Glaucocalyxin A
(Synonyms: 蓝萼甲素) 目录号 : GC38606Glaucocalyxin A is a biologically active ent-kauranoid diterpenoid isolated from Rabdosia japonica var. glaucocalyx with antitumor and anti-inflammatory activity. Glaucocalyxin A induces G2/M cell cycle arrest and apoptosis through the PI3K/Akt pathway in human bladder cancer cells.
Cas No.:79498-31-0
Sample solution is provided at 25 µL, 10mM.
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Glaucocalyxin A is a biologically active ent-kauranoid diterpenoid isolated from Rabdosia japonica var. glaucocalyx with antitumor and anti-inflammatory activity. Glaucocalyxin A induces G2/M cell cycle arrest and apoptosis through the PI3K/Akt pathway in human bladder cancer cells.
[1] Wenfeng Lin, et al. Int J Biol Sci . 2018 Mar 10;14(4):418-426.
Cas No. | 79498-31-0 | SDF | |
别名 | 蓝萼甲素 | ||
Canonical SMILES | CC1(C)C(CC[C@@]2(C)[C@@]3([H])[C@@]4(C(C([C@H](CC3)[C@H]4O)=C)=O)[C@H](O)C[C@]12[H])=O | ||
分子式 | C20H28O4 | 分子量 | 332.43 |
溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 3.0082 mL | 15.0408 mL | 30.0815 mL |
5 mM | 0.6016 mL | 3.0082 mL | 6.0163 mL |
10 mM | 0.3008 mL | 1.5041 mL | 3.0082 mL |
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Glaucocalyxin A: a review
Nat Prod Res 2014;28(24):2221-36.PMID:25033290DOI:10.1080/14786419.2014.934235.
Glaucocalyxin A is a natural ent-Kaurane diterpenoid. It has been widely studied for some important biological activities like cytotoxicity and anti-tumour, anti-bacterial, anti-oxidative, anti-coagulative, anti-thrombotic, immune and anti-neuroinflammatory activities. The aim of the present article is to review the available information on Glaucocalyxin A including sources, biological activities and derivatives and also have a look at the future perspectives.
Glaucocalyxin A reverses EMT and TGF-β1-induced EMT by inhibiting TGF-β1/Smad2/3 signaling pathway in osteosarcoma
Chem Biol Interact 2019 Jul 1;307:158-166.PMID:31059706DOI:10.1016/j.cbi.2019.05.005.
Metastatic osteosarcoma usually has an unsatisfactory response to the current standard chemotherapy and causes poor prognosis. Currently, epithelial-mesenchymal transition (EMT) is reported as a critical event in osteosarcoma metastasis. Glaucocalyxin A, a bioactive ent-kauranoid diterpenoid, exerts anti-cancer effect on osteosarcoma by inducing apoptosis in previous study. However, the effect of Glaucocalyxin A on EMT and metastasis of osteosarcoma is unclear. In this study, we investigated the potential mechanisms of Glaucocalyxin A on EMT and metastasis of osteosarcoma. We found that Glaucocalyxin A inhibited migration and invasion of MG-63 and 143B cells. Moreover, Glaucocalyxin A increased the protein and mRNA levels of E-cadherin and decreased the protein and transcription expression of N-cadherin, Vimentin. Glaucocalyxin A also inhibited the protein and mRNA levels of EMT-associated transcription factor including Snail and Slug. Furthermore, Glaucocalyxin A inhibited transforming growth factor-β1 (TGF-β1)-induced migration, invasion and EMT of low-metastatic osteosarcoma U2OS cells. Glaucocalyxin A inhibited TGF-β-induced phosphorylation of Smad 2/3 in osteosarcoma U2OS cells. Finally, we established transplanted metastatic models of highly metastatic osteosarcoma 143B cells. Glaucocalyxin A inhibited lung metastasis in vivo. Interestingly, Glaucocalyxin A increased the protein expression of E-cadherin and reduced the protein expression of N-cadherin and Vimentin. Glaucocalyxin A inhibited the protein expression of Snail and Slug in vivo. In summary, this study demonstrated that Glaucocalyxin A inhibited EMT and TGF-β1-induced EMT by inhibiting TGF-β1/Smad2/3 signaling pathway in osteosarcoma. Therefore, Glaucocalyxin A might be a promising candidate against the metastasis of human osteosarcoma.
Glaucocalyxin A protect liver function via inhibiting platelet over-activation during sepsis
Phytomedicine 2022 Jun;100:154089.PMID:35398736DOI:10.1016/j.phymed.2022.154089.
