Sheu JR.5. It also restored the decrement in the glutathione content and catalase activity of hepatic tissues in CCl(4)-intoxicated mice.1-diphenyl-2-picrylhydrazyl (DPPH). Republic of China.5%. camphorata extract significantly improved the CCl(4)-induced increase in hepatic glutathione peroxidase. camphorata extract exerts effective protection against chronic chemical-induced hepatic injury in vivo.1% in control mice to 34. Publication Types: Research Support. the mice serum interleukin-12 levels increased significantly by AC-PS treatment. Besides. Taiwan. Antrodia camphorata (A.1 mg/mL. Taipei Medical University. The protective effects and the possible mechanisms of dry matter of fermented filtrate (DMF) from Antrodia camphorata in submerged culture (ACSC) on H(2)O(2)-induced cytotoxicity in HepG2 and carbon tetrachloride (CCl(4))-induced hepatotoxicity in Sprague-Dawley rats were investigated. an A. camphorata) is well-known in Taiwan as a traditional Chinese medicine. The purpose of this study was to evaluate the ability of A. Shen MY. camphorata extracts to protect against oxidative stress in vitro and against carbon tetrachloride (CCl(4))-induced hepatic injury in vivo. Chou DS. Lin CH.8 +/.indexed for MEDLINE] 5: J Agric Food Chem. camphorata inhibited nonenzymatic iron-induced lipid peroxidation in rat brain homogenates with an IC(50) value about 3. respectively. Furthermore.S. Gov't PMID: 12744658 [PubMed . Taipei 110. Publication Types: Research Support. Moreover. 2003 May 21. Hsiao G. Department of Food Science. The results showed that the inhibitory effect of DMF and its crude triterpenoids on lipid peroxidation occurred in a dose-response manner in an AAPH/linoleic acid system. and CCl(4)-induced decrease in superoxide dismutase activities. Lan MH. camphorata extract resulting in a decrease of 0. 250 Wu-Hsing Street.5% and 48. It also scavenged the stable free radical 1.1. Su CH.2 +/.51(6):1571-7. camphorata extract in a dose-dependent manner. Song TY.10 mg/mL for 4 h and then induced by 1 h of treatment 3 . after oral and intraperitoneal treatment.cells also increased from 9. Yen GC. These results suggest that A. Protective effects of fermented filtrate from Antrodia camphorata in submerged culture against CCl4-induced hepatic toxicity in rats. Antioxidative and hepatoprotective effects of Antrodia camphorata extract. Gov't PMID: 15541758 [PubMed . by mediating antioxidative and free radical scavenging activities. reductase. it also dose-dependently inhibited the formation of lipid peroxidative products during CCl(4) treatment. The dose of the A. Department of Pharmacology and Graduate Institute of Medical Sciences.0.2. A. Furthermore.S. An extract of A. Non-U. Taiwan.indexed for MEDLINE] 6: J Agric Food Chem. Lin KH. Taichung 40227. Considering all these results. 2003 Mar 12. it is suggested that AC-PS elicit its anti-tumor effect by promoting a Th1-dominant state and killer activities. Histopathological changes of hepatic lesions induced by CCl(4) were significantly ameliorated by treatment with an A. 250 Kuokuang Road.
