Cirsilineol
(Synonyms: 甲基条叶蓟素) 目录号 : GC63591
Cirsilineol 是一种天然黄酮化合物，可选择性抑制肠道 CD4+ T 细胞中的 IFN-γ/STAT1/T-bet 信号。Cirsilineol 具有免疫抑制和抗肿瘤特性。Cirsilineol 显着改善三硝基苯磺酸 (TNBS) 诱导的小鼠 T 细胞介导的实验性结肠炎。
Cas No.:41365-32-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cirsilineol, a natural flavone compound, selectively inhibits IFN-γ/STAT1/T-bet signaling in intestinal CD4+ T cells. Cirsilineol has potent immunosuppressive and anti-tumor properties. Cirsilineol significantly ameliorates trinitro-benzene sulfonic acid (TNBS)-induced T-cell-mediated experimental colitis in mice[1].
Cirsilineol (0.1-10 μM; 96 hours) inhibits single mixed lymphocyte reaction and Concanava A-induced T-cell proliferation in a dose-dependent manner. Cirsilineol (10 μM) does not affect T lymphocyte’s viability. The inhibition of cirsilineol (10 μM) on T-cell proliferation is not due to a cytotoxic activity[1]. Cirsilineol (1-10 μM; pretreatment for 3 hours) completely inhibits IFN-γ-induced Tyr701 phosphorylation of STAT1 and JAK2 activation[1].
cirsilineol (3, 10, and 30 mg/kg) significantly ameliorates TNBS-induced Th1-mediated colitis through inhibiting IFN-γ/STAT1/T-bet signaling in CD4+ T cells.
[1]. Yang Sun, et al. Novel immunomodulatory properties of cirsilineol through selective inhibition of IFN-gamma signaling in a murine model of inflammatory bowel disease. Biochem Pharmacol. 2010 Jan 15;79(2):229-38.
| Cas No. | 41365-32-6 | SDF | |
| 别名 | 甲基条叶蓟素 | ||
| 分子式 | C18H16O7 | 分子量 | 344.32 |
| 溶解度 | 储存条件 | 4°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 | 2.9043 mL | 14.5214 mL | 29.0428 mL |
| 5 mM | 0.5809 mL | 2.9043 mL | 5.8086 mL |
| 10 mM | 0.2904 mL | 1.4521 mL | 2.9043 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
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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。
Cirsilineol attenuates LPS-induced inflammation in both in vivo and in vitro models via inhibiting TLR-4/NFkB/IKK signaling pathway
J Biochem Mol Toxicol 2021 Aug;35(8):e22799.PMID:33949057DOI:10.1002/jbt.22799.
The anti-inflammatory activity of Cirsilineol in in vivo condition was assessed by measuring the relative organ weight, lung dry/wet weight ratio, protein concentration, and infiltration of inflammatory cells in bronchoalveolar lavage fluid. We estimated the myeloperoxidase activity and levels of cytokines, chemokines, and inflammatory markers to analyze the efficacy of Cirsilineol against lipopolysaccharide (LPS)-induced lung inflammation. Furthermore, we quantified the gene expression of NFkB/IKK signaling molecules in cirsilineol-treated and untreated acute lung injury mice to confirm the anti-inflammatory property of Cirsilineol. The lung histology was assessed with hematoxylin and eosin staining. Apart from in vivo experiments, in vitro tests with LPS-stimulated RAW 264.7 macrophages were also performed. Cell viability assay was performed in the presence and absence of LPS in RAW 264.7 macrophages to determine the cytotoxic effect of Cirsilineol against macrophages. Reverse-transcription polymerase chain reaction (RT-PCR) analysis was done to analyze the gene expression of inflammatory markers in LPS-treated RAW 264.7 macrophages to prove that Cirsilineol effectively inhibits inflammation in vitro. The results of our study prove that Cirsilineol effectively inhibits inflammation in both in vivo and in vitro conditions. RT-PCR analysis results of NFkB/IKK signaling molecules clearly illustrate that Cirsilineol inhibited the expression of NFkB/IKK signaling protein and thereby prevented inflammation in in vivo condition, and it is further confirmed with the results of inflammatory protein expression in vitro model. The lung histopathological studies authentically confirm that Cirsilineol potentially prevented the mice from LPS-induced lung inflammation.
Cirsilineol Treatment Attenuates PM2.5-Induced Lung Injury in Mice
Int J Mol Sci 2022 Nov 12;23(22):13948.PMID:36430427DOI:10.3390/ijms232213948.
Ultrafine particulate matter with less than 2.5 μm diameter (PM2.5) is an air pollutant that causes severe lung damage. Currently, effective treatment and preventive methods for PM2.5-induced lung damage are limited. Cirsilineol (CSL) is a small natural compound isolated from Artemisia vestita. In this study, the efficacy of CSL on PM2.5-induced lung toxicity was tested, and its mechanism was identified. Lung injury was caused by intratracheal administration of PM2.5 suspension in animal models. Two days after PM2.5 pretreatment, CSL was injected via mouse tail vein for two days. The effects of CSL on PM2.5-induced lung damage, autophagy, apoptosis, and pulmonary inflammation in a mouse model and their mechanisms were investigated. CSL significantly suppressed histological lung damage and lung wet/dry weight proportion. CSL also significantly reduced PM2.5-induced autophagy dysfunction, apoptosis, lymphocyte suppression, and inflammatory cytokine levels in bronchoalveolar fluid (BALF). Furthermore, CSL increased mammalian target of rapamycin (mTOR) phosphorylation and significantly inhibited the expression of Toll-like receptors (TLR) 2 and 4, MyD88, and the autophagy proteins, Beclin1 and LC3II. Thus, CSL exerts protective effects on pulmonary damage by regulating mTOR and TLR2,4-myD88 autophagy pathways. Therefore, CSL can be used as an effective treatment for PM2.5-induced lung damage.
