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Actein Sale

(Synonyms: 黄肉楠碱) 目录号 : GC35242

Actein 是从 Cimicifuga foetida 的根茎中分离的三萜糖苷。Actein 通过促进 ROS/JNK 活化和钝化人膀胱癌中的 AKT 途径来抑制细胞增殖,诱导自噬和凋亡。Actein 在体内几乎没有毒性。

Actein Chemical Structure

Cas No.:18642-44-9

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5 mg
¥6,660.00
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产品描述

Actein is a triterpene glycoside isolated from the rhizomes of Cimicifuga foetida. Actein suppresses cell proliferation, induces autophagy and apoptosis through promoting ROS/JNK activation, and blunting AKT pathway in human bladder cancer. Actein has little toxicity in vivo[1][2].

[1]. Yang ZC, et al. Actein enhances TRAIL effects on suppressing gastric cancer progression by activating p53/Caspase-3 signaling. Biochem Biophys Res Commun. 2018 Mar 18;497(4):1177-1183. [2]. Ji L, et al. Actein induces autophagy and apoptosis in human bladder cancer by potentiating ROS/JNK and inhibiting AKT pathways. Oncotarget. 2017 Nov 1;8(68):112498-112515.

Chemical Properties

Cas No. 18642-44-9 SDF
别名 黄肉楠碱
Canonical SMILES C[C@]12[C@@]3([H])[C@@]4(C[C@@H](OC(C)=O)[C@@]1([C@]5([H])[C@](O[C@]6([C@H]7[C@]([C@@H](O)O6)(C)O7)C[C@H]5C)([H])C2)C)[C@@]8([C@@](C(C)([C@@H](O[C@@]9([H])[C@@H]([C@H]([C@H](O)CO9)O)O)CC8)C)([H])CC3)C4
分子式 C37H56O11 分子量 676.83
溶解度 Soluble in DMSO 储存条件 4°C, protect from light
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5 mM 0.2955 mL 1.4775 mL 2.955 mL
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Research Update

Actein Antagonizes Oral Squamous Cell Carcinoma Proliferation through Activating FoxO1

Pharmacology 2021;106(9-10):551-563.PMID:34175854DOI:10.1159/000515601.

Background: Oral squamous cell carcinoma (OSCC) is among the most prevalent head and neck malignancies globally, and it is associated with high mortality rates. Actein is one of the primary active components extractable from the rhizomes of Cimicifuga foetida. This study aimed to evaluate the anti-OSCC effects of Actein and evaluate the potential underlying mechanisms. Methods and results: CCK-8 cell proliferation experiments demonstrated significant dose- and time-dependent anti-OSCC effects of Actein, while Actein had weak cytotoxic effects on normal oral cell lines. Flow cytometry for cell cycle evaluation revealed that Actein could induce cell cycle arrest at the G1 phase among OSCC cell lines. In our Annexin V/PI double staining apoptosis analysis, Actein induced significant apoptosis among OSCC cells, with upregulation of Bax and downregulation of Bcl-2. Our mechanistic study implicated the involvement of the Akt/FoxO1 pathway in the anti-OSCC effects of Actein. Akt1 and Akt2 expression significantly decreased in association with the FoxO1 upregulation. Furthermore, Bim and p21 were significantly upregulated, while survivin expression was downregulated. Finally, Actein treatment was associated with significant p-Akt downregulation and p-FoxO1 upregulation in OSCC cells, demonstrating the validated roles of Akt/FoxO1 in actein-mediated OSCC cell apoptosis and cell cycle arrest. FoxO1 knockdown significantly reversed the anti-OSCC effects of Actein. Additionally, a xenograft model indicated that Actein could inhibit OSCC cell growth in vivo. Conclusions: Our findings demonstrated that Actein could be a strong anti-OSCC candidate. Further evaluations of its safety and effectiveness are necessary before it can be considered for clinical use.

Actein contributes to black cohosh extract-induced genotoxicity in human TK6 cells

J Appl Toxicol 2022 Sep;42(9):1491-1502.PMID:35261072DOI:10.1002/jat.4313.

Black cohosh extract (BCE) is one of the most popular botanical products for relieving menopausal symptoms. However, recent studies indicate that BCE is not only ineffective for menopausal therapy but also induces genotoxicity through an aneugenic mode of action (MoA). In this study, the cytotoxicity of five constituents of BCE was evaluated in human lymphoblastoid TK6 cells. Among the five constituents, Actein (up to 50 μM) showed the highest cytotoxicity and was thus selected for further genotoxicity evaluations. Actein caused DNA damage proportionally to concentration as evidenced by the phosphorylation of the histone protein H2A.X (γH2A.X) and resulted in chromosomal damage as measured by the increased percentage of micronuclei (%MN) in cells. In addition, Actein activated DNA damage response (DDR) pathway through induction of p-ATM, p-Chk1, and p-Chk2, which subsequently induced cell cycle changes and apoptosis. Moreover, both BCE and Actein increased intracellular reactive oxygen species (ROS) production, decreased glutathione levels, and activated the mitogen-activated protein kinases (MAPK) signaling pathway. N-acetylcysteine, a ROS scavenger, attenuated BCE- and actein-induced ROS production, apoptosis, and DNA damage. These findings indicate that BCE- and actein-induced genotoxicity is mediated, at least partially, through oxidative stress. Taken together, our data show that Actein is likely one of the major contributors to BCE-induced genotoxicity.

