Lonicerin
(Synonyms: 忍冬苦苷) 目录号 : GC40909
A flavonoid with diverse biological activities
Cas No.:25694-72-8
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
Lonicerin is a flavonoid that has been found in L. japonica and has diverse biological activities, including antioxidant, anti-inflammatory, and neuroprotective properties. Lonicerin inhibits xanthine oxidase (IC50 = 37.4 µg/ml) and scavenges 2,2-diphenyl-1-picrylhydrazyl , hydroxyl, and superoxide radicals (IC50s = 9.2, 236.8, and 143.9 µg/ml, respectively). It reduces paw edema in a mouse model of C. albicans cell wall- and complete Freund's adjuvant-induced arthritis when administered at doses of 1 and 2 mg/kg three times every other day. It also decreases nitric oxide (NO) production and T cell proliferation in vitro when used at concentrations of 20 and 40 µg/ml, respectively. Lonicerin is neuroprotective against glutamate-induced neurotoxicity in rat primary cortical neurons.
| Cas No. | 25694-72-8 | SDF | |
| 别名 | 忍冬苦苷 | ||
| Canonical SMILES | O[C@H]([C@H]1O[C@@]2([H])[C@H](O)[C@H](O)[C@@H](O)[C@H](C)O2)[C@H](O)[C@@H](CO)O[C@H]1OC3=CC(O)=C(C(C=C(C4=CC(O)=C(O)C=C4)O5)=O)C5=C3 | ||
| 分子式 | C27H30O15 | 分子量 | 594.5 |
| 溶解度 | DMF: 50 mg/ml,DMSO: 50 mg/ml | 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 | 1.6821 mL | 8.4104 mL | 16.8209 mL |
| 5 mM | 0.3364 mL | 1.6821 mL | 3.3642 mL |
| 10 mM | 0.1682 mL | 0.841 mL | 1.6821 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。
Lonicerin targets EZH2 to alleviate ulcerative colitis by autophagy-mediated NLRP3 inflammasome inactivation
Acta Pharm Sin B 2021 Sep;11(9):2880-2899.PMID:34589402DOI:10.1016/j.apsb.2021.03.011.
Aberrant activation of NLRP3 inflammasome in colonic macrophages strongly associates with the occurrence and progression of ulcerative colitis. Although targeting NLRP3 inflammasome has been considered to be a potential therapy, the underlying mechanism through which pathway the intestinal inflammation is modulated remains controversial. By focusing on the flavonoid Lonicerin, one of the most abundant constituents existed in a long historical anti-inflammatory and anti-infectious herb Lonicera japonica Thunb., here we report its therapeutic effect on intestinal inflammation by binding directly to enhancer of zeste homolog 2 (EZH2) histone methyltransferase. EZH2-mediated modification of H3K27me3 promotes the expression of autophagy-related protein 5, which in turn leads to enhanced autophagy and accelerates autolysosome-mediated NLRP3 degradation. Mutations of EZH2 residues (His129 and Arg685) indicated by the dynamic simulation study have found to greatly diminish the protective effect of Lonicerin. More importantly, in vivo studies verify that Lonicerin dose-dependently disrupts the NLRP3-ASC-pro-caspase-1 complex assembly and alleviates colitis, which is compromised by administration of EZH2 overexpression plasmid. Thus, these findings together put forth the stage for further considering Lonicerin as an anti-inflammatory epigenetic agent and suggesting EZH2/ATG5/NLRP3 axis may serve as a novel strategy to prevent ulcerative colitis as well as other inflammatory diseases.
Lonicerin attenuates house dust mite-induced eosinophilic asthma through targeting Src/EGFR signaling
Front Pharmacol 2022 Dec 23;13:1051344.PMID:36618942DOI:10.3389/fphar.2022.1051344.
Eosinophilic asthma is the predominant phenotype of asthma, and although these patients are sensitive to glucocorticoid therapy, they also experience many side effects. Lonicerin is a kind of bioflavonoid isolated from the Chinese herb Lonicera japonica Thunb, which has anti-inflammatory and immunomodulatory effects. The aim of this study was to elucidate the effects of Lonicerin on eosinophilic asthma and its potential mechanisms. Here, we established a house dust mite (house dust mite)-induced eosinophilic asthma model in BALB/c mouse, and evaluated the effects of Lonicerin on it. Our results showed that Lonicerin significantly reduced airway hyperresponsiveness the number of inflammatory cells (especially eosinophils) and the elevation of interleukin (IL)-4, IL-5, IL-13 and eotaxin in bronchoalveolar lavage fluid (BALF) supernatants of mice. Additionally, Lonicerin also eminently blunted inflammatory infiltration and mucus secretion, as well as mRNA levels of Mucin 5AC (MUC5AC) in lung tissue. Furthermore, results of network pharmacology and molecular docking revealed that Src kinase and epidermal growth factor receptor may be the potential targets responsible for the effects of Lonicerin. Finally, in vivo experiments confirmed that Lonicerin inhibited activation of the Src/EGFR pathway by decreasing their phosphorylation. Taken together, the present study demonstrated that Lonicerin could suppress HDM-induced eosinophilic asthma in mice through inhibiting the activation of Src/EGFR pathway, which also provides a basis for further research as a new potentially therapeutic agent for eosinophilic asthma and its underlying mechanisms in the future.