Gov't PMID: 12617586 [PubMed . Ng LT. Hsu YL. EAC treatment increased the level 4 . Department of Pharmacy. Our results indicate that EAC inhibits the activation of NF-kappaB. as measured by the formation of malondialdehyde. EAC also inhibited the TNF-alpha-activated NF-kappaB-dependent reporter gene expression of MMP-9 and VEGF. Hsu YL. Chia-Nan University of Pharmacy and Science. Kuo YH. Tainan. Lin CC. Publication Types:Research Support. and necrosis induced by CCl(4) in rats. Histopathological evaluation of the rat liver revealed that DMF reduced the incidence of liver lesions. 2006 Aug. MMP-9 and MT1-MMP. glutathione reductase.10 mL/100 g of bw. Kuo YH. lipid peroxidation was significantly (p < 0. Taiwan. Furthermore. Department of Biotechnology. Ni WC. including neutrophil infiltration. cinnamomea (EAC) fruiting bodies in Hep 3B. EAC inhibited constitutively activated and inducible NF-kappaB in both its DNA-binding activity and transcriptional activity. Non-U. Cho CY. and glutathione S-transferase) and the GSH/GSSG ratio were significantly improved in the oral pretreatment DMF of rats (p < 0. Cho CY. PMID: 17316946 [PubMed . we first report the anti-invasive effect of ethylacetate extract from Antrodia cinnamomea (EAC) fruiting bodies in the human liver cancer cell line PLC/PRF/5.05) decreased. Epub 2006 Feb 28. Chia-Nan University of Pharmacy and Science. This effect was strongly associated with a concomitant decrease in either the level or activity of VEGF.in process] 8: Food Chem Toxicol. Kuo PL. reduced glutathione (GSH)-dependent enzymes (glutathione peroxidase. and may provide a molecular basis for drug development using EAC as an anti-invasive agent in the prevention and treatment of cancer. and an increase in the expression of TIMP-1 and TIMP-2. The results suggest that DMF may play a role in preventing oxidative damage in living systems by up-regulating hepatic GSH-dependent enzymes to preserve the normal GSH/GSSH ratio and scavenging free radicals formed during CCl(4) metabolism. Taiwan.with H(2)O(2) (100 microM). hydropic swelling. Ng LT.25 and 0.50 mg/kg of body weight (bw)] for 5 consecutive days prior to the administration of a single dose of 40% CCl(4) (0.44(8):1316-26. Moreover.S. In this study. The oral pretreatment with DMF [0. Tainan. EAC also exhibited an inhibitory effect on angiogenesis in a Matrigel Plug Angiogenesis Assay. Tzeng TF. a liver cancer cell line.05).indexed for MEDLINE] 7: Antrodia cinnamomea fruiting bodies extract suppresses the invasive potential of human liver cancer cell line PLC/PRF/5 through inhibition of nuclear factor kappaB pathway. The purpose of this study was to evaluate the apoptotic effects of ethylacetate 乙酸乙酯 extract from A. Further investigation revealed that EAC's inhibition of cancer cell growth and invasion was also evident in a nude mice model. and the invasion of cancer cells. EAC decreased cell proliferation of Hep 3B cells by inducing apoptotic cell death. MMP-2. Antrodia cinnamomea is well known in Taiwan as a traditional medicine for treating cancer and inflammation. Kuo PL.01). Lin CC. Apoptotic effects of Antrodia cinnamomea fruiting bodies extract are mediated through calcium and calpain-dependent pathways in Hep 3B cells. ip) significantly prevented the increase in serum levels of hepatic enzyme markers (alanine and aspartate aminotransferase) and liver lipid peroxidation (p < 0. Treatment with EAC decreased the cancer invasion of PLC/PRF/5 cells in a dose-dependent manner.
(3)破壞粒線體的功能 (4)而細胞內同時發生 calpain/Bid/Bax 與 Ca2+/粒線體的細胞自殺路徑，進而誘導整個細 胞內的細胞自殺訊號出現!) Publication Types: • Research Support. (3) disruption of mitochondrial function. and (4) apoptotic signaling being amplified by cross-talk between the calpain/Bid/Bax and Ca2+/mitochondrial apoptotic pathways. The ratio of branch points was about 16% of the total residual numbers. Non-U. [eta]=0. ACN2a had an average molecular weight of 12. indicating hepatoprotective activity in vivo.S. Publication Types: • Research Support. Nakamura N.indexed for MEDLINE] J Ethnopharmacol. 2008 May 7.54(4):496-500. and activation of caspase-9 in Hep 3B cells. University of Toyama. EAC also initiated the mitochondrial apoptotic pathway through regulation of Bcl-2 family proteins expression. Hattori M. [Epub ahead of print] 5 .07:0. The administration of ACN2a (0. Non-U. Glc.g-1. 