Helichrysetin
(Synonyms: 蜡菊亭； 4,2',4'-三羟基-6'-甲氧基查耳酮) 目录号 : GC64662
Helichrysetin，分离于 Helichrysum odoratissimum 的花朵中, 是一种ID2 (DNA 结合抑制剂 2) 抑制剂，可抑制DCIS (原位导管癌) 的形成。Helichrysetin 对细胞生长具有很强的抑制作用，并且能够诱导 A549 细胞凋亡 (apoptosis)。
Cas No.:62014-87-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
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Helichrysetin, isolated from the flowers of Helichrysum odoratissimum, is an ID2 (inhibitor of DNA binding 2) inhibitor, and suppresses DCIS (ductal carcinoma in situ) formation. Helichrysetin possess strong inhibitory effects on cell growth and is capable of inducing apoptosis in A549 cells[1][2].
[1]. Liu Y, et al. ID2 and GJB2 promote early-stage breast cancer progression by regulating cancer stemness. Breast Cancer Res Treat. 2019 May;175(1):77-90.
[2]. Ho YF, et al. Induction of apoptosis and cell cycle blockade by helichrysetin in a549 human lung adenocarcinoma cells. Evid Based Complement Alternat Med. 2013;2013:857257.
| Cas No. | 62014-87-3 | SDF | Download SDF |
| 别名 | 蜡菊亭； 4,2',4'-三羟基-6'-甲氧基查耳酮 | ||
| 分子式 | C16H14O5 | 分子量 | 286.28 |
| 溶解度 | 储存条件 | -20°C, protect from light | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.4931 mL | 17.4654 mL | 34.9308 mL |
| 5 mM | 0.6986 mL | 3.4931 mL | 6.9862 mL |
| 10 mM | 0.3493 mL | 1.7465 mL | 3.4931 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Helichrysetin inhibits gastric cancer growth by targeting c-Myc/PDHK1 axis-mediated energy metabolism reprogramming
Acta Pharmacol Sin 2022 Jun;43(6):1581-1593.PMID:PMC9160019DOI:10.1038/s41401-021-00750-0.
Helichrysetin (HEL), a chalcone isolated from Alpinia katsumadai Hayata, has an antitumor activity in human lung and cervical cancers. However, the inhibitory effect and underlying mechanism of HEL in gastric cancer have not been elucidated. Here, HEL significantly inhibited the growth of gastric cancer MGC803 cells in vitro and in vivo. HEL decreased expression and transcriptional regulatory activity of c-Myc and mRNA expression of c-Myc target genes. HEL enhanced mitochondrial oxidative phosphorylation (OXPHOS) and reduced glycolysis as evidenced by increased mitochondrial adenosine triphosphate (ATP) production and excessive reactive oxygen species (ROS) accumulation, and decreased the pPDHA1/PDHA1 ratio and Glyco-ATP production. Pyruvate enhanced OXPHOS after HEL treatment. c-Myc overexpression abolished HEL-induced inhibition of cell viability, glycolysis, and protein expression of PDHK1 and LDHA. PDHK1 overexpression also counteracted inhibitory effect of HEL on cell viability. Conversely, c-Myc siRNA decreased cell viability, glycolysis, and PDHK1 expression. NAC rescued the decrease in viability of HEL-treated cells. Additionally, HEL inhibited the overactivated mTOR/p70S6K pathway in vitro and in vivo. HEL-induced cell viability inhibition was counteracted by an mTOR agonist. mTOR inhibitor also decreased cell viability. Similar results were obtained in SGC7901 cells. HEL repressed lactate production and efflux in MGC803 cells. These results revealed that HEL inhibits gastric cancer growth by targeting mTOR/p70S6K/c-Myc/PDHK1-mediated energy metabolism reprogramming in cancer cells. Therefore, HEL may be a potential agent for gastric cancer treatment by modulating cancer energy metabolism reprogramming.
Helichrysetin and TNF‑α synergistically promote apoptosis by inhibiting overactivation of the NF‑κB and EGFR signaling pathways in HeLa and T98G cells
Int J Mol Med 2021 Apr;47(4):49.PMID:33576459DOI:10.3892/ijmm.2021.4882.
Tumor necrosis factor‑α (TNF‑α) has different effects on apoptosis depending on activation or inactivation of the nuclear factor‑κB (NF‑κB) and epidermal growth factor receptor (EGFR) signaling pathways. Helichrysetin, a natural chalcone, inhibits NF‑κB nuclear translocation in mouse pancreatic β cells. The present study aimed to identify the effect of Helichrysetin on activation of the NF‑κB and EGFR signaling pathways induced by TNF‑α, and the synergistic effect of Helichrysetin and TNF‑α on apoptosis of HeLa and T98G cells. Cell proliferation was measured by Cell Counting Kit‑8 assay, while apoptosis was measured by Hoechst 33258 and Annexin V/PI staining. NF‑κB activity was detected by luciferase assay, protein expression was measured by western blotting and mRNA expression was detected by quantitative PCR assay. The results revealed that in HeLa and T98G cells Helichrysetin blocked the increased phosphorylation of NF‑κB p65 induced by TNF‑α. Although Helichrysetin alone decreased cell viability, Helichrysetin and TNF‑α synergistically decreased cell viability. Helichrysetin, not TNF‑α, promoted apoptosis, while the combination of Helichrysetin and TNF‑α synergistically increased apoptosis. In addition, Helichrysetin and TNF‑α synergistically enhanced the activation of caspase‑3 and poly‑(ADP‑ribose)‑polymerase compared with Helichrysetin alone. Helichrysetin inhibited the phosphorylation of transforming growth factor‑β activated kinase (TAK1), IκB kinase‑α/β (IKK‑α/β), NF‑κB p65 and EGFR induced by TNF‑α. Consistent with the inhibition of NF‑κB activation, the increased TNF‑α‑induced mRNA expression levels of TNF‑α, IL‑1β, CCL2, CCL5 and CXCL10 were significantly downregulated by Helichrysetin. Therefore, Helichrysetin and TNF‑α synergistically promoted apoptosis by inhibiting TAK1/IKK/NF‑κB and TAK1/EGFR signaling pathways in HeLa and T98G cells, indicating a potential therapeutic strategy for cancer.
