Gomisin J
(Synonyms: 戈米辛J) 目录号 : GC36178
A lignan with diverse biological activities
Cas No.:66280-25-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Gomisin J is a lignan that has been found in Schisandra chinensis and has diverse biological activities.1,2 It inhibits HIV-1 IIIB replication in H9 T cells (EC50 = 1.5 ?g/ml).1 Gomisin J (20 ?M) decreases LPS-induced increases in nitric oxide (NO) production and p38, ERK, and JNK phosphorylation in RAW 264.7 cells.2 It induces relaxation of isolated, precontracted endothelium-intact rat aortic rings when used at concentrations of 3, 10, and 30 ?g/ml.3 Gomisin J is cytotoxic to 13 cancer cell lines, including breast, colon, and cervical cancer cells, when used at a concentration of 30 ?g/ml.4
1.Chen, D.-F., Zhang, S.-X., Xie, J.-X., et al.Anti-AIDS agents—XXVI. Structure-activity correlations of gomisin-G-related anti-HIV lignans from Kadsura interior and of related synthetic analoguesBioorg. Med. Chem.5(8)1715-1723(1997) 2.Oh, S.-Y., Kim, Y.H., Bae, D.S., et al.Anti-inflammatory effects of gomisin J, and Schisandrin C isolated from the fruit of Schisandra chinensisBiosci. Biotechnol. Biochem.74(2)285-291(2010) 3.Park, J.Y., Hoi, Y.W., Yun, J.W., et al.Gomisin J from Schisandra chinensis induces vascular relaxation via activation of endothelial nitric oxide synthaseVascul. Pharmacol.57(2-4)124-130(2012) 4.Jung, S., Moon, H.-I., Kim, S., et al.Anticancer activity of gomisin J from Schisandra chinensis fruitOncol. Rep.41(1)711-717(2019)
| Cas No. | 66280-25-9 | SDF | |
| 别名 | 戈米辛J | ||
| Canonical SMILES | OC1=C(OC)C(OC)=C(C2=C(OC)C(OC)=C(O)C=C2CC(C)C(C)C3)C3=C1 | ||
| 分子式 | C22H28O6 | 分子量 | 388.45 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 30 mg/ml,Ethanol:PBS (pH 7.2) (1:5): 0.16 mg/ml | 储存条件 | 4°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 | 2.5743 mL | 12.8717 mL | 25.7433 mL |
| 5 mM | 0.5149 mL | 2.5743 mL | 5.1487 mL |
| 10 mM | 0.2574 mL | 1.2872 mL | 2.5743 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。
Anticancer activity of Gomisin J from Schisandra chinensis fruit
Oncol Rep 2019 Jan;41(1):711-717.PMID:30542721DOI:10.3892/or.2018.6850.
In attempting to identify effective anticancer drugs from natural products that are harmless to humans, we found that the Gomisin J from Schisandra chinensis fruit has anticancer activity. Schisandra chinensis fruits are used in traditional herbal medicine and Gomisin J is one of their chemical constituents. In the present study, we examined the anticancer activity of Gomisin J in MCF7 and MDA-MB-231 breast cancer cell lines and in MCF10A normal cell line, in a time- and concentration-dependent manner. Our data revealed that Gomisin J exerted a much stronger cytotoxic effect on MCF7 and MDA-MB-231 cancer cells than on MCF10A normal cells. Gomisin J suppressed the proliferation and decreased the viability of MCF7 and MDA-MB-231 cells at relatively low (<10 µg/ml) and high (>30 µg/ml) concentrations, respectively. Our data also revealed that Gomisin J induced necroptosis, a programmed form of necrosis, as well as apoptosis. Notably, Gomisin J predominantly induced necroptosis in MCF7 cells that are known to have high resistance to many pro-apoptotic anticancer drugs, while MDA-MB-231 exhibited a much lower level of necroptosis but instead a higher level of apoptosis. This data indicated the possibility that it may be used as a more effective anticancer drug, especially in apoptosis-resistant malignant cancer cells. In an extended study, Gomisin J exhibited a strong cytotoxic effect on all tested various types of 13 cancer cell lines, indicating its potential to be used against a wide range of different types of cancer cells.
Gomisin J attenuates cerebral ischemia/reperfusion injury by inducing anti-apoptotic, anti-inflammatory, and antioxidant effects in rats
Bioengineered 2022 Mar;13(3):6908-6918.PMID:35235758DOI:10.1080/21655979.2022.2026709.
Ischemic stroke is one of the leading causes of morbidity and mortality in humans. Cerebral ischemia-reperfusion (CIR) injury serves as a leading cause of stroke. Schisandra chinensis is a well-known Chinese traditional medicine. In this study, we explored the role of Gomisin J (GJ), a compound of S. chinensis, in CIR using a middle cerebral artery occlusion/reperfusion rat model and the possible mechanisms. We identified that GJ reduced neurological scores, cerebral infarction, and water content in the I/R rat brain. Importantly, GJ rescued I/R treatment-reduced neuron survival in the hippocampus, inhibited apoptosis of ischemic tissues in I/R rats, increased B-cell lymphoma-extra-large (Bcl-XL) expression, and reduced the levels of cleaved caspase-3, Bax, cyclooxygenase-2, nuclear factor kappa-B, and nitric oxide in I/R rat brain tissues. Furthermore, GJ treatment enhanced nuclear factor E2 related factor 2 (Nrf2) translocation, heme oxygenase-1 (HO-1) expression, superoxide dismutase and glutathione peroxidase activities, and glutathione level. Overall, GJ treatment GJ attenuates CIR injury by inducing anti-apoptotic, antioxidant, and anti-inflammatory effects in vivo.
