Mediation of the Cytotoxicity of Lanostanoids and Steroids of <i>Ganoderma tsugae</i> through Apoptosis and Cell Cycle

Gan, Kim-Hong; Fann, Yih-Fen; Hsu, Shu-Hui; Kuo, Kou‐Wha; Lin, Chun‐Nan

doi:10.1021/np9704664

Cited by 65 publications

(62 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Traditionally, Ganoderma is highly regarded as a herbal treatment and is claimed to alleviate or cure virtually all diseases. Current research is focused on purification and characterization of the bioactive components and determination of their clinical value, especially their putative antitumor and anti-ageing properties (2,4,12,14,21). Many biologically active oxygenated lanostane-type triterpenoids have already been isolated from G. lucidum, and some of them have been shown to inhibit histamine release from rats mast cells (9,10) and angiotensin-converting enzyme (15).…”

mentioning

confidence: 99%

Effect of 26-Oxygenosterols from Ganoderma lucidum and Their Activity as Cholesterol Synthesis Inhibitors

Hajjaj

Macé

Roberts

et al. 2005

Appl Environ Microbiol

View full text Add to dashboard Cite

Ganoderma lucidum is a medicinal fungus belonging to the Polyporaceae family which has long been known in Japan as Reishi and has been used extensively in traditional Chinese medicine. We report the isolation and identification of the 26-oxygenosterols ganoderol A, ganoderol B, ganoderal A, and ganoderic acid Y and their biological effects on cholesterol synthesis in a human hepatic cell line in vitro. We also investigated the site of inhibition in the cholesterol synthesis pathway. We found that these oxygenated sterols from G. lucidum inhibited cholesterol biosynthesis via conversion of acetate or mevalonate as a precursor of cholesterol. By incorporation of 24,25-dihydro-[24,25-3 H 2 ]lanosterol and [3-3 H]lathosterol in the presence of ganoderol A, we determined that the point of inhibition of cholesterol synthesis is between lanosterol and lathosterol. These results demonstrate that the lanosterol 14␣-demethylase, which converts 24,25-dihydrolanosterol to cholesterol, can be inhibited by the 26-oxygenosterols from G. lucidum. These 26-oxygenosterols could lead to novel therapeutic agents that lower blood cholesterol.

show abstract

mentioning

confidence: 99%

Effect of 26-Oxygenosterols from Ganoderma lucidum and Their Activity as Cholesterol Synthesis Inhibitors

Hajjaj

Macé

Roberts

et al. 2005

Appl Environ Microbiol

View full text Add to dashboard Cite

show abstract

“…The majority of anticancer drugs in clinical use induce tumor cell apoptosis, via activating several apoptotic signaling pathways, including those of the mitochondria and endoplasmic reticulum. FPOA has previously been revealed to cause Hep 3B cell death by apoptosis (14). However, the apoptotic pathway induced by FPOA remains unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Lucialdehyde c has been revealed to exert cytotoxic effects on Lewis lung carcinoma, T-47D, sarcoma 180 and meth-A tumor cell lines (13). Furthermore, 3-acetoxylanosta-8,24-dien-21-oic acid (FPOA), which was initially isolated from Ganoderma tsugae, has been identified to induce human hepatoma Hep3B cell death by apoptosis (14,15). With increasing research into triterpenoids, the mechanisms of their antitumor effects have been demonstrated to include induction of apoptosis, cell cycle inhibition and regulation of the immune response (16,17).…”

Section: Introductionmentioning

confidence: 99%

FPOA induces the apoptosis of HepG2 cells

2018

View full text Add to dashboard Cite

Abstract. The triterpenoid 3-acetoxylanosta-8,24-dien-21-oic acid (FPOA) is isolated from the fruiting body of Fomitopsis pinicola. The present study reports that FPOA exerts cytotoxic activity and describes the molecular mechanism of FPOA-induced apoptosis on human HepG2 hepatoma cells. FPOA exhibited significant cytotoxic effects against HepG2, MCF-7 and HeLa cells. However, FPOA was particularly cytotoxic towards HepG2 cells, with a half maximal inhibitory concentration value of 42.10 µM, thus these cells were taken forward for further analysis. Flow cytometry results demonstrated that FPOA significantly increased the apoptotic rate of HepG2 cells in a dose-dependent manner, explaining its potent cytotoxicity. In addition, western blot analysis revealed that FPOA significantly increased the B-cell lymphoma 2 (Bcl-2)-associated X/Bcl-2 ratio, and cytochrome c, caspase-9 and caspase-3 release, in addition to significantly decreasing poly(ADP) ribose polymerase levels. These observations indicate that FPOA induces the apoptosis of HepG2 cells by activating members of the caspase protein family and triggering the mitochondrial apoptosis signaling pathway. Based on these results, FPOA is a potential agent for the treatment of cancer.