Helichrysetin Induces DNA Damage that Triggers JNK-Mediated Apoptosis in Ca Ski Cells
Pharmacogn Mag 2017 Oct-Dec;13(52):607-612.PMID:29200721DOI:10.4103/pm.pm_53_17.
Background: Cervical cancer has become one of the most common cancers in women and currently available treatment options for cervical cancer are very limited. Naturally occurring chalcones and its derivatives have been studied extensively as a potential anticancer agent in different types of cancer and Helichrysetin is naturally occurring chalcone that possess potent antiproliferative activity toward human cancer cells. Materials and methods: Inhibitory activity of Helichrysetin was evaluated at different concentrations. Ability of Helichrysetin to induce apoptosis and its relation with c-Jun N-terminal kinase (JNK)-mediated mechanism of apoptosis was assessed using flow cytometry and Western blotting. Results: Helichrysetin inhibited Ca Ski cells at half maximal inhibitory concentration 30.62 ± 0.38 μM. This compound has the ability to induce DNA damage, mitochondrial membrane disruption, and loss of cell membrane integrity. We have shown that apoptosis was induced through the activation of JNK-mediated apoptosis by DNA damage in the cells then triggering p53-downstream apoptotic pathway with increased expression of pro-apoptotic proteins, Bax and caspase 3, and suppression of Bcl-2 anti-apoptotic protein. DNA damage in the cells also caused phosphorylation of protein ataxia-telangiectasia mutated, an activator of DNA damage response. Conclusion: We conclude that Helichrysetin can inhibit Ca Ski cells through DNA damage-induced JNK-mediated apoptotic pathway highlighting the potential of this compound as anticancer agent for cervical cancer. Summary: Helichrysetin induced DNA damage in Ca Ski cellsDNA damage caused JNK-mediated phosphorylation of p53 resulting in p53-mediated apoptosisHelichrysetin is a potential DNA damage inducing agent through JNK activation to kill human cervical carcinoma cells. Abbreviations used: ATM: Ataxia-telangiectasia mutated, DAPI: 4',6-diamidino-2-phenylindole, DMSO: Dimethyl sulfoxide, FITC: Fluorescein isothiocyanate, IC50: Half maximal inhibitory concentration, JC1-5,5',6,6'-Tetrachloro: 1',3,3'-tetraethylbenzimidazolylcarbocyanine, iodide, JNK: c-Jun N-terminal kinase, MMP: Mitochondrial membrane potential, PBS: Phosphate-buffered saline, SRB: Sulforhodamine B, TUNEL: Terminal deoxynucleotidyl transferase dUTP nick labeling.
The role of chalcones: Helichrysetin, xanthohumol, and flavokawin-C in promoting neurite outgrowth in PC12 Adh cells
Nat Prod Res 2018 May;32(10):1229-1233.PMID:28539058DOI:10.1080/14786419.2017.1331226.
Chalcones are a group of compounds widely distributed in plant kingdom. The aim of this study was to assess the neurite outgrowth stimulatory activity of selected chalcones, namely Helichrysetin, xanthohumol and flavokawin-C. Using adherent rat pheochromocytoma (PC12 Adh) cells, the chalcones were subjected to neurite outgrowth assay and the extracellular nerve growth factor (NGF) levels were determined. Xanthohumol (10 μg/mL) displayed the highest (p < 0.05) percentage of neurite-bearing PC12 Adh cells and the highest (p < 0.05) NGF level in the culture medium of xanthohumol-treated cells. While, Helichrysetin induced a moderately high numbers of neurite-bearing cells, flavokawin-C did not stimulate neurite outgrowth. This work supports the potential use of xanthohumol as a potential neuroactive compound to stimulate neurite outgrowth.
Induction of apoptosis and cell cycle blockade by Helichrysetin in a549 human lung adenocarcinoma cells
Evid Based Complement Alternat Med 2013;2013:857257.PMID:23533528DOI:10.1155/2013/857257.
Researchers are looking into the potential development of natural compounds for anticancer therapy. Previous studies have postulated the cytotoxic effect of Helichrysetin towards different cancer cell lines. In this study, we investigated the cytotoxic effect of Helichrysetin, a naturally occurring chalcone on four selected cancer cell lines, A549, MCF-7, Ca Ski, and HT-29, and further elucidated its biochemical and molecular mechanisms in human lung adenocarcinoma, A549. Helichrysetin showed the highest cytotoxic activity against Ca Ski followed by A549. Changes in the nuclear morphology of A549 cells such as chromatin condensation and nuclear fragmentation were observed in cells treated with Helichrysetin. Further evidence of apoptosis includes the externalization of phosphatidylserine and the collapse of mitochondrial membrane potential which are both early signs of apoptosis. These signs of apoptosis are related to cell cycle blockade at the S checkpoint which suggests that the alteration of the cell cycle contributes to the induction of apoptosis in A549. These results suggest that Helichrysetin has great potentials for development as an anticancer agent.