Actein antagonizes colorectal cancer through blocking PI3K/Akt pathways by downregulating IMPDH2

Anticancer Drugs 2021 Sep 1;32(8):864-874.PMID:33929996DOI:10.1097/CAD.0000000000001080.

Actein, a triterpene glycoside, isolated from rhizomes of Cimicifuga foetida, was reported to exhibit anticancer effects in vitro and in vivo. However, the effects of Actein on colorectal cancer (CRC) remains unclear. As one of the most popular cancers all over the world, CRC ranked third place in both men and women. Recently, we investigated the potential anti-CRC effects of Actein and its mechanisms. The Cell counting kit-8 cell proliferation assays, cell cycle detection, apoptosis detection, reactive oxygen species and mitochondrial membrane potential evaluation, western blot, as well as SW480 xenograft mice model were conducted to illustrate the mechanisms of action on anti-CRC effects of Actein. Actein could significantly inhibit the human CRC cell lines SW480 and HT-29 proliferation, whereas less antiproliferation effects were found in normal colorectal cell lines HCoEpiC and FHC. Administration of Actein resulted in G1 phase cell cycle arrest in both SW480 and HT-29 cells. Moreover, mitochondria-mediated apoptosis was also observed after treatment with Actein in SW480 and HT-29 cell lines. Further investigation of mechanisms of action on actein-mediated anti-CRC proliferation effects indicated that the phosphoinositide 3-kinases (PI3K)/Akt pathways were involved. Actein significantly downregulated the phosphorylation of key molecules in PI3K/Akt pathways, including mTOR, glycogen synthesis kinase 3β (GSK-3β), as well as FOXO1. In addition, inosine 5'-monophosphate dehydrogenase type II (IMPDH2) was also observed decreasing in both SW480 and HT-29 cell lines after Actein treatment, suggesting that Actein may inhibit the PI3K/Akt pathways by decreasing IMPDH2. Finally, our SW480 xenograft model verified the anti-CRC effects and the safety of Actein in vivo. Our findings suggest Actein is worthy of further investigation as a novel drug candidate for the treatment of CRC.

Actein inhibits glioma growth via a mitochondria-mediated pathway

Cancer Biomark 2017;18(4):329-338.PMID:28128733DOI:10.3233/CBM-160095.

Previous studies indicate that the triterpene glycoside Actein from the herb black cohosh inhibits growth of human breast cancer cells. This study sought to investigate the effects of Actein on glioma cell growth and explore the potential mechanisms. Our results showed that administration of Actein significantly inhibited glioma cell viability in a dose- and time-dependent manner. Actein also increasingly inhibited the colony formation processes in glioma U87 cells and U251 cells. Administration of Actein also induced mitochondria-related apoptosis by increasing expression of pro-apoptotic factors Bax, cleaved caspase-3, cleaved caspase-9 and cleaved poly (ADP-ribose) polymerase 1 (PARP1) as well as decreasing anti-apoptotic Bcl-2 expression in U87 cells and U251 cells. In a xenograft model of glioma, Actein suppressed tumor growth and consistently induced cell apoptosis with the same mechanisms observed in vitro. In all, this study is the first report to address the growth inhibitory effects of Actein on glioma growth and propose that mitochondria-mediated apoptosis pathway may underlie the biological activities of Actein in glioma. Our study suggests that administration of Actein may serve as a potent therapeutic strategy for treatment of glioma.

Actein induces apoptosis in leukemia cells through suppressing RhoA/ROCK1 signaling pathway

Int J Oncol 2017 Dec;51(6):1831-1841.PMID:29039493DOI:10.3892/ijo.2017.4150.

Actein is a tetracyclic triterpenoid compound, extracted from the rhizome of Cimicifuga foetida, exhibiting anticancer activities as previously reported. However, the effects of Actein on human leukemia have not been explored before. In this study, the role of Actein in regulating apoptosis induction in human leukemia cells was investigated. Actein administration significantly enhanced apoptosis, especially in human leukemia cell line of U937 and the primary human leukemia cells. The promotion was accompanied by caspase-9, caspase-3 and poly(ADP-ribose) polymerase (PARP) cleavage, and cytochrome c (Cyto-c) release. Additionally, translocation of Bax into mitochondria was increased by Actein, while anti-apoptotic signals of myeloid cell leukemia-1 (Mcl-1) and B cell CLL/lymphoma 2 (Bcl-2) were decreased, accompanied by reduced phosphorylated Bcl-2-associated death promoter (Bad). Furthermore, protein kinase B (AKT) activation was downregulated by Actein treatment in U937 cells. RhoA, but not caspase-3, regulated Rho kinase 1 (ROCK1) expression induced by Actein. Suppression of RhoA and ROCK1 reduced ROCK1 expression, caspase-9, caspase-3 and PARP cleavage. In contrast, AKT inactivity enhanced apoptosis levels, as well as caspase signaling pathway expression. The anticancer role of Actein was potentiated by inactivating AKT. In vivo, U937-bearing tumor growth was suppressed by Actein, which was related to ROCK1 suppression, AKT dephosphorylation and apoptosis induction. These results indicated that Actein has a suppressive role in human leukemia progression through inactivating RhoA/ROCK1 and inducing caspases.