Gomisin J inhibits the glioma progression by inducing apoptosis and reducing HKII-regulated glycolysis
Biochem Biophys Res Commun 2020 Aug 13;529(1):15-22.PMID:32560813DOI:10.1016/j.bbrc.2020.05.109.
Glioma is a leading cause of central nervous system malignant tumor-associated deaths in the world. However, the molecular mechanisms for glioma progression are still unclear, lacking effective therapeutic strategies. Gomisin J (GomJ) is a derivative of lignan compound, and shows regulatory effects on virus, oxidative stress and tumor progression. However, the role of GomJ in the meditation of glioma progression has not been explored. In this study, we found that GomJ markedly reduced the proliferation of glioma cell lines. Mitochondrial apoptosis was highly induced by GomJ, as evidenced by the significantly up-regulated expression of cytoplastic Cyto-c and cleaved Caspase-3. In addition, mitochondrial membrane potential (MMP) and oxidative stress were highly triggered in GomJ-incubated glioma cells, accompanied with the glycolysis suppression. Importantly, we found that GomJ could dramatically reduce the expression of hexokinase II (HKII) in glioma cells. At the same time, the dissociation of HKII from voltage-dependent anion channel (VDAC) in mitochondria was markedly induced by GomJ, contributing to glycolytic repression. The in vivo experiments confirmed that GomJ obviously reduced the growth of glioma with HKII reduction and few side effects. Taken together, these results demonstrated that GomJ could inhibit the proliferation, induce apoptosis and restrain HKII-regulated glycolysis during glioma progression. Herein, GomJ with few toxicity might be served as a potential therapeutic strategy for the treatment of glioma in humans.
Gomisin J Inhibits Oleic Acid-Induced Hepatic Lipogenesis by Activation of the AMPK-Dependent Pathway and Inhibition of the Hepatokine Fetuin-A in HepG2 Cells
J Agric Food Chem 2015 Nov 11;63(44):9729-39.PMID:26455261DOI:10.1021/acs.jafc.5b04089.
The aim of our study is to investigate the molecular mechanism of Gomisin J from Schisandra chinensis on the oleic acid (OA)-induced lipid accumulation in HepG2 cells. Gomisin J attenuated lipid accumulation in OA-induced HepG2 cells. It also suppressed the expression of lipogenic enzymes and inflammatory mediators and increased the expression of lipolytic enzymes in OA-induced HepG2 cells. Furthermore, the use of specific inhibitors and fetuin-A siRNA and liver kinase B1 (LKB1) siRNA transfected cells demonstrated that Gomisin J regulated lipogenesis and lipolysis via inhibition of fetuin-A and activation of an AMP-activated protein kinase (AMPK)-dependent pathway in HepG2 cells. Our results showed that Gomisin J suppressed lipid accumulation by regulating the expression of lipogenic and lipolytic enzymes and inflammatory molecules through activation of AMPK, LKB1, and Ca(2+)/calmodulin-dependent protein kinase II and inhibition of fetuin-A in HepG2 cells. This suggested that Gomisin J has potential benefits in treating nonalcoholic fatty liver disease.
Gomisin J from Schisandra chinensis induces vascular relaxation via activation of endothelial nitric oxide synthase
Vascul Pharmacol 2012 Sep-Oct;57(2-4):124-30.PMID:22728282DOI:10.1016/j.vph.2012.06.002.
Gomisin J (GJ) is a lignan contained in Schisandra chinensis (SC) which is a well-known medicinal herb for improvement of cardiovascular symptoms in Korean. Thus, the present study examined the vascular effects of GJ, and also determined the mechanisms involved. Exposure of rat thoracic aorta to GJ (1-30μg/ml) resulted in a concentration-dependent vasorelaxation, which was more prominent in the endothelium (ED)-intact aorta. ED-dependent relaxation induced by GJ was markedly attenuated by pretreatment with L-NAME, a nitric oxide synthase (NOS) inhibitor. In the intact endothelial cells of rat thoracic aorta, GJ also enhanced nitric oxide (NO) production. In studies using human coronary artery endothelial cells, GJ enhanced phosphorylation of endothelial NOS (eNOS) at Ser(1177) with increased cytosolic translocation of eNOS, and subsequently increased NO production. These effects of GJ were attenuated not only by calcium chelators including EGTA and BAPTA-AM, but also by LY294002, a PI3K/Akt inhibitor, indicating calcium- and PI3K/Akt-dependent activation of eNOS by GJ. Moreover, the levels of intracellular calcium were increased immediately after GJ administration, but Akt phosphorylation was started to increase at 20min of GJ treatment. Based on these results with the facts that ED-dependent relaxation occurred rapidly after GJ treatment, it was suggested that the ED-dependent vasorelaxant effects of GJ were mediated mainly by calcium-dependent activation of eNOS with subsequent production of endothelial NO.