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Dracorhodin perchlorate Sale

(Synonyms: 血竭素高氯酸盐; Dracohodin perochlorate) 目录号 : GC35898

A pro-apoptotic compound

Dracorhodin perchlorate Chemical Structure

Cas No.:125536-25-6

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产品描述

Dracorhodin perchlorate is a pro-apoptotic compound and a synthetic analog of dracorhodin, an anthocyanin that has been found in D. draco fruit.1,2 It induces cell cycle arrest at the G0/G1 phase as well as apoptosis in U87MG and T98G glioma cells when used at concentrations of 40 and 80 μM.2 It also increases levels of p53, p21, Bim, and Bax and decreases levels of Bcl-2 in glioma cells in vitro. Dracorhodin perchlorate is cytotoxic to U937, A375-S2, and MCF-7 cells in a concentration-dependent manner.1 It is also cytotoxic to HeLa cells, an effect that can be reversed by Ac-YVAD-CMK , Z-DEVD-FMK , Z-IETD-FMK, and Z-LEHD-FMK, which are inhibitors of caspase-1, -3, -8, and -9, respectively.

1.Xia, M., Wang, D., Wang, M., et al.Dracorhodin perchlorate induces apoptosis via activation of caspases and generation of reactive oxygen speciesJ. Pharmacol. Sci.95(2)273-283(2004) 2.Chen, X., Luo, J., Meng, L., et al.Dracorhodin perchlorate induces the apoptosis of glioma cellsOncol. Rep.35(4)2364-2372(2016)

Chemical Properties

Cas No. 125536-25-6 SDF
别名 血竭素高氯酸盐; Dracohodin perochlorate
Canonical SMILES CC1=C(OC)C2=CC=C(C3=CC=CC=C3)[O+]=C2C=C1O.O=Cl(=O)([O-])=O
分子式 C17H15ClO7 分子量 366.75
溶解度 DMF: 30 mg/ml,DMSO: 30 mg/ml,DMSO:PBS (pH 7.2) (1:4): 0.20 mg/ml 储存条件 Store at -20°C,protect from light
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1 mM 2.7267 mL 13.6333 mL 27.2665 mL
5 mM 0.5453 mL 2.7267 mL 5.4533 mL
10 mM 0.2727 mL 1.3633 mL 2.7267 mL
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Research Update

[Retracted] Dracorhodin perchlorate induces the apoptosis of glioma cells

Oncol Rep 2021 Jun;45(6):98.PMID:33846807DOI:10.3892/or.2021.8049.

Following the publication of the above paper, a concerned reader drew to the Editor's attention that certain of the western blotting data appeared to have been duplicated, comparing Fig. 2B with Fig. 4A; furthermore, the flow cytometric data panels featured in Fig. 3A appeared to contain repeated patternings of data within those data panels. After having conducted an independent investigation in the Editorial Office, the Editor of Oncology Reports has determined that this paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Oncology Reports 35: 2364‑2372, 2016; DOI: 10.3892/or.2016.4612].

Dracorhodin perchlorate enhances wound healing via β-catenin, ERK/p38, and AKT signaling in human HaCaT keratinocytes

Exp Ther Med 2021 Aug;22(2):822.PMID:34131445DOI:10.3892/etm.2021.10254.

Dracorhodin can be isolated from the exudates of the fruit of Daemonorops draco. Previous studies suggested that Dracorhodin perchlorate can promote fibroblast proliferation and enhance angiogenesis during wound healing. In the present study, the potential bioactivity of Dracorhodin perchlorate in human HaCaT keratinocytes, were investigated in vitro, with specific focus on HaCaT wound healing. The results of in vitro scratch assay demonstrated the progressive closure of the wound after treatment with Dracorhodin perchlorate in a time-dependent manner. An MTT assay and propidium iodide exclusion detected using flow cytometry were used to detect cell viability of HaCaT cells. Potential signaling pathways underlying the effects mediated by Dracorhodin perchlorate in HaCaT cells were clarified by western blot analysis and kinase activity assays. Dracorhodin perchlorate significantly increased the protein expression levels of β-catenin and activation of AKT, ERK and p38 in HaCaT cells. In addition, Dracorhodin perchlorate did not induce HaCaT cell proliferation but promoted cell migration. Other mechanisms may yet be involved in the dracorhodin perchlorate-induced wound healing process of human keratinocytes. In summary, Dracorhodin perchlorate may serve to be a potential molecularly-targeted phytochemical that can improve skin wound healing.

