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Ganoderic Acid D Sale

(Synonyms: 灵芝酸 D) 目录号 : GC40900

An oxygenated triterpenoid

Ganoderic Acid D Chemical Structure

Cas No.:108340-60-9

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产品描述

Ganoderic acid D, a highly oxygenated tetracyclic triterpenoid, is the major active component of Ganoderma lucidum. Ganoderic acid D upregulates the protein expression of SIRT3 and induces the deacetylated cyclophilin D (CypD) by SIRT3. Ganoderic acid D inhibits the energy reprogramming of colon cancer cells including glucose uptake, lactate production, pyruvate and acetyl-coenzyme production in colon cancer cells[1].

Ganoderic acid D can inhibit the growth of numerous cancer cell lines and it inhibits HeLa human cervical carcinoma cells with an IC50 of 17.3 mM[2].

References:
[1]. Liu Z, et al. Effect of ganoderic acid D on colon cancer Warburg effect: Role of SIRT3/cyclophilin D. Eur J Pharmacol. 2018 Apr 5;824:72-77.
[2]. Yue QX,et al. Proteomics characterization of the cytotoxicity mechanism of ganoderic acid D and computer-automated estimation of the possible drug target network. Mol Cell Proteomics. 2008 May;7(5):949-61.

Chemical Properties

Cas No. 108340-60-9 SDF
别名 灵芝酸 D
Canonical SMILES O=C1CC[C@@]2(C)[C@](C[C@H](O)C([C@@](C(C[C@]3([H])[C@H](C)CC(CC(C)C(O)=O)=O)=O)(C)[C@]3(C)C4)=C2C4=O)([H])C1(C)C
分子式 C30H42O7 分子量 514.7
溶解度 DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 30 mg/ml,Ethanol:PBS (pH 7.2) (1:3): 0.25 mg/ml 储存条件 Store at -20°C, protect from light
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1 mM 1.9429 mL 9.7144 mL 19.4288 mL
5 mM 0.3886 mL 1.9429 mL 3.8858 mL
10 mM 0.1943 mL 0.9714 mL 1.9429 mL
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Research Update

Ganoderic Acid D prevents oxidative stress-induced senescence by targeting 14-3-3ε to activate CaM/CaMKII/NRF2 signaling pathway in mesenchymal stem cells

Aging Cell 2022 Sep;21(9):e13686.PMID:35929187DOI:10.1111/acel.13686.

Stem cell senescence is an important cause of aging. Delaying senescence may present a novel way to combat aging and age-associated diseases. This study provided a mechanistic insight into the protective effect of Ganoderic Acid D (GA-D) against human amniotic mesenchymal stem cell (hAMSCs) senescence. GA-D, a Ganoderma lucidum-derived triterpenoid, markedly prevented hAMSCs senescence via activating the Ca2+ calmodulin (CaM)/CaM-dependent protein kinase II (CaMKII)/nuclear erythroid 2-related factor 2 (Nrf2) axis, and 14-3-3ε was identified as a target of GA-D. 14-3-3ε-encoding gene (YWHAE) knockdown in hAMSCs reversed the activation of the CaM/CaMKII/Nrf2 signals to attenuate the GA-D anti-aging effect and increase senescence-associated β-galactosidase (SA-β-gal), p16 and p21 expression levels, including reactive oxygen species (ROS) production, thereby promoting cell cycle arrest and decreasing differentiation potential. YWHAE overexpression maintained or slightly enhanced the GA-D anti-aging effect. GA-D prevented d-galactose-caused aging in mice by significantly increasing the total antioxidant capacity, as well as superoxide dismutase and glutathione peroxidase activity, and reducing the formation of malondialdehyde, advanced glycation end products, and receptor of advanced glycation end products. Consistent with the protective mechanism of GA-D against hAMSCs senescence, GA-D delayed the senescence of bone-marrow mesenchymal stem cells in this aging model in vivo, reduced SA-β-gal and ROS production, alleviated cell cycle arrest, and enhanced cell viability and differentiation via regulating 14-3-3ε and CaM/CaMKII/Nrf2 axis. Therefore, GA-D retards hAMSCs senescence by targeting 14-3-3ε to activate the CaM/CaMKII/Nrf2 signaling pathway. Furthermore, the in vivo GA-D anti-aging effect may involve the regulation of stem cell senescence via the same signal axis.

Ganoderic Acid D induces synergistic autophagic cell death except for apoptosis in ESCC cells

J Ethnopharmacol 2020 Nov 15;262:113213.PMID:32755651DOI:10.1016/j.jep.2020.113213.

Ethnophamacological relevance: Ganoderma lucidum has been used as a medicinal mushroom for more than 2000 years in China. Ganoderic Acid D (GAD) as a representative active triterpenoid from Ganoderma lucidum is known to possess anticancer activity. However, the mechanism involved in its anticancer cell process is still largely elusive. Aim of the study: Our study aimed to investigate the anticancer effects of GAD on the esophageal squamous cell carcinoma (ESCC) cells and the underlying mechanisms at the cell level. Materials and methods: EC9706 and Eca109 cells were treated with GAD (0, 10, 20, 40 μM) for 24 h. The cell viability, cell cycle, reactive oxygen species (ROS), mitochondrial membrane potential (MMP), apoptosis rate, caspase-3 activity, autophagic flux, lysosomal function were examined. Cell cycle, apoptotic, autophagy and mTOR signal pathway related proteins such as P53, Cyclin B1, CytoC, PARP, Beclin-1, P62, LC3, PI3K, AKT and mTOR were analyzed by Western blot approach. Results: GAD inhibited cell proliferation and induced both apoptosis and autophagic cell death. In particular, we found that in the early stage of the autophagic process, GAD could initiate and enhance the autophagy signal while in the late stage it on the contrary could block the autophagic flux by impairing the autophagosome-lysosome fusion and inhibited the lysosomal degradation. Besides the autophagic cell death, GAD also induced the apoptosis mediated by caspase-related process in parallel. The mechanism involved for the synergistic apoptotic and autophagic cell death was also explored. We found that GAD down-regulated the expression of PI3K, AKT and mTOR phosphorylated proteins in the mTOR signaling pathway which thus led to the synergistic effect on apoptosis and autophagic cell death in the ESCC cells. Conclusions: In summary, this study has documented that GAD may inhibit cell proliferation through the mTOR pathway in ESCC cells, and induce synergistic apoptosis and autophagic cell death by disrupting the autophagic flux. This work therefore also suggests that GAD may be used as an efficient anticancer adjuvant for ESCC cancer therapy.

