Alisol B
(Synonyms: 泽泻醇 B) 目录号 : GC35286
A triterpene with diverse biological activities
Cas No.:18649-93-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Alisol B is a triterpene that has been found in A. orientale and has diverse biological activities.1,2,3 It increases the number of LC3 puncta, a marker of autophagy, as well as induces cell cycle arrest at the G1 phase and apoptosis, in MCF-7 breast cancer cells when used at a concentration of 30 ?M.1 Alisol B (0.5-5 ?M) inhibits RANKL-induced osteoclast differentiation of mouse bone marrow-derived macrophages (BMDMs).2 It reduces increases in ear thickness in a mouse model of delayed-type hypersensitivity induced by picryl chloride when administered at doses of 10 or 50 mg/kg.3
1.Law, B.Y.K., Wang, M., Ma, D.-L., et al.Alisol B, a novel inhibitor of the sarcoplasmic/endoplasmic reticulum Ca2+ ATPase pump, induces autophagy, endoplasmic reticulum stress, and apoptosisMol. Cancer Ther.9(3)718-730(2010) 2.Lee, J.-W., Kobayashi, Y., Nakamichi, Y., et al.Alisol-B, a novel phyto-steroid, suppresses the RANKL-induced osteoclast formation and prevents bone loss in miceBiochem. Pharmacol.80(3)352-361(2010) 3.Lee, J.H., Kwon, O.S., Jin, H.-G., et al.The rhizomes of Alisma orientale and alisol derivatives inhibit allergic response and experimental atopic dermatitisBiol. Pharm. Bull.35(9)1581-1587(2012)
| Cas No. | 18649-93-9 | SDF | |
| 别名 | 泽泻醇 B | ||
| Canonical SMILES | C[C@]([C@@]1(C2=C([C@H](C)C[C@@H]([C@]3([H])C(C)(C)O3)O)CC1)C)(CC[C@@]4([H])C5(C)C)[C@]([C@H](C2)O)([H])[C@]4(CCC5=O)C | ||
| 分子式 | C30H48O4 | 分子量 | 472.7 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at 2-8°C,protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.1155 mL | 10.5775 mL | 21.1551 mL |
| 5 mM | 0.4231 mL | 2.1155 mL | 4.231 mL |
| 10 mM | 0.2116 mL | 1.0578 mL | 2.1155 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Alisol B 23-Acetate Increases the Antitumor Effect of Bufalin on Liver Cancer through Inactivating Wnt/ β-Catenin Axis
Comput Math Methods Med 2022 May 6;2022:6249534.PMID:35572840DOI:10.1155/2022/6249534.
Objective: Liver cancer seriously threatens the health of people. Meanwhile, it has been reported that bufalin could act as an inhibitor in liver cancer. In addition, Alisol B 23-acetate is a natural product derived from Alisma plantago-aquatica Linn which has an antitumor effect. In this study, we aimed to explore whether Alisol B 23-acetate could increase the antitumor effect of bufalin on liver cancer. Methods: In order to detect the effect of Alisol B 23-acetate in combination with bufalin on liver cancer, human liver cancer SMMC-7721 and MHCC97 cells were used as subjects. Bufalin and Alisol B 23-acetate were performed on cells. Cell viability was tested by MTT assay. In addition, flow cytometry was performed to assess the cell apoptosis. Autophagy-related protein levels were tested by western blotting. Results: The data revealed that bufalin significantly decreased the viability of liver cancer cells, and the inhibitory effect was further increased by Alisol B 23-acetate. In addition, Alisol B 23-acetate notably enhanced the apoptotic effect of bufalin on liver cancer cells through mediation of Mcl-1, Bax, Bcl-2, and cleaved caspase-3. Meanwhile, Alisol B 23-acetate in combination with bufalin induced the autophagy in liver cancer cells through mediation of Beclin-1 and p62. Furthermore, Alisol B 23-acetate in combination with bufalin significantly downregulated the level of GSK-3β and increased the expression of β-catenin in liver cancer cells. Conclusion: In summary, these findings provide the first evidence that Alisol B 23-acetate improves the anticancer activity of bufalin on liver cancer through activation of the Wnt/β-catenin axis, and these outcomes might shed new lights on exploring the new methods against liver cancer.
Alisol B Alleviates Hepatocyte Lipid Accumulation and Lipotoxicity via Regulating RARα-PPARγ-CD36 Cascade and Attenuates Non-Alcoholic Steatohepatitis in Mice
Nutrients 2022 Jun 10;14(12):2411.PMID:35745142DOI:10.3390/nu14122411.
Non-alcoholic steatohepatitis (NASH) is a common chronic liver disease worldwide, with no effective therapies available. Discovering lead compounds from herb medicine might be a valuable strategy for the treatment of NASH. Here, we discovered Alisol B, a natural compound isolated from Alisma orientalis (Sam.), that attenuated hepatic steatosis, inflammation, and fibrosis in high-fat diet plus carbon tetrachloride (DIO+CCl4)-induced and choline-deficient and amino acid-defined (CDA)-diet-induced NASH mice. RNA-seq showed Alisol B significantly suppressed CD36 expression and regulated retinol metabolism in NASH mice. In mouse primary hepatocytes, Alisol B decreased palmitate-induced lipid accumulation and lipotoxicity, which were dependent on CD36 suppression. Further study revealed that Alisol B enhanced the gene expression of RARα with no direct RARα agonistic activity. The upregulation of RARα by Alisol B reduced HNF4α and PPARγ expression and further decreased CD36 expression. This effect was fully abrogated after RARα knockdown, suggesting Alisol B suppressed CD36 via regulating RARα-HNF4α-PPARγ cascade. Moreover, the hepatic gene expression of RARα was obviously decreased in murine NASH models, whereas Alisol B significantly increased RARα expression and decreased CD36 expression, along with the downregulation of HNF4α and PPARγ. Therefore, this study showed the unrecognized therapeutic effects of Alisol B against NASH with a novel mechanism by regulating RARα-PPARγ-CD36 cascade and highlighted Alisol B as a promising lead compound for the treatment of NASH.
