Capillarisin
(Synonyms: 茵陈色原酮) 目录号 : GC65429
Capillarisin 作为蒿属植物蒿的一种成分，具有抗炎和抗氧化作用。Capillarisin 可为哮喘介导并发症的研究，并且可以作为一种潜在的神经保护剂来对抗布比卡因引起的神经毒性。
Cas No.:56365-38-9
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
Capillarisin, as a constituent from Artemisiae Capillaris herba, is found to exert anti-inflammatory and antioxidant properties. Capillarisin can be used for the research of asthma-mediated complications and can be a potential neuroprotectant against bupivacaine-induced neurotoxicity[1][2][3].
Capillarisin (0~40 μM; 24 hours; SH-SY5Y cells) does not produce any significant changes on the viability of SH-SY5Y cells[3]..Capillarisin (40 μM; 24 hours; SH-SY5Y cells) induces PI3K/PKB pathway inactivation, which inhibiting apoptosis in bupivacaine-challenged SH-SY5Y cells is overturned by LY294002 treatment and counteracts bupivacaine-induced injury via activating the PI3K/PKB pathway[3]..Capillarisin antagonizes bupivacaine-induced oxidative stress via activating the PI3K/PKB pathway in SH-SY5Y cells. Capillarisin inhibits bupivacaine-induced mitochondrial injury and endoplasmic reticulum stress via activating PI3K/PKB pathway[3].
Capillarisin (20 and 80 mg/kg; i.p.; 1 hour) pretreatment strongly inhibits NF-κB mediated genes (iNOS, COX-2)[4].Capillarisin significantly reduces the plasma leading nitrite production. Capillarisin markedly suppresses the adenosine 5'-triphosphate (ATP) in plasma and substance P in CFA-induced paw tissue[4].
[1]. Peng G, et al. Capillarisin exerts antiasthmatic activity in neonatal rats via modulating the matrix remodeling. Pak J Pharm Sci. 2020;33(4(Supplementary)):1907-1915.
[2]. Komiya T, et al. Capillarisin, a Constituent from Artemisiae Capillaris Herba. Chemical and Pharmaceutical Bulletin, 1975
[3]. Zhao T, Wang Q. Capillarisin protects SH-SY5Y cells against bupivacaine-induced apoptosis via ROS-mediated PI3K/PKB pathway. Life Sci. 2020;259:118279.
[4]. Khan S, et al. Anti-hyperalgesic and anti-allodynic activities of capillarisin via suppression of inflammatory signaling in animal model. J Ethnopharmacol. 2014;152(3):478-486.
| Cas No. | 56365-38-9 | SDF | Download SDF |
| 别名 | 茵陈色原酮 | ||
| 分子式 | C16H12O7 | 分子量 | 316.26 |
| 溶解度 | 储存条件 | Store at -20°C | |
| 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 | 3.162 mL | 15.8098 mL | 31.6196 mL |
| 5 mM | 0.6324 mL | 3.162 mL | 6.3239 mL |
| 10 mM | 0.3162 mL | 1.581 mL | 3.162 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 | ||||||||||
计算结果:
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。
Capillarisin protects SH-SY5Y cells against bupivacaine-induced apoptosis via ROS-mediated PI3K/PKB pathway
Life Sci 2020 Oct 15;259:118279.PMID:32798562DOI:10.1016/j.lfs.2020.118279.
