Juglanin
(Synonyms: 胡桃宁) 目录号 : GC32983
Juglanin是一个JNK激活剂。
Cas No.:5041-67-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Cell experiment: | Breast cancer cells are planted in 96-well plates with a density of 5×103 cells/well. After 12 h, the cells are treated with different concentrations of Juglanin (0 to 40 μM) for different periods of time (24 h and 48 h). Then the fresh mixture of MTS and PMS is added and incubated for 4 h at 37°C according to the manufacturer's protocol. A microplate reader is conducted to determine the absorbance at 500 nm, and the IC50 values are assessed with the probit model. Each one is performed in triplicate[1]. |
Animal experiment: | Male BALB/c-nude mice, aged 5 weeks, are used. They are maintained under specific pathogenfree conditions and supplied with sterilized food and water. On day 0, about 5×106 MCF-7 cells suspended in 0.1 mL PBS are inoculated subcutaneously in the right flank of each mouse (six mice each group). On day 9, when the tumors reach palpable size of around 200 mm3, mice are randomly assigned to three groups and receive daily intraperitoneal injection with 100 μL of vehicle (10% DMSO, 70% Cremophor/ethanol (3: 1), and 20% PBS), and 5 or 10 Juglanin mg/kg of celastrol. Tumor sizes are measured daily to observe dynamic changes in tumor growth. Body weights are also measured daily. After 7 days of drug administration, when the tumors of control group reach around 1600 mm3, all mice are killed. Tumors are dissected and stored in liquid nitrogen or fixed in formalin for further analysis[1]. |
References: [1]. Sun ZL, et al. Juglanin induces apoptosis and autophagy in human breast cancer progression via ROS/JNK promotion. Biomed Pharmacother. 2017 Jan;85:303-312. | |
Juglanin is a JNK activator.
Juglanin inhibits the proliferation of breast cancer cell in a dose- and time-dependent manner and presents less cytotoxic against the normal cells. Juglanin results in the accumulation of cancer cells in G2/M phase and a corresponding decrease in G0/G1 and S phases in both MCF-7 and SKBR3 cells. Juglanin up-regulates the expressions of phosphorylated Chk2, Chk2, phosphorylated Cdc25C, phosphorylated Cdc2, p27, cyclin D and down-regulates the levels of Cdc25C as well as Cdc2. The proportion of apoptosis is negligible for control cells, whereas 24 h of exposure of cells to Juglanin leads to a dose-dependent increase of apoptotic cells in both MCF-7 and SKBR3 cells. Juglanin significantly suppresses anti-apoptotic factor of Bcl-2 expression, and in contrast Bad and Bax are both up-regulated for Juglanin treatment. Juglanin markedly activates caspases and leads to Casapse-9, Casapse-8 and Caspase-3 cleavage. ROS generation is initiated by Juglanin and significantly increased by high concentrations of Juglanin. Juglanin also increases the level of JNK phosphorylation in both MCF-7 and SKBR3 cells[1].
Juglanin at doses of 5 and 10 mg/kg leads to significant decrease in tumor volume after 7 days of drug administration. 5 and 10 mg/kg Juglanin treatments do not cause weight loss in mice[1].
[1]. Sun ZL, et al. Juglanin induces apoptosis and autophagy in human breast cancer progression via ROS/JNK promotion. Biomed Pharmacother. 2017 Jan;85:303-312.
| Cas No. | 5041-67-8 | SDF | |
| 别名 | 胡桃宁 | ||
| Canonical SMILES | O=C1C(O[C@@H]2O[C@@H](CO)[C@H](O)[C@H]2O)=C(C3=CC=C(O)C=C3)OC4=CC(O)=CC(O)=C41 | ||
| 分子式 | C20H18O10 | 分子量 | 418.35 |
| 溶解度 | Methanol : 16.67 mg/mL (39.85 mM) | 储存条件 | Store at -20°C |
| 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 | 2.3903 mL | 11.9517 mL | 23.9034 mL |
| 5 mM | 0.4781 mL | 2.3903 mL | 4.7807 mL |
| 10 mM | 0.239 mL | 1.1952 mL | 2.3903 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。
Juglanin inhibits IL-1β-induced inflammation in human chondrocytes
Artif Cells Nanomed Biotechnol 2019 Dec;47(1):3614-3620.PMID:31468982DOI:10.1080/21691401.2019.1657877.