show abstract

“…Pat. 1887 (24S)-24-Methyl-5α-cholest-7-ene-3β-ol and (24S)-24-Methyl-5α-cholest-7, l6-diene-3β-ol Strigina et al 1971 Alnusenone, Furanoganoderic acid, Friedelin, Ganoderenic acid F, Ganoderenic acid G, Ganoderic acid B8, 5,, Methyl ganoderenate H and Methyl ganoderenate AP Nishitoba et al 1989 Applanoxidic acid A and Applanoxidic acid B Tokuyama et al 1991Yoshikawa et al 2002 Applanoxidic acid F, Applanoxidic acid G, Applanoxidic acid H and Applanoxidic acid E Chairul & Hayashi 1994 24ξ-Methyl-5α-lanosta-25-one and Ergosta-4, 6, 8(14), 22-tetraen-3-one Gan et al 1998a Lucidone A, 24ξ-Methyl-5α-lanosta-25-one, Epidioxyergosta-6,9(11), 22-trien-3β-ol (9,11-Dehy-droergosterol peroxide), Ergosta-7, 22-dien-3-one and Ergosta-7, 22-dien-3β-yl palmitate Gan et al 1998b Ergosterol, Ganoderenic acid A, Ganoderenic acid D, β-Amyrenone, β-Amyrin acetate, Ganoderma aldehyde and 2, 5-Dihydroxy benzoic acid Ming et al 2002 Ergosterol; (24S) as C28 sterols from G. applanatum Cole & Schweikert 2003 Methyl ganoderenate D, 23-Dihydroganoderenic acid I, 11,15,methyl ester 3β,7β ,20,7β,20,11,11,20E (22)-dien-26-oic acid Shim et al 2004 D-mannitol, 2-methoxy fatty acids, cerebrosides, Daucosterol, 2, 5-Dihydroxyacetophenone, 2, 5-dihydro-xyacetophenone, 2,5-dihydroxybenzoic acid and Protocatechualdehyde Lee et al 2005 3α-Carboxyacetoxy-24-methylene-23-oxolanost-8-en-26-oic acid, 3α-Carboxyacetoxy-24-methyl-23-oxolanost-8-en-26-oic acid, 3α, 16α-Dihydroxylanosta-7,9(11),24-trien-21-oic acid, 16α-Hydroxy-3-oxolanosta-7,9(11), 24-trien-21-oic acid and 3α, 16α, 26-Trihydroxylanosta-7,9(11),24-trien-21-oic acid De Silva et al 2006 Ergosterol peroxide (5,8-epidioxy-5α-8α-ergosta-6,22E-dien-3-βol), 22E,24R-Ergosta-7,22-diene-3β,5α,6β-triol (Cerevisterol) Lee et al 2006 Methyl australate, 5α-ergost-7-en-3β-ol, 5α-ergost-7, 22-dien-3β-ol, 5, 8-epidioxy-5α, 8α-ergost-6, 22-dien-3β-ol, Methyl australate and Australic acid Smania et al 2007 Two laccase enzymes from G. australe Elissetche et al 2007 Fornicatin G (7β-hydroxy-11-oxo-3, 4-seco-25, 26, 27-trinorlanosta-4(28),8-dien-24-oic-3-acetyl ester) Fornicatin H Peng et al 2012 3β, 22S-Dih...…”

Section: G Annulare Lloyd) Boedijn 1940mentioning

confidence: 99%

Mycosphere Essays 20: Therapeutic potential of Ganoderma species: Insights into its use as traditional medicine

Hapuarachchi¹

2017

Mycosphere

View full text Add to dashboard Cite

The genus Ganoderma (Ganodermataceae) has a long history in traditional medicine to improve longevity and health in Asia. Ganoderma has been widely used in multiple therapeutic activities as well as dietary supplements to prevent and treat many diseases. Several classes of bioactive substances have been isolated and identified from Ganoderma, such as polysaccharides, triterpenoids, nucleosides, sterols, fatty acids, protein and alkaloids. There are numerous research publications, which report the abundance and variety of biological actions initiated by the metabolites of Ganoderma. Investigation on different metabolic activities of Ganoderma species has been performed both in vitro and in vivo. In many cases, however, it has been questioned whether Ganoderma is solely a nourishment supplement for wellbeing or merely a helpful "medication" for restorative purposes. There has been no any conclusive report of human trials using Ganoderma species as a direct control agent for diseases. In addition, there is no evidence supporting the usage of Ganoderma species (excluding G. lucidum) as potential supplements for cancer or other diseases in humans since no preclinical trials have been performed up to date. In this review, the beneficial medicinal properties of several species of Ganoderma (excluding G. lucidum) and their secondary metabolites are discussed. Ganoderma species can be used as a therapeutic drug, but more direct scientific evidence should be made available in the future. The efficiency of Ganoderma in clinical treatments should be substantiated with more biomedical research and their true impact assessed on human health with more standardized clinical evaluations so that the feasibility of biologically active extracts of Ganoderma species in alternative treatments can be recommended.

show abstract

Mediation of the Cytotoxicity of Lanostanoids and Steroids of Ganoderma tsugae through Apoptosis and Cell Cycle

Cited by 65 publications

References 8 publications

Effect of 26-Oxygenosterols from Ganoderma lucidum and Their Activity as Cholesterol Synthesis Inhibitors

Effect of 26-Oxygenosterols from Ganoderma lucidum and Their Activity as Cholesterol Synthesis Inhibitors

FPOA induces the apoptosis of HepG2 cells

Mycosphere Essays 20: Therapeutic potential of Ganoderma species: Insights into its use as traditional medicine

Contact Info

Product

Resources

About