Pharmacodynamics of Dracorhodin perchlorate and Its Inflammation-Targeting Emulsion Gel for Wound Healing

Gels 2022 Nov 4;8(11):712.PMID:36354620DOI:10.3390/gels8110712.

The mechanism of Dracorhodin perchlorate for the repair of rat skin wounds was investigated. In order to screen a more favorable drug delivery system for wound repair, the therapeutic effect of Dracorhodin perchlorate inflammation-targeted emulsion gel was compared with that of non-targeted emulsion gel on rat wounds. Compared with non-targeted emulsion gels, inflammation-targeted emulsion gels had a better transdermal penetration and lower potentials (-51.6 mV and -17.1 mV, respectively). The recovery of the wound from the Dracorhodin perchlorate inflammation targeted emulsion gel group was better than that of the Dracorhodin perchlorate inflammation non-targeted emulsion gel group and the positive drug group. Compared with the no-target emulsion gel group, the bFGF expression on day 7 and the EGF expression on day 14 in the targeted emulsion group showed 45.5% and 49.9% improvement, respectively. Pathological tissue slices showed that the epidermis, dermis, and basal layer inflammatory cells in the inflammation-targeted emulsion gel group and non-targeted emulsion gel group were significantly reduced, the granulation tissue proliferation was obvious, and the inflammation-targeted emulsion gel group was more effective. The results proved that Dracorhodin perchlorate had a repairing effect on rat skin wounds, and its mechanism might be related to the promotion of the expression of EGF and bFGF in tissues.

Dracorhodin perchlorate inhibits osteoclastogenesis through repressing RANKL-stimulated NFATc1 activity

J Cell Mol Med 2020 Mar;24(6):3303-3313.PMID:31965715DOI:10.1111/jcmm.15003.

Osteolytic skeletal disorders are caused by an imbalance in the osteoclast and osteoblast function. Suppressing the differentiation and resorptive function of osteoclast is a key strategy for treating osteolytic diseases. Dracorhodin perchlorate (D.P), an active component from dragon blood resin, has been used for facilitating wound healing and anti-cancer treatments. In this study, we determined the effect of D.P on osteoclast differentiation and function. We have found that D.P inhibited RANKL-induced osteoclast formation and resorbed pits of hydroxyapatite-coated plate in a dose-dependent manner. D.P also disrupted the formation of intact actin-rich podosome structures in mature osteoclasts and inhibited osteoclast-specific gene and protein expressions. Further, D.P was able to suppress RANKL-activated JNK, NF-κB and Ca2+ signalling pathways and reduces the expression level of NFATc1 as well as the nucleus translocation of NFATc1. Overall, these results indicated a potential therapeutic effect of D.P on osteoclast-related conditions.

Dracorhodin perchlorate Regulates the Expression of Inflammatory Cytokines through the TLR4 Pathway and Improves Skin Wound Healing in Diabetic Rats

Evid Based Complement Alternat Med 2022 Apr 14;2022:9050686.PMID:35463063DOI:10.1155/2022/9050686.

Background: Dragon's blood is a natural medicine with hemostatic and blood-activating effects and is used to promote wound healing. Dracorhodin perchlorate (DP) is a stable form of dracarhod and is used as a substitute for cochinchinenin. DP promotes the proliferation of rat fibroblasts and promotes wound healing in rats. Methods: DP ointment (0.2 mg/mL) was applied to the skin wounds of nondiabetic and diabetic rats, and the skin of the wound was collected. Wound healing rate, H&E staining, Masson staining, TLR4 pathway, related inflammatory factors, nitric oxide synthase, and so forth were detected. Results: DP treatment alleviated the prolonged inflammatory cell infiltration time and the increase in the TLR4 pathway and inflammatory factors caused by diabetes. DP also promoted wound healing by increasing eNOS protein expression and NO content in the later stage of wound healing. Conclusion: DP promotes wound healing in diabetic rats by regulating the TLR4 pathway and related inflammatory factors. Therefore, adjuvant treatment of DP can be developed for diabetic wound healing.