Ganoderic Acid D Protects Human Amniotic Mesenchymal Stem Cells against Oxidative Stress-Induced Senescence through the PERK/NRF2 Signaling Pathway

Oxid Med Cell Longev 2020 Jul 27;2020:8291413.PMID:32774686DOI:10.1155/2020/8291413.

Aging is an important risk factor in the occurrence of many chronic diseases. Senescence and exhaustion of adult stem cells are considered as a hallmark of aging in organisms. In this study, a senescent human amniotic mesenchymal stem cell (hAMSC) model subjected to oxidative stress was established in vitro using hydrogen peroxide. We investigated the effects of Ganoderic Acid D (GA-D), a natural triterpenoid compound produced from Ganoderma lucidum, on hAMSC senescence. GA-D significantly inhibited β-galactosidase (a senescence-associated marker) formation, in a dose-dependent manner, with doses ranging from 0.1 μM to 10 μM, without inducing cytotoxic side-effects. Furthermore, GA-D markedly inhibited the generation of reactive oxygen species (ROS) and the expression of p21 and p16 proteins, relieved the cell cycle arrest, and enhanced telomerase activity in senescent hAMSCs. Furthermore, GA-D upregulated the expression of phosphorylated protein kinase R- (PKR-) like endoplasmic reticulum kinase (PERK), peroxidase III (PRDX3), and nuclear factor-erythroid 2-related factor (NRF2) and promoted intranuclear transfer of NRF2 in senescent cells. The PERK inhibitor GSK2656157 and/or the NRF2 inhibitor ML385 suppressed the PERK/NRF2 signaling, which was activated by GA-D. They induced a rebound for the generation of ROS and β-galactosidase-positive cells and attenuated the differentiation capacity. These findings suggest that GA-D retards hAMSC senescence through activation of the PERK/NRF2 signaling pathway and may be a promising candidate for the discovery of antiaging agents.

Effect of Ganoderic Acid D on colon cancer Warburg effect: Role of SIRT3/cyclophilin D

Eur J Pharmacol 2018 Apr 5;824:72-77.PMID:29374515DOI:10.1016/j.ejphar.2018.01.026.

Ganoderic Acid D (GAD) is a highly oxygenated tetracyclic triterpenoid. This study aims to assess the effects of GAD on the energy metabolism of colon cancer through the regulation of SIRT3 expression and whether this effect is related to acetylated cyclophilin D. The results demonstrated that GAD inhibits the energy reprogramming of colon cancer cells including glucose uptake, lactate production, pyruvate and acetyl-coenzyme production in colon cancer cells. Meanwhile, GAD upregulated the protein expression of SIRT3. Furthermore, the interruption of SIRT3 expression significantly reversed all the effects of SIRT3 on the energy reprogramming of colon cancer. In addition, GAD induced the deacetylated cyclophilin D (CypD) by SIRT3, whereas SIRT3-shRNA inhibited its combining effect on CypD. The energy reprogramming effects of GAD on colon cancer seem to be mediated by SIRT3 upregulation via acetylated CypD inhibition.

Pharmacokinetics of Ganoderic Acid D and its main metabolite by liquid chromatography-tandem mass spectrometry

J Chromatogr B Analyt Technol Biomed Life Sci 2013 Jul 1;930:1-6.PMID:23692850DOI:10.1016/j.jchromb.2013.04.015.

The present study aims to investigate the pharmacokinetics of Ganoderic Acid D (GD), a representative active triterpenoid from Ganoderma lucidum. A sensitive and selective liquid chromatography-tandem mass spectrometry method was developed for the simultaneous determination of the concentrations of GD and its main metabolite (ganoderic acid B) in rat plasma. Following protein precipitation, the analytes were separated on a reversed-phase C18 column. Acetonitrile-water-acetic acid (40:60:0.01) was used at a flow-rate of 0.2ml/min. A triple quadrupole mass spectrometer equipped with an electrospray ionization source was used as the detector and was operated in the negative ion mode. Multiple reaction monitoring using the characteristic transitions was performed to quantify the analytes. The method had a lower limit of quantification of 8.19ng/ml for GD, and 8.59ng/ml for ganoderic acid B (GB). The calibration curves were demonstrated to be linear over the concentration range of 8.19-4096ng/ml and 8.59-2149ng/ml, respectively. Variations within- and between-batch were less than 6.4% and 4.6%, respectively. The extraction recovery rates ranged from 98.8 to 105.2% and 100.7 to 113.6%, respectively. The validated method was successfully applied to the quantification of GD and GB concentrations in rat plasma after oral administration (or intravenous administration) of GD preparations at a dose of 15mg/kg. The data showed that the absolute bioavailability increased from 22% to 70% after the GD suspension was changed to GD loaded solid lipid nanoparticles. In the meantime, the Cmax increased from 107.2 to 1555.6ng/ml; the tmax changed from 2.0h to 0.3h. These results are very helpful in the further studies.