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Acetylshikonin Sale

(Synonyms: 乙酰紫草素) 目录号 : GC35236

Acetylshikonin,来源于紫草根,具有抗癌、抗炎作用。Acetylshikonin 是一种非选择性的细胞色素 P450 抑制剂,对所有 P450 亚型抑制的 IC50 值范围为 1.4-4.0 μM。Acetylshikonin 是一种 AChE 抑制剂,具有很强的抗凋亡活性。

Acetylshikonin Chemical Structure

Cas No.:24502-78-1

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产品描述

Acetylshikonin, derived from the root of Lithospermum erythrorhizon, has anti-cancer and antiinflammation activity. Acetylshikonin is a non-selective cytochrome P450 inhibitor against all P450s (IC50 values range from 1.4-4.0 μM). Acetylshikonin is an AChE inhibitor and exhibits potent antiapoptosis activity[1][2][3]. IC50: 1.4-4.0 μM (all P450s)[2]AChE[3]

[1]. Park SH, et al. Identification of acetylshikonin as the novel CYP2J2 inhibitor with anti-cancer activity in HepG2 cells. Phytomedicine. 2017 Jan 15;24:134-140. [2]. Shon JC, et al. Acetylshikonin is a novel non-selective cytochrome P450 inhibitor. Biopharm Drug Dispos. 2017 Dec;38(9):553-556. [3]. Wang Y, et al. Acetylshikonin, a Novel AChE Inhibitor, Inhibits Apoptosis via Upregulation of Heme Oxygenase-1 Expression in SH-SY5Y Cells. Evid Based Complement Alternat Med. 2013;2013:937370.

Chemical Properties

Cas No. 24502-78-1 SDF
别名 乙酰紫草素
Canonical SMILES O=C1C([C@H](OC(C)=O)C/C=C(C)\C)=CC(C2=C1C(O)=CC=C2O)=O
分子式 C18H18O6 分子量 330.33
溶解度 DMSO : 50 mg/mL (151.36 mM) 储存条件 4°C, protect from light
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Research Update

Pharmacology, toxicity and pharmacokinetics of Acetylshikonin: a review

Pharm Biol 2020 Dec;58(1):950-958.PMID:32956595DOI:10.1080/13880209.2020.1818793.

Context: Acetylshikonin, a naphthoquinone derivative, is mainly extracted from some species of the family Boraginaceae, such as Lithospermum erythrorhizon Sieb. et Zucc., Arnebia euchroma (Royle) Johnst., and Arnebia guttata Bunge. As a bioactive compound, Acetylshikonin has attracted much attention because of its broad pharmacological properties. Objective: This review provides a comprehensive summary of the pharmacology, toxicity, and pharmacokinetics of Acetylshikonin focussing on its mechanisms on the basis of currently available literature. Methods: The information of Acetylshikonin from 1977 to 2020 was collected using major databases including Elsevier, Scholar, PubMed, Springer, Web of Science, and CNKI. Acetylshikonin, pharmacology, toxicity, pharmacokinetics, and naphthoquinone derivative were used as key words. Results: According to emerging evidence, Acetylshikonin exerts a wide spectrum of pharmacological effects such as anticancer, anti-inflammatory, lipid-regulatory, antidiabetic, antibacterial, antifungal, antioxidative, neuroprotective, and antiviral properties. However, only a few studies have reported the adverse effects of Acetylshikonin, with respect to reproductive toxicity and genotoxicity. Pharmacokinetic studies demonstrate that Acetylshikonin is associated with a wide distribution and poor absorption. Conclusions: Although experimental data supports the beneficial effects of this compound, Acetylshikonin cannot be considered as a therapy drug without further investigations, especially, on the toxicity and pharmacokinetics.

Acetylshikonin, A Novel CYP2J2 Inhibitor, Induces Apoptosis in RCC Cells via FOXO3 Activation and ROS Elevation

Oxid Med Cell Longev 2022 Mar 9;2022:9139338.PMID:35308176DOI:10.1155/2022/9139338.