0. H2O). Yokozawa T. release of cytochrome c.9x10(5) Daltons. the mitochondrial apoptotic pathway amplified the calpain pathway by Bid and Bax interaction and Ca2+ translocation. Man and GalN (in the ratio 1:0.2663 cal/(g. and branches were attached to C-2 of galactosyl residues of the main chain.o. 2006 Apr. A neutral polysaccharide named ACN2a separated from the water extract was purified using 10% CCl3COOH. in which an alpha-D-(1-->6)-Gal linkage accounted for 73% of all linkages. acnes-LPS.026:faint). Han HF.4. [alpha]D25=+115 degrees (c=0. (研究結果發現 EAC 會藉由誘導細胞自我毀滅(細胞凋亡)來減少 Hep 3B 細胞的增生數目。加 入 EAC，會使細胞質中的鈣離子濃度增加，並啟動 calpain 跟 caspase-12 的活化。EAC 也 會啟動粒線體的自殺計劃，這個自殺計劃是藉由調節 Bcl-2 家族蛋白質的表現，釋放出 cytochrome c，以及活化 caspase-9 蛋白質。此外，粒線體的自殺計劃路徑會使得 Bid and Bax 這兩個蛋白質交互作用，以及改變鈣離子的分佈位置，來增強 calpain 的作用路徑。因此 EAC 誘導了(1)細胞凋亡的誘導(2)啟動了 Ca2+/calpain pathway.). ACN2a was composed of Gal. Mycelia of Antrodia cinnamomea were extracted with chloroform and hot water. acnes) and lipopolysaccharide (LPS). p. Institute of Natural Medicine. degrees C). and repeated column chromatography on HW-65 and DE-52 cellulose. Gov't PMID: 16595952 [PubMed . Gov't PMID: 16600460 [PubMed . Protective effects of a neutral polysaccharide isolated from the mycelium of Antrodia cinnamomea on Propionibacterium acnes and lipopolysaccharide induced hepatic injury in mice.indexed for MEDLINE] 9: Chem Pharm Bull (Tokyo). We have therefore concluded that the molecular mechanisms during EAC-mediated proliferation inhibition in Hep 3B cells were due to: (1) apoptosis induction.44.8 g/kg/d. Cp=0. Fuc. Furthermore.0417dl. (2) triggering of Ca2+/calpain pathway. significantly prevented increases in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzyme activities in mice treated with P. Japan.24:0.S. Its structure was determined by chemical and spectroscopic analyses. Hirakawa A. Zuo F. The hepatoprotective effect of ACN2a was evaluated using a mouse model of hepatic injury that was induced by Propionibacterium acnes (P.of calcium (Ca2+) in the cytoplasm and triggered the subsequent activation of calpain and caspase-12.
dependent inhibition of p-AKT. Chang LH. Tainan. Chuu JJ. Western blot analysis for MDR-1 and apoptosis. College of Engineering. Yu HH. RESULTS: We have found that Antrodia camphorata extracts. The percentage of human hepatoma cells undergoing apoptosis and distributing in different phases of cell cycle were determined by Flow cytometric analysis. when combined with anti-tumor agents. showed adjuvant antiproliferative effects on hepatoma cells (in vitro) and on xenografted cells in tumor-implanted nude mice (in vivo).as supplied by publisher] 6 . Institute of Biotechnology. showed adjuvant antiproliferative effects on hepatoma cells (in vitro) and on xenografted cells in tumor-implanted nude mice (in vivo). Tainan Hsien. Furthermore. solid-state extracts of Antrodia camphorata (AC-SS) showed its adjuvant effects through the inhibition of MDR gene expressions and the pathway of COX-2. Department of Medicine. Southern Taiwan University. Yung-Kang City. Li SL. Huang ZN. The measurements of tumor growth and survival analysis of hepatoma implanted nude mice treated with Antrodia camphorata extracts and anti-tumor agents alone or in combinations. Chi-Mei Medical Center. Lee KY. which then extended their median survival days. AIM OF THE STUDY: The objectives of this study were to investigate the adjuvant anti-tumor effects of Antrodia camphorate in human hepatoma cells (C3A and PLC/PRF/5) which are resistance to most anti-tumor agents. Chang CY. elucidate the possible regulation pathways. we have found that Antrodia camphorata extract. when combined with anti-tumor agents. Chen YP. Taiwan. PMID: 18571350 [PubMed . MATERIALS AND METHODS: The AC extracts were measured by using a phenol/sulfuric acid method as previously described. The in vitro cell proliferation assay of ACs and anti-tumor agents was tested on C3A and PLC/PRF/5 cell lines.The adjuvant effects of Antrodia Camphorata extracts combined with anti-tumor agents on multidrug resistant human hepatoma cells. which ultimately resulted in the induction of apoptosis in hepatoma cells. Taiwan. and measure the tumor growth and survival rate in xenograft-nude mice after combined with anti-tumor agents. CONCLUSIONS: In this study.related proteins.