Cirsilineol Inhibits the Proliferation of Human Prostate Cancer Cells by Inducing Reactive Oxygen Species (ROS)-Mediated Apoptosis
Evid Based Complement Alternat Med 2022 Jul 9;2022:7975664.PMID:35855832DOI:10.1155/2022/7975664.
Cirsilineol has been reported to exhibit anticancer effects against several human cancer cell lines. The present study was designed to evaluate the anticancer effects of Cirsilineol against the human DU-145 prostate cancer cells. The results showed that Cirsilineol suppressed the proliferation of DU-145 cancer cells in a dose-dependent manner with minimal cytotoxic effects against the normal cells. The IC50 of Cirsilineol was found to be 7 μM and 110 μM against prostate cancer DU-145 and normal HPrEC prostate cells, respectively. Acridine orange and ethidium bromide (AO/EB) staining showed that Cirsilineol induced apoptosis in DU-145 prostate cancer cells. The Annexin V/PI staining further confirmed the induction of apoptosis in DU-145 cells. The western blot analysis showed that Cirsilineol suppressed the expression of Bax and upregulated the expression of Bcl-2 in prostate cancer DU-145 cells. Moreover, Cirsilineol caused a dose-dependent increase in reactive oxygen species (ROS) levels in prostate cancer. Wound healing and Transwell assays showed that Cirsilineol inhibits migration and invasion of DU-145 prostate cancer cells. Summing up, the results suggest that Cirsilineol suppresses the proliferation of prostate cancer cells and may prove to be a beneficial lead molecule for the development of chemotherapy for prostate cancer.
Cirsilineol inhibits proliferation of lung squamous cell carcinoma by inducing ROS mediated apoptosis
Food Chem Toxicol 2020 Sep;143:111550.PMID:32640357DOI:10.1016/j.fct.2020.111550.
Cirsilineol belonging to the flavones category have not been explored in detail for anti-proliferative potential, therefore selected for the investigation. Hence, the antiproliferative potential of Cirsilineol has been established in NCIH-520 cells. Cirsilineol exhibited good binding-energy and inhibited the activity of ODC, CATD, DHFR, HYAL, LOX-5, and COX-2 up to 45.14% at 100 μM. It significantly inhibited the proliferation of NCIH-520 cells (81.96%) and likewise, the proliferation of other cell lines up to 48.50%. It also induced an increase in the sub-diploid cell population, which then leads to an increase in apoptosis by 2.64 and 5.12 fold at 10 μM and 100 μM respectively. Further, the Annexin-V-FITC assay confirmed the late apoptosis and necrosis in the NCIH-520 cell line induced by Cirsilineol. The ROS production was enhanced by 1.16 and 2.22 folds at 10 μM and 100 μM respectively. Besides, Cirsilineol revealed acceptable ADME properties, non-toxic and non-mutagenic compound. Altogether, these findings provide evidence that Cirsilineol inhibited the proliferation of NCIH-520 cells by inducing ROS-mediated apoptosis and offer new insight into the anti-proliferative potential of Cirsilineol, which can further be exploited to either synthesise new derivatives or its candid usage as a herbal lead for cancer treatment.
Gastroprotective effect of Cirsilineol against hydrochloric acid/ethanol-induced gastric ulcer in rats
Korean J Physiol Pharmacol 2021 Sep 1;25(5):403-411.PMID:34448458DOI:10.4196/kjpp.2021.25.5.403.
This study was designed to evaluate the gastroprotective activity of Cirsilineol in hydrochloric acid (HCl)/ethanol-induced gastric ulcer model. Cirsilineol was administered at the doses of 20 and 40 mg/kg in HCl/ethanol-induced rats. The gastroprotective ability was verified by determining the ulcer score, total acidity, hemoglobin, inflammatory cytokines, lipid peroxides, and enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT) in gastric tissue and serum biochemical analysis. The results showed a favorable increase in the hemoglobin level, antioxidant enzymes (SOD and CAT), restored electrochemical balance (carbon dioxide & anion gap) while a noticeable decrease in ulcer index, total acidity, lipid peroxides, inflammatory cytokines (interleukin-1 beta [IL-1β], IL-6, and tumor necrosis factor alpha) in rats treated with the Cirsilineol. The serum biochemical analysis on liver markers (alkaline phosphatases, alanine aminotransferase, and aspartate aminotransferase), kidney markers (urea, creatinine, albumin, globulin, total protein), and lipid profile (triglyceride, high-density lipoprotein, total cholesterol) were attenuated by Cirsilineol treatment in rats. Histopathology showed enhanced gastric protection and preserved the integrity of gastric mucosa upon Cirsilineol administration. These results ultimately suggest that Cirsilineol has gastroprotective effects that prevent the development of gastric ulcer.