Lonicerin prevents inflammation and apoptosis in LPS-induced acute lung injury
Front Biosci (Landmark Ed) 2020 Jan 1;25(3):480-497.PMID:31585898DOI:10.2741/4815.
Acute lung injury (ALI) is a life-threatening condition caused by severe inflammation of lung tissues. We hypothesized that lipopolysaccharide induced acute lung inflammation and injury in mice might be controlled by Lonicerin (LCR), a plant flavonoid that impacts immunity, oxidative stress, and cell proliferation. LCR reduced pathological changes including pulmonary edema, elevation of protein in bronchoalveolar lavage, inflammation, pro-inflammatory gene expression, expression of toll-like receptor 4/nuclear factor-kappa B, apoptosis, and significantly reduced mortality. Together, the results suggest that LCR might be a potential and effective candidate for the treatment of ALI that acts by inhibiting inflammation and apoptosis.
Lonicerin, an anti-algE flavonoid against Pseudomonas aeruginosa virulence screened from Shuanghuanglian formula by molecule docking based strategy
J Ethnopharmacol 2019 Jul 15;239:111909.PMID:31026553DOI:10.1016/j.jep.2019.111909.
Ethnopharmacological relevance: The Shuanghuanglian formula (SF) is a famous antimicrobial and antiviral traditional Chinese medicine that is made of Lonicera japonica Thunb., Scutellaria baicalensis Georgi, and Forsythia suspensa (Thunb.) Vahl. According to the Chinese Pharmacopoeia, the SF is commonly administered in the forms of oral liquid, tablets, and injection. It has long been used to treat acute respiratory tract infections, especially lung infection. Aim of the study: In the light of the increasing incidence of multidrug resistance to conventional antibiotics, the aim of this study was to screen potential anti-virulence agents against Pseudomonas aeruginosa from the extract of the SF. Materials and methods: The SF was used for effective compounds screening via the combination of the molecule docking approach and ultra-high-performance liquid chromatography-quadrupole/time of flight mass spectrometry. Fifty-one anti-virulence-related proteins were docked, 26 identified compounds were from SF. Subsequently, the top-scoring screened compound was assessed via bioactive-related assays, including the quantification of alginate biosynthesis, anti-biofilm assays, and the A549 human lung cells infection. Result: A flavonoid Lonicerin was found to be bonded with the active site of the alginate secretion protein (AlgE) with the highest score in molecule docking. Furthermore, we validated that Lonicerin could significantly reduce alginate secretion (25 μg/mL) and biofilm formation (12.5 μg/mL) at a sub-MIC concentration without inhibiting the proliferation of P. aeruginosa or influencing the expression of AlgE, which suggested that Lonicerin may directly inhibit AlgE. In addition, Lonicerin was proven to inhibit the infection of P. aeruginosa in the A549 cells. Conclusion: This work reported on the first potential AlgE antagonist that was derived from herbal resources. Lonicerin was proven to be an effective inhibitor in-vitro of P. aeruginosa infection.
Antiarthritic effect of Lonicerin on Candida albicans arthritis in mice
Arch Pharm Res 2011 May;34(5):853-9.PMID:21656372DOI:10.1007/s12272-011-0520-6.
Fungal arthritis is a potentially serious disease resulting in rapid destruction of the joint. Among the various Candida species, Candida albicans is the most commonly associated with fungal arthritis. In the present study, we examined the effect of Lonicerin, a flavonoid isolated from Lonicerae Flos, on an arthritis caused by C. albicans cell wall (CACW) in mice. To examine the effect, an emulsified mixture of CACW and complete Freund's adjuvant (CACW/CFA) was injected into BALB/c mice via hind footpad route on days -3, -2, and -1. On Day 0, mice with the swollen footpad received Lonicerin at 1 or 2 mg/dose/time intraperitoneally 3 times every other day. The footpad-swelling was measured for 20 days. Results showed that the Lonicerin treatment reduced the edema at all dose levels, and, furthermore, there was app. 54% edema reduction in animals given the 2 mg-dose at the peak (day 10) of septic arthritis (p < 0.05). Since the peak, the edema was reduced in similar rates. This antiarthritic activity appeared to be mediated by Lonicerin's ability to suppress T cell proliferation, nitric oxide production from macrophages, and shift of cellular immunity from Th1- toward Th2-type responses, all of which are beneficial to treat arthritis. In addition, the flavonoid had anticandidal activity (p < 0.01). These data suggest that Lonicerin alone, which has both anti-arthritic and antifungal activities, can result in a combination therapy for the treatment of fungal arthritis due to C. albicans infection.