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Luteoloside Sale

(Synonyms: 木犀草苷; Luteolin 7-glucoside; Luteolin 7-O-β-D-glucoside) 目录号 : GC41452

A flavanoid with diverse biological activities

Luteoloside Chemical Structure

Cas No.:5373-11-5

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5mg
¥855.00
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10mg
¥1,197.00
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25mg
¥2,610.00
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50mg
¥4,500.00
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产品描述

Luteoloside is a flavonoid that has been found in many Chinese herbs with diverse biological activities. It reduces lactate dehydrogenase (LDH) and caspase-3 activities and production of reactive oxygen species (ROS) and increases cell viability and 14-3-3η protein levels in H9C2 cardiomyocytes after anoxia/reoxygenation injury. Luteoloside blocks 3C protease activity (IC50 = 0.36 mM) and reduces the cytopathic effect of enterovirus 71 in rhabdomyosarcoma cells (EC50 = 0.43 mM). It inhibits the growth of hepatocellular carcinoma (HCC) cells in vitro via reduction in ROS accumulation, caspase-1 activity, and expression of the NLRP3 inflammasome and reduces the number of lung metastases in an SMMC-7721 HCC mouse xenograft model when administered at a dose of 2 mg/kg. Luteoloside also reduces acanthosis and expression of epidermal differentiation markers in a mouse model of psoriasis induced by imiquimod .

Chemical Properties

Cas No. 5373-11-5 SDF
别名 木犀草苷; Luteolin 7-glucoside; Luteolin 7-O-β-D-glucoside
Canonical SMILES OC1=C(C(C=C(C2=CC(O)=C(O)C=C2)O3)=O)C3=CC(O[C@H]4[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O4)=C1
分子式 C21H20O11 分子量 448.4
溶解度 DMF: 20 mg/ml,DMSO: 10 mg/ml,DMSO:PBS (pH 7.2)(1:5): 1 mg/ml,Ethanol: 5 mg/ml 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 2.2302 mL 11.1508 mL 22.3015 mL
5 mM 0.446 mL 2.2302 mL 4.4603 mL
10 mM 0.223 mL 1.1151 mL 2.2302 mL
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Research Update

Reduning injection and its effective constituent Luteoloside protect against sepsis partly via inhibition of HMGB1/TLR4/NF-κB/MAPKs signaling pathways

J Ethnopharmacol 2021 Apr 24;270:113783.PMID:33421596DOI:10.1016/j.jep.2021.113783.

Ethnopharmacological relevance: Reduning injection (RDN), a popular traditional Chinese medicine, formulated by three herbs (i.e., Artemisia carvifolia Buch.-Ham. ex Roxb., Lonicera japonica Thunb., and Gardenia jasminoides J. Ellis), has been widely used to treat upper respiratory infectious diseases in China. Aim of the study: To investigate the protective effect of RDN on both lipopolysaccharides (LPS)- and cecal ligation and puncture (CLP)-induced septic mice. To identify the potentially effective constituent, and to determine its protective effect and underlying mechanism in vivo and in vitro. Materials and methods: Male C57BL/6 mice were used to establish septic model by tail intravenous injection of 4 mg/kg LPS or CLP surgery. After modeling, mice were administered by tail intravenous injection of RDN in the dose of 16 or 8 mL/kg/day. The mortality, histopathology, plasma levels of inflammatory cytokines were evaluated respectively. In addition, we screened the potentially effective substances of RDN against sepsis by detecting the nitric oxide (NO) production in LPS-stimulated Raw 264.7 cells and verified the effect of Luteoloside in CLP-induced septic mice subsequently. Finally, the underlying mechanisms of RDN and Luteoloside were investigated in the inflammatory model in vitro. Results: Administration of RDN significantly reduced the mortality and increased the survival rate in both LPS- and CLP-induced septic mice. Meanwhile, RDN reduced the release of inflammatory cytokines accompanied by alleviating the organs damage of lung, liver, and kidney in CLP-induced septic mice. Moreover, several components from Gardenia jasminoides J. Ellis extract (ZZ) or Lonicera japonica Thunb and Artemisia carvifolia Buch.-Ham. ex Roxb extract (JQ) as well as the constituents of Luteoloside, quercetin, and caffeic acid were screened out to have obvious anti-inflammatory activity, which may be the potentially effective substances of RDN against sepsis. We further verified the protective role of Luteoloside in CLP-induced septic mice. In addition, RDN and Luteoloside significantly inhibited both the secretion and translocation of mobility group box (HMGB)1, and HMGB1-mediated activation of TLR4/NF-κB/MAPKs signaling pathways. Conclusion: RDN and its effective constituent Luteoloside exhibited a significant protective effect against sepsis, which were potential candidate drugs for treatment of sepsis. The mechanism of antisepsis partly was related to inhibition of HMGB1/TLR4/NF-κB/MAPKs signaling pathways. The results provide an evidence base for the follow-up clinical application of RDN in treatment of sepsis.

Luteoloside Protects the Uterus from Staphylococcus aureus-Induced Inflammation, Apoptosis, and Injury

Inflammation 2018 Oct;41(5):1702-1716.PMID:29987481DOI:10.1007/s10753-018-0814-7.