Osteoarthritis (OA) is one of the most characterized joint diseases associated with chondrocyte apoptosis. Juglanin has been reported to have anti-inflammation activity. This study aimed to evaluate the protective anti-inflammatory effects of Juglanin in human OA chondrocytes. Human OA chondrocytes were pretreated with Juglanin (10, 20 and 40 μM) for 2 h and subsequently stimulated with IL-1β for 24 h. Nitric oxide (NO) production was determined using the Griess method and prostaglandin E2 (PGE2), matrix metalloproteinase-3, -9 and -13 (MMP-3, MMP-9 and MMP-13), TNF-α, and IL-6 were assessed using ELISA. The expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), a disintegrin and metalloproteinase with thrombospondin motifs-4 and -5 (ADAMTS-4 and ADAMTS-5) were detected by qRT-PCR and western blot analysis. NF-κB signalling molecules were detected by western blot analysis. The results showed that Juglanin dose-dependently suppressed PGE2, NO, MMP-1, MMP3, MMP13, TNF-α and IL-6 production induced by IL-1β. The expression of COX-2, iNOS, ADAMTS-4 and ADAMTS-5 induced by IL-1β were also suppressed by Juglanin pretreatment. Western blot analysis showed that Juglanin suppressed IL-1β-induced NF-κB activation. Taken together, we found that Juglanin inhibits IL-1β-induced inflammation through the regulation of NF-κB signalling. Juglanin might be used as a therapeutic agent for treating OA.
Juglanin Inhibits Osteoclastogenesis in Ovariectomized Mice via the Suppression of NF-κB Signaling Pathways
Front Pharmacol 2021 Jan 27;11:596230.PMID:33708115DOI:10.3389/fphar.2020.596230.
Bone metabolism is a physiological process that involves both osteoblasts and osteoclasts. Pathological changes of osteoclasts are commonly seen in osteoporosis diseases. Juglanin is a natural compound, reported to have an inhibitory effect on inflammation, oxidative stress and cancer progression. The purpose of this study is to explore the role that Juglanin plays on the osteoclast functions and underlying signaling pathways. In vitro study demonstrated that Juglanin had negative influence on osteoclastic differentiation by suppressing the transcription activity of osteoclastogenesis-related genes and proteins. To determine the underlying mechanism, Western blot was employed to show that Juglanin could significantly have negative effect on the phosphorylation of P50, P65, I-κB， ultimately suppressing the expression and transcriptional activity of nuclear factor of activated T cells (NFATc1). In vivo Juglanin treatment attenuate bone reducing in mice with removed ovary through suppressing osteoclast functioning. Taken together, our study demonstrated that in the molecular mechanism, JUG inhibited the expression of receptor activator of nuclear factor-κ B ligand (RANKL) induced NF - κ B signaling pathway, thus may play a vital part in preventing postmenopausal osteoporosis.
The Inhibitory Effects of Juglanin on Adipogenesis in 3T3-L1 Adipocytes
Drug Des Devel Ther 2020 Dec 2;14:5349-5357.PMID:33293796DOI:10.2147/DDDT.S256504.
Introduction: Deregulation of adipogenesis plays an important role in obesity and other metabolism disorders. PPAR, C/EBP and SREBP1c are key transcriptional factors involved in adipogenesis and lipogenesis. Juglanin is a natural compound belonging to flavonoids, and it has been reported that Juglanin has a potent inhibitory effect on inflammation and certain type of cancers. However, the effects of Juglanin in adipogenesis have not been reported before. Materials and methods: 3T3-L1 preadipocytes were incubated with differentiation induction medium in the presence or absence of 0.5, 2.5, or 5 µM Juglanin for an 8-day differentiation period. The lipid droplets accumulated in the cytoplasm were monitored by Oil Red O staining on days 0, 2, 5, and 8. The regulatory effects of Juglanin on adipogenesis-related genes and proteins were investigated by real-time polymerase chain reaction and Western blot analysis. Results: Juglanin significantly decreased lipid accumulation in differentiated adipocytes. Our findings show that Juglanin reduced the expression of C/EBPα, C/EBPβ, and SREBP-1c without affecting PPARα or PPARγ expression. Additionally, Juglanin increased the activation of the SIRT1/AMPK signaling pathway through the phosphorylation of AMPKα. Finally, we performed an AMPK inhibitor experiment, which revealed that the inhibitory effects of Juglanin on adipogenesis are mediated through AMPK. Discussion: Juglanin can prevent adipogenesis by suppressing lipid accumulation and the differentiation of preadipocytes. The mechanism of Juglanin regulating adipogenesis requires further investigation. Future clinical study in vivo could shed more light on its implication in modulating obesity and metabolic disorders.