Acetylshikonin is a shikonin derivative originated from Lithospermum erythrorhizon roots that exhibits various biological activities, including granulation tissue formation, promotion of inflammatory effects, and inhibition of angiogenesis. The anticancer effect of Acetylshikonin was also investigated in several cancer cells; however, the effect against renal cell carcinoma (RCC) have not yet been studied. In this study, we aimed to investigate the anticarcinogenic mechanism of Acetylshikonin in A498 and ACHN, human RCC cell lines. MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide), cell counting, and colony forming assay showed that Acetylshikonin induced cytotoxic and antiproliferative effects in a dose- and time-dependent manner. Cell cycle analysis and annexin V/propidium iodide (PI) double staining assay indicated the increase of subG1 phase and apoptotic rates. Also, DNA fragmentation was observed by using the TUNEL and comet assays. The intracellular ROS level in acetylshikonin-treated RCC was evaluated using DCF-DA. The ROS level was increased and cell viability was decreased in a dose- and time-dependent manner, while those were recovered when cotreated with NAC. Western blotting analysis showed that Acetylshikonin treatment increased the expression of FOXO3, cleaved PARP, cleaved caspase-3, -6, -7, -8, -9, γH2AX, Bim, Bax, p21, and p27 while decreased the expressions of CYP2J2, peroxiredoxin, and thioredoxin-1, Bcl-2, and Bcl-xL. Simultaneously, nuclear translocation of FOXO3 and p27 was observed in cytoplasmic and nuclear fractionated western blot analysis. Acetylshikonin was formerly identified as a novel inhibitor of CYP2J2 protein in our previous study and it was evaluated that CYP2J2 was downregulated in acetylshikonin-treated RCC. CYP2J2 siRNA transfection augmented that apoptotic effect of Acetylshikonin in A498 and ACHN via up-regulation of FOXO3 expression. In conclusion, we showed that the apoptotic potential of Acetylshikonin against RCC is mediated via increase of intracellular ROS level, activation of FOXO3, and inhibition of CYP2J2 expressions. This study offers that Acetylshikonin may be a considerable alternative therapeutic option for RCC treatment by targeting FOXO3 and CYP2J2.

Acetylshikonin exerts anti-tumor effects on non-small cell lung cancer through dual inhibition of STAT3 and EGFR

Phytomedicine 2022 Jul;101:154109.PMID:35526322DOI:10.1016/j.phymed.2022.154109.

Background: Lung cancer is one of the most common types of malignant tumor. It has one of the highest morbidity and mortality rates worldwide, and approximately 85% of cases are non-small cell lung cancer (NSCLC). Clinically, several EGFR inhibitors have been used to treat NSCLC, but resistance can develop. Studies have shown that cross talk between signal transducer and activator of transcription 3 (STAT3) and epidermal growth factor receptor (EGFR) can mediate drug resistance. Acetylshikonin has obvious antitumor effects, but the mechanism of action is still unclear. Purpose: To analyze the antitumor activity of Acetylshikonin in lung cancer and clarify its molecular mechanism. Methods: Methyl thiazolyl tetrazolium (MTT), colony formation and 5-ethynyl-2'-deoxyuridine (EDU) assays were performed to examine the effects of Acetylshikonin in inhibiting the proliferation of NSCLC cells (PC-9, H1975 and A549). Scratch wound and transwell assays were used to evaluate the migration and invasion of NSCLC cells. Flow cytometry was employed to determine whether Acetylshikonin could induce apoptosis. Proteome sequencing was used to identify the targets of Acetylshikonin. Immunofluorescence staining and western blotting were utilized to verify the inhibition of STAT3 and EGFR phosphorylation. A xenotransplantation model was established to evaluate the efficacy of Acetylshikonin in nude mice. Results: Our data demonstrated that Acetylshikonin significantly decreased the survival rate of human NSCLC cells, increased the apoptotic rate and inhibited cell migration dose-dependently. Immunofluorescence staining and western blotting analyses revealed that Acetylshikonin inhibited EGFR and STAT3 pathways. Acetylshikonin also inhibited tumor growth in a xenograft model better than inhibitors of EGFR and STAT3. Conclusion: Acetylshikonin has anti-cancer effects on NSCLC cells by inhibiting EGFR and STAT3, indicating that Acetylshikonin may be a new antitumor drug to treat NSCLC.