Background: Rabdosia japonica (Burm. f.) var. glaucocalyx (Maxim.) is a perennial herb, and is traditionally used as folk medicine for treating inflammatory diseases and cancer. Gaucocalyxin A (GLA) is an ent‑kaurane diterpenoid that is isolated from the aerial parts of R. japonica (Burm. f.) var. glaucocalyx (Maxim.). In a recent study, we found that GLA protects against acute liver dysfunction induced by Escherichia coli, which is likely related to its anti-inflammatory effects. However, the mechanism by which GLA protects liver injury during sepsis is unknown. Aim: To evaluate the anti-inflammatory function of GLA and its regulatory effect on platelet function. Method: An in vivo model of sepsis was established by inoculating mice with E. coli. Live function and platelet activation were evaluated through standard assays. The levels of pro-inflammatory factors were measured through ELISA and qRT-PCR. Results: GLA alleviated liver dysfunction in the mouse model of sepsis. GLA-treated mice displayed lower complement activation and liver dysfunction after E. coli infection. GLA alleviated the decrease in peripheral platelet counts by inhibiting their clearance by Kupffer cells in liver. Furthermore, GLA inhibited platelet activation through the RIP1/RIP3/AKT pathway and downregulated C3aR expression on the platelets, thereby inhibiting liver injury and dysfunction due to excessive complement activation. Conclusion: GLA can inhibit platelet activation by reducing surface expression of C3aR, which protect the liver from injury induced by excessive complement activation. GLA is a novel therapeutic agent for controlling sepsis-related liver dysfunction.
Protective effects of Glaucocalyxin A on the airway of asthmatic mice
Open Med (Wars) 2022 Jul 7;17(1):1158-1171.PMID:35859797DOI:10.1515/med-2022-0513.
The aim of this study is to investigate the protective effects of Glaucocalyxin A (GLA) on airways in mouse models of asthma, concerning the inflammatory mediators, Th1/Th2 subgroup imbalance, and Toll-like receptor 4 (TLR4)/NF-κB signaling pathway. Hematoxylin and eosin/periodic acid-Schiff staining was used to observe the pathological changes in lung tissues. Inflammatory cytokine contents in the bronchoalveolar lavage fluid were detected by enzyme-linked immunosorbent assay. Protein expression levels were detected with Western blot, immunohistochemistry, and immunofluorescence. In vivo studies showed that, in ovalbumin (OVA)-induced asthmatic mouse models, the GLA treatments reduced the airway hyperresponsiveness and the secretion of inflammatory cells, declined the proliferation of goblet cells, decreased the levels of IL-4, IL-5, and IL-13, and increased the contents of interferon-γ and IL-12. Moreover, GLA inhibited the protein expression levels of TLR4, MyD88, TRAF6, and NF-κB in OVA-induced asthmatic mouse models. Further in vitro studies showed that GLA inhibited the expression of NF-κB, p-IκBα, tumor necrosis factor-α, IL-6, and IL-1β and blocked the nuclear transfer of NF-κB in lipopolysaccharide-stimulated RAW264.7 macrophages. Conclusively, GLA can inhibit the inflammatory responses in OVA-induced asthmatic mice and inhibit the release of inflammatory factors in LPS-induced RAW264.7 macrophages, which may be related to the inhibition of TLR4/NF-κB signaling pathway.
Glaucocalyxin A prevents hypoxia-induced epithelial-mesenchymal transition in human gastric cancer cells through the PI3K/Akt signaling pathway
J Recept Signal Transduct Res 2022 Apr;42(2):109-116.PMID:33307912DOI:10.1080/10799893.2020.1853160.
Hypoxia is a frequent occurrence in most solid tumors and associated with multiple cancer progression. Glaucocalyxin A (GLA) has been found to exhibit anti-tumor effect in several types of cancer, except gastric cancer (GC). The present study aimed to evaluate the function of GLA in GC and explore the underlying mechanism under hypoxia condition. Our results showed that GLA suppressed cell viability of MGC-803 cells in both normoxic or hypoxic conditions. MGC-803 cells were more sensitive to GLA in hypoxic condition. GLA attenuated hypoxia-induced migration and invasion of GC cells. Western blot assay proved that GLA elevated E-cadherin expression, as well reduced N-cadherin and vimentin expressions in hypoxia-induced GC cells. Moreover, we also found that GLA suppressed the expression of HIF-1α in both mRNA and protein levels. Furthermore, GLA blocked hypoxia-induced activation of PI3K/Akt pathway in GC cells. Notably, insulin like growth factor 1 (IGF-1), an activator of PI3K/Akt pathway, reversed the effects of GLA on cell migration, invasion and EMT in hypoxia-treated MGC-803 cells. In conclusion, these findings demonstrated that GLA exerted inhibitory effects on cell migration, invasion and epithelial to mesenchymal transition (EMT) via the PI3K/Akt signaling pathway in GC cells.