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Asatone Sale

(Synonyms: 细辛酮) 目录号 : GC35401

Asatone 是从细辛中分离到的一种活性成分,具有抗炎活性,通过活化 NF-κB 及下调 p-MAPK (ERK,JNK 和 p38) 通路起作用。

Asatone Chemical Structure

Cas No.:38451-63-7

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1mg
¥1,620.00
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5mg
¥3,150.00
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产品描述

Asatone is an active component isolated from Radix et Rhizoma Asari, with anti-inflammatory effect via activation of NF-κB and donwn regulation of p-MAPK (ERK, JNK and p38) pathways[1]. NF-κB[1]

[1]. Chang HY, et al. Asatone Prevents Acute Lung Injury by Reducing Expressions of NF-[Formula: see text]B, MAPK and Inflammatory Cytokines. Am J Chin Med. 2018;46(3):651-671.

Chemical Properties

Cas No. 38451-63-7 SDF
别名 细辛酮
Canonical SMILES O=C1C(OC)(OC)[C@@]2([H])[C@@](C(OC)(OC)C3=O)([H])C(CC=C)=C[C@@]3(OC)[C@@]2(CC=C)C=C1OC
分子式 C24H32O8 分子量 448.51
溶解度 Soluble in DMSO 储存条件 4°C, protect from light
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1 mg 5 mg 10 mg
1 mM 2.2296 mL 11.148 mL 22.296 mL
5 mM 0.4459 mL 2.2296 mL 4.4592 mL
10 mM 0.223 mL 1.1148 mL 2.2296 mL
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Research Update

Protective activity of Asatone against ovalbumin-induced allergic asthma

Int J Clin Exp Pathol 2020 Oct 1;13(10):2487-2494.PMID:33165354doi

Allergic asthma is a chronic lung disease characterized by wheezing, coughing, chest tightness and shortness of breath. Clinically, the treatments against asthma focus on controlling the symptoms rather than inhibiting recurrence radically. Additionally, local and systemic side effects caused by current treatments are worthy of attention. Therefore, a novel therapeutic strategy against asthma is needed. Asatone is a pharmacologically active component from Radix et Rhizoma Asari, which has anti-inflammatory effects in lipopolysaccharide-induced lung injury. In the present study, we showed that Asatone could protect mice against OVA-induced asthma, as manifested by attenuating inflammation infiltration, mucus production, and airway hyperreactivity and suppressing the elevation of IL-4, IL-5, and IL-13 in broncho-alveolar lavage fluid. Overall, results of the present study support use of Asatone as a potent therapeutic strategy for clinical treatment of allergic asthma.

Asatone and Isoasatone A Against Spodoptera litura Fab. by Acting on Cytochrome P450 Monoxygenases and Glutathione Transferases

Molecules 2019 Oct 31;24(21):3940.PMID:31683670DOI:10.3390/molecules24213940.

Asatone and isoasatone A from Asarum ichangense Cheng were determined to be defensive compounds to some insects in a previous investigation. However, the anti-insect activity mechanisms to caterpillar are still unclear. The compounds Asatone and isoasatone A from A. ichangense were induced by Spodoptera litura. The anti-insect activity of Asatone and isoasatone A to S. litura was further tested by weight growth rate of the insect through a diet experiment. Isoasatone A showed a more significant inhibitory effect on S. litura than Asatone on the second day. The concentration of Asatone was higher than isoasatone A in the second instar larvae of S. litura after 12 h on the feeding test diet. Both compounds caused mid-gut structural deformation and tissue decay as determined by mid-gut histopathology of S. litura. Furthermore, some detoxification enzyme activity were measured by relative expression levels of genes using a qPCR detecting system. Asatone inhibited the gene expression of the cytochrome P450 monooxygenases (P450s) CYP6AB14. Isoasatone A inhibited the relative expression levels of CYP321B1, CYP321A7, CYP6B47, CYP6AB14, and CYP9A39. Asatone increased the relative gene expression of the glutathione transferases (GSTs) SIGSTe1 and SIGSTo1, in contrast, isoasatone A decreased the relative gene expression of SIGSTe1 by about 33 fold. Neither compound showed an effect on acetylcholinesterase SIAce1 and SIAce2. The mechanism of anti-insect activity by both compounds could be explained by the inhibition of enzymes P450s and GSTs. The results provide new insights into the function of unique secondary metabolites Asatone and isoasatone A in genus Asarum, and a new understanding of why A. ichangense is largely free of insect pests.

Asatone Prevents Acute Lung Injury by Reducing Expressions of NF-[Formula: see text]B, MAPK and Inflammatory Cytokines

Am J Chin Med 2018;46(3):651-671.PMID:29595073DOI:10.1142/S0192415X18500349.

Asatone is an active component extracted from the Chinese herb Radix et Rhizoma Asari. Our preliminary studies have indicated that Asatone has an anti-inflammatory effect on RAW 264.7 culture cells challenged with lipopolysaccharide (LPS). Acute lung injury (ALI) has high morbidity and mortality rates due to the onset of serious lung inflammation and edema. Whether Asatone prevents ALI LPS-induced requires further investigation. In vitro studies revealed that Asatone at concentrations of 2.5-20[Formula: see text][Formula: see text]g/mL drastically prevented cytotoxicity and concentration-dependently reduced NO production in the LPS-challenged macrophages. In an in vivo study, the intratracheal administration of LPS increased the lung wet/dry ratio, myeloperoxidase activity, total cell counts, white blood cell counts, NO, iNOS, COX, TNF-[Formula: see text], IL-1[Formula: see text], and IL-6 in the bronchoalveolar lavage fluid as well as mitogen-activated protein kinases in the lung tissues. Pretreatment with Asatone could reverse all of these effects. Asatone markedly reduced the levels of TNF-[Formula: see text] and IL-6 in the lung and liver, but not in the kidney of mice. By contrast, LPS reduced anti-oxidative enzymes and inhibited NF-[Formula: see text]B activations, whereas Asatone increased anti-oxidative enzymes in the bronchoalveolar lavage fluid and NF-[Formula: see text]B activations in the lung tissues. Conclusively, Asatone can prevent ALI through various anti-inflammatory modalities, including the major anti-inflammatory pathways of NF-[Formula: see text]B and mitogen-activated protein kinases. These findings suggest that Asatone can be applied in the treatment of ALI.