Aims: Bupivacaine, a common local anesthetic, can induce neurotoxicity and neurological complications. Capillarisin, a bioactive ingredient of Artemisia capillaris root extracts, has been reported to protect SH-SY5Y cells against oxidative stress-mediated neuronal cell death. Nevertheless, the effects of Capillarisin on bupivacaine-induced neurotoxicity in SH-SY5Y cells remain unclear. Main methods: Cell viability, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production, and apoptosis were detected. Malondialdehyde (MDA) content, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase (CAT) activities were measured for evaluation of oxidative stress. Western blot was performed to detect the changes of phosphatidylinositol-3-kinase (PI3K)/protein kinase B (PKB) pathway, and expression of cleaved poly ADP ribose polymerase (PARP), cleaved caspase-3, glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP). Activities of mitochondrial respiratory chain complexes I-III and adenosine triphosphate (ATP) content were measured to evaluate mitochondrial damage. Key findings: Bupivacaine treatment dose-dependently reduced cell viability, increased LDH release, and induced ROS production and PI3K/PKB pathway inactivation in SH-SY5Y cells, which were overturned by Capillarisin treatment. Capillarisin inhibited bupivacaine-induced apoptosis in SH-SY5Y cells by decreasing cleaved PARP and cleaved caspase-3 expression. Capillarisin inhibited bupivacaine-induced oxidative stress, decrease of mitochondrial respiratory chain complex I, II, and III activities and ATP content, and increase of GRP78 and CHOP expression in SH-SY5Y cells. However, treatment with LY294002 abolished the effects of Capillarisin on bupivacaine-induced neurotoxicity in SH-SY5Y cells. Significance: Capillarisin protected SH-SY5Y cells against bupivacaine-induced apoptosis by inhibiting oxidative stress, mitochondrial injury, and endoplasmic reticulum stress via ROS-mediated of PI3K/PKB pathway.
Capillarisin augments anti-oxidative and anti-inflammatory responses by activating Nrf2/HO-1 signaling
Neurochem Int 2017 May;105:11-20.PMID:28161468DOI:10.1016/j.neuint.2017.01.018.
Capillarisin is a naturally isolated chromone, which is one of the major bioactive constituents of Artemisia capillaries. Capillarisin has antioxidant, anti-inflammatory, and anti-tumor potential, but the underlying molecular mechanisms remain largely unclear. In the present study, we demonstrate that the transcription factor nuclear factor E2-related factor-2 (Nrf2) is activated by Capillarisin in neuroblastoma SH-SY5Y cells and microglial BV2 cells. Capillarisin leads to Nrf2 phosphorylation, subsequent activation of antioxidant response element (ARE)-mediated transcription, and up-regulation of downstream molecules, such as heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1. Capillarisin protects SH-SY5Y cells from 6-hydroxydopamine-induced oxidative stress and attenuates inflammatory responses in lipopolysaccharide-treated BV2 cells. The cytoprotective and anti-inflammatory effects of Capillarisin are significantly abolished in cells transfected with specific Nrf2 or HO-1 siRNA, suggesting that these pharmacological properties of Capillarisin are primarily due to increased HO-1 activity. Capillarisin induces the activation of c-Jun N-terminal kinase in SH-SY5Y and BV2 cells, which is responsible for Nrf2 phosphorylation and HO-1 upregulation. Together, this study demonstrates that Capillarisin is a potential activator of the Nrf2/ARE-dependent pathway and could be an attractive candidate for the regulation of oxidative stress and inflammatory responses in the brain.
Capillarisin Suppresses Lipopolysaccharide-Induced Inflammatory Mediators in BV2 Microglial Cells by Suppressing TLR4-Mediated NF-κB and MAPKs Signaling Pathway
Neurochem Res 2015 Jun;40(6):1095-101.PMID:25894679DOI:10.1007/s11064-015-1567-4.
Capillarisin, one of the major bioactive compounds derived from Artemisia capillaries Thunb, has been reported to have extensive pharmacological properties, such as ant-inflammatory and anti-nociceptive activities. However, the molecular mechanisms responsible for the anti-inflammatory activity of Capillarisin have not been elucidated in microglia. In the present study, we investigated the anti-inflammatory effects and molecular mechanisms of Capillarisin on LPS-stimulated BV2 microglial cells. The effects of Capillarisin on inflammatory mediators TNF-α, IL-6, IL-1β, NO and PGE2 were detected. The effects of Capillarisin on NF-κB and MAPK activation were detected by western blotting. The results showed that Capillarisin suppressed LPS-induced TNF-α, IL-6, IL-1β, NO and PGE2 production in a dose-dependent manner. Capillarisin also inhibited LPS-induced TLR4 expression, NF-κB and MAPKs activation in BV2 microglia. In conclusion, Capillarisin inhibited LPS-induced inflammation by blocking TLR4-mediated NF-κB and MAPKs activation in BV2 microglia.