Juglanin inhibits lung cancer by regulation of apoptosis, ROS and autophagy induction
Oncotarget 2017 Sep 28;8(55):93878-93898.PMID:29212196DOI:10.18632/oncotarget.21317.
Juglanin (Jug) is obtained from the crude extract of Polygonum aviculare, exerting suppressive activity against cancer cell progression in vitro and in vivo. Juglanin administration causes apoptosis and reactive oxygen species (ROS) in different types of cells through regulating various signaling pathways. In our study, the effects of Juglanin on non-small cell lung cancer were investigated. A significant role of Juglanin in suppressing lung cancer growth was observed. Juglanin promoted apoptosis in lung cancer cells through increasing Caspase-3 and poly ADP-ribose polymerase (PARP) cleavage, which is regulated by TNF-related apoptosis-inducing ligand/Death receptors (TRAIL/DRs) relied on p53 activation. Anti-apoptotic members Bcl-2 and Bcl-xl were reduced, and pro-apoptotic members Bax and Bad were enhanced in cells and animals receiving Juglanin. Additionally, nuclear factor-κB (NF-κB), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) and mitogen-activated protein kinases (MAPKs) activation were inhibited by Juglanin. Further, Juglanin improved ROS and induced autophagy. ROS inhibitor N-acetyl-l-cysteine (NAC) reversed apoptosis induced by Juglanin in cancer cells. The formation of autophagic vacoules and LC3/autophagy gene7 (ATG7)/Beclin1 (ATG6) over-expression were observed in juglanin-treated cells. Also, Juglanin administration to mouse xenograft models inhibited lung cancer progression. Our study demonstrated that Juglanin could be a promising candidate against human lung cancer progression.
Juglanin administration protects skin against UVB‑induced injury by reducing Nrf2‑dependent ROS generation
Int J Mol Med 2020 Jul;46(1):67-82.PMID:32377697DOI:10.3892/ijmm.2020.4589.
Extensive solar ultraviolet B (UVB) exposure of the skin results in inflammation and oxidative stress, which may contribute to skin cancer. Natural products have attracted attention for their role in the effective treatment of cutaneous neoplasia. Juglanin is purified from the crude extract of Polygonum aviculare, exhibiting anti‑oxidant, anti‑inflammatory and anti‑cancer activities. Jugalanin was used in the current study to investigate whether it may ameliorate UVB irradiation‑induced skin damage by reducing oxidative stress and suppressing the inflammatory response in vivo and in vitro. In the present study, hairless mice were exposed to UVB irradiation in the absence or presence of Juglanin administration for 10 weeks. The findings indicated that Juglanin inhibited UVB‑induced hyperplasia and decreased infiltration in the skin of mice. UVB exposure‑induced oxidative stress in mice and cells was inhibited by Juglanin via enhancing anti‑oxidant activity. Additionally, Juglanin markedly reduced pro‑inflammatory cytokine release, including cyclic oxidase 2, interleukin‑1β and tumor necrosis factor‑α, triggered by chronic UVB irradiation. Juglanin‑ameliorated skin damage was associated with its suppression of mitogen activated protein kinases (MAPKs), including p38, extracellular signal regulated 1/2, and c‑Jun N‑terminal kinases, as well as nuclear factor (NF)‑κB signaling pathways, which was dependent on nuclear factor‑E2‑related factor 2 (Nrf2)‑modulated reactive oxygen species generation. Taken together, these data indicate that Juglanin protected against UVB‑triggered oxidative stress and inflammatory responses by suppressing MAPK and NF‑κB activation via enhancing Nrf2 activity.