Chemokine (C-C motif) ligand 18/membrane-associated 3/forkhead box O1 axis promotes the proliferation, migration, and invasion of intrahepatic cholangiocarcinoma

Bioengineered 2022 May;13(5):12738-12748.PMID:35609322DOI:10.1080/21655979.2022.2069383.

Phosphatidylinositol Transfer Protein, Membrane-Associated 3 (PITPNM3) often bind with chemokine (C-C motif) ligand 18 (CCL18) to promote tumor progression. However, the role of PITPNM3 in intrahepatic cholangiocarcinoma (ICC) is unclear. We first searched GEPIA database and detected the PITPNM3 expression using immunohistochemistry and real-time quantitative PCR. The results showed that PITPNM3 is high expression in ICC tissues and cells. Then we investigated the cell function of CLL18 and PITPNM3 through cell clone formation assay and transwell assay. The results indicated that CCL18 treatment promoted the proliferation, migration, and invasion of ICC cells. Silence of PITPNM3 reversed the effect of CCL18 on cell function. Simultaneously, we detected key protein expression of forkhead box O1 (FOXO1) and nuclear factor kappa B (NF-KB) through western blotting and found that CCL18 activated NF-KB pathway while inhibited FOXO1 pathway, the effect of which were attenuated by silence of PITPNM3. Finally, we confirmed which pathway affected the cell function using inhibitor of FOXO1 (AS1842856) and activator of NF-KB (Asatone). The results showed that AS1842856, not Asatone, relieved the inhibitory effect of si-PITPNM3 on the cell function of CCL18. In short, CCL18 treatment activated PITPNM3 to promote the proliferation, migration, and invasion of ICC via FOXO1 signaling pathway. These results provided a new insight for the diagnosis and therapy of ICC.

Effect of TLR7 gene expression mediating NF-κB signaling pathway on the pathogenesis of bronchial asthma in mice and the intervention role of IFN-γ

Eur Rev Med Pharmacol Sci 2021 Jan;25(2):866-879.PMID:33577041DOI:10.26355/eurrev_202101_24655.

Objective: To explore the mechanism of TLR7 mediating NF-κB signaling pathway on the pathogenesis of bronchial asthma in mice and the intervention effect of IFN-γ in the process. Materials and methods: The experimental animals were 70 C57BL/6J female mice of clean grade, which were divided into 7 groups according to different treatment protocols, including Normal group, Asthma group, Model+1-MT group, Model+IFN-γ group, Model+TLR7 agonist group, TLR7 deficient group, and Model+TLR7 deficient group. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of lung tissues. The positive expression rates of TLR7, p-IKKα and NF-κBp65 were detected by immunohistochemistry. bronchoalveolar lavage fluid (BALF) cells were classified and counted. The contents of interleukin (IL)-4, IL-10, IL-12 and interferon (IFN)-γ in BALF supernatant were detected by enzyme-linked immunosorbent assay (ELISA). Following isolation, culture and plasmid construction of airway smooth muscle cells (ASMCS) from normal mice and asthmatic mice, cells were transfected and divided into the Control group, pcDNA-TLR7 NC group, siRNA-TLR7 NC group, pcDNA-TLR7 group, siRNA-TLR7 group, Asatone group, Triptolide group, and pcDNA-TLR7 +Asatone group. The expression of TLR7, IDO, p-IKKα and NF-κBp65 was detected by real-time polymerase chain reaction (RT-PCR) and Western blot, respectively. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) was used to detect the proliferation of ASMCS. The cell cycle and apoptosis of ASMCS were detected by flow cytometry. Results: HE staining showed successful modeling of asthma. Immunohistochemical test showed that the positive expression rate of TLR7 in the Asthma group was significantly decreased, and that of IKKα and NF-κBp65 was significantly increased, with significantly increased IL-4, IL-10, IL-12 and IFN-γ levels (all p<0.05). Model+1-MT group and Model+TLR7 deficient group had a large number of inflammatory cell infiltration, increased IL-4, IL-10, IL-12 and IFN-γ levels, decreased expression levels of TLR7 and IDO, and increased expression of p-IKKα and NF-κBp65 (all p<0.05); while the opposites results were detected in Model+IFN-γ group and Model+TLR7 agonist group (all p<0.05). Cell transfection experiments revealed that pcDNA-TLR7 group and Triptolide group had increased TLR7 expression while decreased p-IKKα and NF-κBp65, decreased proliferation level, and increased cell apoptosis (all p<0.05); while the contrary results were found in siRNA-TLR7 group and Asatone group (all p<0.05); yet without significant difference in pcDNA-TLR7+Asatone group (all p>0.05). Conclusions: Upregulation of TLR7 can inhibit the activation of NF-κB signaling pathway, reduces airway inflammation, inhibits ASMCS proliferation and thus promotes cell apoptosis in asthmatic mice. Besides, IFN-γ can exert a protective role in suppressing the progression of inflammation in asthma.