Luteoloside is a flavonoid extracted from several natural herbs that exhibits anti-microbial and anti-inflammation properties. Our study mainly identified the anti-inflammatory mechanism of action of Luteoloside in Staphylococcus aureus-induced endometritis. Histopathological observations and myeloperoxidase (MPO) activity showed that Luteoloside could protect the uterus from S. aureus-induced damage and ameliorate the infiltration of inflammatory cells. Quantitative PCR (qPCR) and ELISA analysis also revealed that Luteoloside could decrease the expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 and increase the expression of the anti-inflammatory cytokine IL-10 both in vivo and in vitro. However, western blot analysis revealed that Luteoloside inhibited the expression of TLR2 and IL-8 and inhibited the phosphorylation of IκBα and NF-κB p65. Moreover, Luteoloside inhibited the apoptosis of endometrial epithelial cells (EECs), suppressed the phosphorylation of p53, and decreased the expression of caspase-3 induced by S. aureus. Furthermore, this study showed that Luteoloside inhibited the expression of Bax but increased the expression of Bcl-2. These results indicate that Luteoloside has anti-inflammatory properties by inhibiting the TLR2 and NF-κB signaling pathways and plays an anti-apoptotic role in S. aureus-induced endometritis, which may be valuable for the clinical treatment of S. aureus-induced inflammation.

Luteoloside Acts as 3C Protease Inhibitor of Enterovirus 71 In Vitro

PLoS One 2016 Feb 12;11(2):e0148693.PMID:26870944DOI:10.1371/journal.pone.0148693.

Luteoloside is a member of the flavonoids family that exhibits several bioactivities including anti-microbial and anti-cancer activities. However, the antiviral activity of Luteoloside against enterovirus 71 (EV71) and the potential mechanism(s) responsible for this effect remain unknown. In this study, the antiviral potency of Luteoloside against EV71 and its inhibitory effects on 3C protease activity were evaluated. First, we investigated the cytotoxicity of Luteoloside against rhabdomyosarcoma (RD) cells, which was the cell line selected for an in vitro infection model. In a subsequent antiviral assay, the cytopathic effect of EV71 was significantly and dose-dependently relieved by the administration of Luteoloside (EC50 = 0.43 mM, selection index = 5.3). Using a plaque reduction assay, we administered Luteoloside at various time points and found that the compound reduced EV71 viability in RD cells rather than increasing defensive mobilization or viral absorption. Moreover, biochemical studies focused on VP1 (a key structural protein of EV71) mRNA transcript and protein levels also revealed the inhibitory effects of Luteoloside on the EV71 viral yield. Finally, we performed inhibition assays using Luteoloside to evaluate its effect on recombinant 3C protease activity. Our results demonstrated that Luteoloside blocked 3C protease enzymatic activity in a dose-dependent manner (IC50 = 0.36 mM) that was similar to the effect of rutin, which is a well-known C3 protease inhibitor. Collectively, the results from this study indicate that Luteoloside can block 3C protease activity and subsequently inhibit EV71 production in vitro.

Luteoloside prevents lipopolysaccharide-induced osteolysis and suppresses RANKL-induced osteoclastogenesis through attenuating RANKL signaling cascades

J Cell Physiol 2018 Feb;233(2):1723-1735.PMID:28681916DOI:10.1002/jcp.26084.

Bone destruction or osteolysis marked by excessive osteoclastic bone resorption is a very common medical condition. Identification of agents that can effectively suppress excessive osteoclast formation and function is crucial for prevention and treatment of osteolytic conditions such as periprosthetic joint infection and periprosthetic loosening. Luteoloside, a flavonoid, is a natural bioactive compound with anti-inflammation and anti-tumor properties. However, the effect of Luteoloside on inflammation-induced osteolysis is unknown. Here, we found that Luteoloside exhibited a strong inhibitory effect on lipopolysaccharide (LPS)-induced osteolysis in vivo. In addition, Luteoloside suppressed RANKL-induced osteoclast differentiation and abrogated bone resorption in a dose-dependent manner. Further, we found that the anti-osteoclastic and anti-resorptive actions of Luteoloside are mediated via blocking NFATc1 activity and the attenuation of RANKL-mediated Ca2+ signaling as well as NF-κB and MAPK pathways. Taken together, this study shows that Luteoloside may be a potential therapeutic agent for osteolytic bone diseases associated with abnormal osteoclast formation and function in inflammatory conditions.

Luteoloside attenuates neuroinflammation in focal cerebral ischemia in rats via regulation of the PPARγ/Nrf2/NF-κB signaling pathway

Int Immunopharmacol 2019 Jan;66:309-316.PMID:30502652DOI:10.1016/j.intimp.2018.11.044.

Luteoloside, a flavonoid compound, has been reported to have anti-inflammatory, anti-oxidative, antibacterial, antiviral, anticancer, and cardioprotective effects, among others, but its neuroprotective effects have rarely been studied. The purpose of this study was to investigate the protective effect of Luteoloside on cerebral ischemia and explore its potential mechanism. Middle cerebral artery occlusion (MCAO) was performed to investigate the effects of Luteoloside on cerebral ischemia-reperfusion (I/R). Male Sprague-Dawley rats were randomly divided into six groups: sham, MCAO, Luteoloside (20 mg/kg, 40 mg/kg, 80 mg/kg) and nimodipine (4 mg/kg). The results showed that Luteoloside alleviated neurologic deficits and cerebral edema as well as improved cerebral infarction and histopathological changes in MCAO rats. Luteoloside significantly inhibited I/R-induced neuroinflammation, as demonstrated by reduced levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the brain tissues of MCAO rats. Furthermore, our results demonstrated that Luteoloside significantly suppressed the activation of nuclear factor-kappa B (NF-κB) signaling, upregulated the protein expression of peroxisome proliferator activated receptor gamma (PPARγ) and increased NF-E2-related factor (Nrf2) nuclear accumulation in MCAO rats. Collectively, our findings suggested that Luteoloside played a crucial neuroprotective role by inhibiting NF-κB signaling in focal cerebral ischemia in rats. Furthermore, PPARγ and Nrf2 were also important for the anti-inflammatory effect of Luteoloside. In addition, our data suggested that Luteoloside might be an effective treatment for cerebral ischemia and other neurological disorders.