Alisol B 23-Acetate Ameliorates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction by Inhibiting TLR4-NOX1/ROS Signaling Pathway in Caco-2 Cells
Front Pharmacol 2022 Jun 14;13:911196.PMID:35774596DOI:10.3389/fphar.2022.911196.
Alisol B 23-Acetate (AB23A) is a naturally occurring triterpenoid, which can be indicated in the rhizome of medicinal and dietary plants from Alisma species. Previous studies have demonstrated that AB23A could inhibit intestinal permeability by regulating tight junction (TJ)-related proteins. Even so, the AB23A protective mechanism against intestinal barrier dysfunction remains poorly understood. This investigation seeks to evaluate the AB23A protective effects on intestinal barrier dysfunction and determine the mechanisms for restoring intestinal barrier dysfunction in LPS-stimulated Caco-2 monolayers. According to our findings, AB23A attenuated the inflammation by reducing pro-inflammatory cytokines production like IL-6, TNF-α, IL-1β, and prevented the paracellular permeability by inhibiting the disruption of TJ in LPS-induced Caco-2 monolayers after treated with LPS. AB23A also inhibited LPS-induced TLR4, NOX1 overexpression and subsequent ROS generation in Caco-2 monolayers. Transfected with NOX1-specific shRNA diminished the up-regulating AB23A effect on ZO-1 and occludin expression. Moreover, transfected with shRNA of TLR4 not only enhanced ZO-1 and occludin expression but attenuated NOX1 expression and ROS generation. Therefore, AB23A ameliorates LPS-induced intestinal barrier dysfunction by inhibiting TLR4-NOX1/ROS signaling pathway in Caco-2 monolayers, suggesting that AB23A may have positive impact on maintaining the intestinal barrier's integrity.
Alisol B 23-acetate adjusts bile acid metabolisim via hepatic FXR-BSEP signaling activation to alleviate atherosclerosis
Phytomedicine 2022 Jul;101:154120.PMID:35523117DOI:10.1016/j.phymed.2022.154120.
Background: Postmenopausal women have a high incidence of atherosclerosis. Phytosterols have been shown to have cholesterol-lowering properties. Alisa B 23-acetate (AB23A) is a biologically active plant sterol isolated from Chinese herbal medicine Alisma. However, the atherosclerosis effect of AB23A after menopause and its possible mechanism have not been reported yet. Purpose: To explore whether AB23A can prevent atherosclerosis by regulating farnesoid X receptor and subsequently increasing fecal bile acid and cholesterol excretion to reduce plasma cholesterol levels. Methods: Aortic samples from premenopausal and postmenopausal women with ascending aortic arteriosclerosis were analyzed, and bilateral ovariectomized (OVX) female LDLR-/- mice and free fatty acid (FFA)-treated L02 cells were used to analyze the effect of AB23A supplementation therapy. Results: AB23A increased fecal cholesterol and bile acids (BAs) excretion dependent on activation of hepatic farnesoid X receptor (FXR) in ovariectomized mice. AB23A inhibited hepatic cholesterol 7α-hydroxylase (CYP7A1) and sterol 12α-hydroxylase (CYP8B1) via inducing small heterodimer partner (SHP) expression. On the other hand, AB23A increased the level of hepatic chenodeoxycholic acid (CDCA), and activated the hepatic BSEP signaling. The activation of hepatic FXR-BSEP signaling by AB23A in ovariectomized mice was accompanied by the reduction of liver cholesterol, hepatic lipolysis, and bile acids efflux, and reduced the damage of atherosclerosis. In vitro, AB23A fixed abnormal lipid metabolism in L02 cells and increased the expression of FXR, BSEP and SHP. Moreover, the inhibition and silencing of FXR canceled the regulation of BSEP by AB23A in L02 cells. Conclusion: Our results shed light into the mechanisms behind the cholesterol-lowering of AB23A, and increasing FXR-BSEP signaling by AB23A may be a potential postmenopausal atherosclerosis therapy.
Apoptotic effects of Alisol B 23‑acetate on gastric cancer cells
Mol Med Rep 2021 Apr;23(4):248.PMID:33537833DOI:10.3892/mmr.2021.11887.
Alisol B 23‑acetate (AB23A) is a natural triterpenoid isolated from Alismatis rhizoma, which exhibits a number of pharmacological activities. In the present study, AB23A‑induced anticancer efficacy was examined in AGS gastric cancer cells. Cell viability assay, cell cycle analysis, caspase activity assay, western blotting and reactive oxygen species (ROS) assay were used to investigate the anticancer effects of AB23A on AGS cells. AB23A reduced the viability of AGS cells, increased the sub‑G1 cell fraction and depolarized the mitochondrial membrane. Notably, AB23A‑induced cell death was associated with downregulation of the B‑cell lymphoma 2 and survivin proteins, and upregulation of the Bax protein. In addition, AB23A increased caspase‑3 and ‑9 activities, and regulated the activation of mitogen‑activated protein kinases (MAPK). Moreover, AB23A increased the production of reactive oxygen species. These results suggested that AB23A may induce apoptosis through cell cycle arrest and the mitochondrial pathway, accompanied by the caspase and MAPK signaling cascades. In conclusion, AB23A may have potential as a novel anticancer drug for the treatment of gastric cancer.