Capillarisin Exhibits Anticancer Effects by Inducing Apoptosis, Cell Cycle Arrest and Mitochondrial Membrane Potential Loss in Osteosarcoma Cancer Cells (HOS)
Drug Res (Stuttg) 2015 Aug;65(8):422-7.PMID:25368903DOI:10.1055/s-0034-1387728.
The aim of the present study was to assess the anticancer activity of Capillarisin against human osteosarcoma (HOS) cancer cells in vitro. Cell viability after Capillarisin drug treatment and evaluated by MTT assay. The extent of cell death induced by Capillarisin was estimated by using lactate dehydrogenase (LDH) assay. The effect of Capillarisin on cell cycle phase distribution and mitochondrial membrane potential (ΛΨm) was demonstrated via flow cytometry using propidium iodide (PI) and rhodamine-123 (Rh-123) DNA-binding fluorescent dyes respectively. Fluorescence microscopy was employed to examine the morphological changes in osteosarcoma cancer cells and presence of apoptotic bodies following Capillarisin treatment. The results of this study revealed that Capillarisin induced dose-dependent growth inhibition of these cancer cells after 12-h of incubation. Further, Capillarisin induced significant release of LDH from these cell cultures and this LDH release was much more noticeable at higher concentrations of Capillarisin. Hoechst 33258 staining revealed characteristic morphological features of apoptosis triggered by Capillarisin treatment. Cell cycle analysis revealed that Capillarisin induced dose-dependent G0/G1-phase cell cycle arrest. Capillarisin also trigerred a progressive and dose-dependent reduction in the mitochondrial membrane potential. In conclusion, Capillarisin inhibits cancer cell growth of osteosarcoma cells by inducing apoptosis accompanied with G0/G1-phase cell cycle arrest and loss in mitochondrial membrane potential.
Capillarisin attenuates exercise-induced muscle damage through MAPK and NF-κB signaling
Phytomedicine 2017 Aug 15;32:30-36.PMID:28732805DOI:10.1016/j.phymed.2017.04.007.
Background: Intense exercise has the potential to increase oxidative stress and cause muscle damage. Mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) are two major regulators of gene transcription in response to oxidative stress in the skeletal muscle. Pure Capillarisin (CAP) isolated from Artemisia capillaris Thunberg is known to have antioxidant and anti-inflammatory effects. Hypothesis/purpose: We hypothesized CAP to exert antioxidant activity against exercise-induced oxidative stress and suppress acute inflammatory response. We aimed to investigate skeletal muscle recovery after intense exercise with or without CAP administration. Study design: Eccentric exercise was conducted to induce muscle damage (C57BL6 mice, 13m/min for 60min downhill running). Mice were divided into four groups (n=6): the rested control, exercised, and exercised with CAP treatments (20mg/kg and 80mg/kg, ip injection 24h prior to exercise) groups. Method: After the intense exercise, mice were sacrificed immediately, and after 24h the gastrocnemius muscles and blood plasma were collected for further study. The DCFH-DA and TBARS assays were conducted for anti-oxidative capacity. Muscle damage markers, creatinine phosphate kinase (CPK) and lactate dehydrogenase (LDH) were investigated at plasma level. Muscle data were examined with H&E staining and microscopy. MAPK and NF-κB pathway, chemokine and cytokine productions were confirmed by western blotting and RT-PCR. Results: From DCFH-DA and TBARS assays, exercise increased the level of ROS production, but these changes were suppressed by CAP treatment. Exercise induced muscle damage by raising the levels of soluble muscle enzymes, such as CPK and LDH. However, this result was improved in CAP-treated groups at plasma level. Exercise activated MAPK (ERK 1/2 and JNK but not p38) and NF-κB (nuclear p50 and p65, and cytosolic p-IκBα) subunits at protein level but CAP attenuated these increase in a dose dependent manner. At the mRNA level, the chemokines CINC-1 and MCP-1, and cytokine IL-6 in gastrocnemius muscle were increased by exercise, whereas CAP suppressed these increase. Conclusion: Overall, our results indicate that CAP, as a single compound, can attenuate muscle damage by exerting antioxidant and anti-inflammatory effects. Thus, CAP is a potential candidate for the muscle protective agent in the future.