Acetylshikonin is a novel non-selective cytochrome P450 inhibitor

Biopharm Drug Dispos 2017 Dec;38(9):553-556.PMID:28866862DOI:10.1002/bdd.2101.

Acetylshikonin is a biologically active compound with anti-cancer and anti-inflammatory activity, which is isolated from the roots of Lithospermum erythrorhizoma. An inhibitory effect of Acetylshikonin against CYP2J2 activity was discovered recently. Based on this result, this study was expanded to evaluate the inhibitory effects of Acetylshikonin against nine different cytochrome P450 (P450) isoforms in human liver microsomes (HLMs) using substrate cocktails incubation assay. Acetylshikonin showed a strong inhibitory effect against all P450s tested with IC50 values of 1.4-4.0 μ m. Pre-incubation of Acetylshikonin with HLMs and NADPH did not alter the inhibition potency, indicating that Acetylshikonin is not a mechanism-based inhibitor. SKF-525A, a widely used non-specific P450 inhibitor, had no inhibitory activity against CYP1A2, 2A6, 2E1 and 2J2, while it showed an inhibitory effect against CYP2B6, CYP2C19 and 2D6 with IC50 values of 2.5, 3.6 and 0.5 μ m, respectively. Our findings indicate that Acetylshikonin may be a novel general P450 inhibitor, which could replace SKF-525A.

Acetylshikonin inhibits growth of oral squamous cell carcinoma by inducing apoptosis

Arch Oral Biol 2016 Oct;70:149-157.PMID:27371806DOI:10.1016/j.archoralbio.2016.06.020.

Objectives: Recently, shikonin derivatives from Lithospermum erythrorhizon have been suggested as potential chemotherapeutic agents against numerous types of cancers in addition to their traditional uses, e.g., as anti-inflammatory agents. Acetylshikonin, one of shikonin derivatives, has also been reported to possess anticancer activity. However, few studies of the effectiveness of Acetylshikonin against cancer cells have been conducted, and there are no studies of oral cancers. In this study, we investigated the usefulness of Acetylshikonin as a treatment regimen for oral cancers by observing the growth inhibitory function of Acetylshikonin and the involved mechanisms. Designs: The viability, cell cycle, and ratio of apoptotic cells of oral squamous cell carcinoma (OSCC) cells were observed after treatment with Acetylshikonin using MTT assay, flow cytometric analysis, and Annexin V/PI staining, respectively. In addition, molecular changes of apoptosis-related pathways and the role of reactive oxygen species (ROS) were analyzed in acetylshikonin-treated cells. Results: We observed that Acetylshikonin significantly suppressed the growth of OSCC cells by inducing apoptotic cell death, and Acetylshikonin affected the viability of a normal keratinocyte cell line HaCaT to a lesser degree, suggesting that Acetylshikonin may be a good chemotherapeutic reagent with less toxicity to normal tissues. In addition, we found that acetylshikonin-induced apoptosis of OSCC cells is mediated by ROS as well as G2 cell cycle arrest. ROS production in response to Acetylshikonin treatment enhanced the phosphorylation of JNK and p38 MAPK, which are in the major pathways of apoptotic cell death mechanisms. Conclusions: In summary, our data suggest that Acetylshikonin is a strong candidate for use as a selective chemotherapeutic agent for the treatment of OSCC.