Nigericin
(Synonyms: 尼日利亚霉素) 目录号 : GC39719
A potassium ionophore
Cas No.:28380-24-7
Sample solution is provided at 25 µL, 10mM.
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Related Biological Data
Lysosomal accumulation and cellular pH-responsive capability of NRhD-PEG-4 NPs. (b) Fluorescence images of A549 and MCF-7 cells incubated with NRhD-PEG-4 NPs at different pH values (4.5, 5.5, 6.5, and 7.5). (c) Fluorescence quantification in (a).
For the intracellular pH-reactive test, the cells were treated with 1.0 mg/mL nigericin (GLPBIO) in a high K+ buffer of different pH values for 30 min.
Acta Biomaterialia (2022). PMID: 36087865 IF: 10.6335 -
Related Biological Data
IPI-2I cells were transfected with siR-SLC9A3, NC, pEGFP-SLC9A3 or pEGFP. (G-H) NHE3 activity were analyzed by using pH sensitive dye BCECF-AM.
Finally, the re-addition of the Na+-solution and measurement of the pH at the end of each experiment, thefluorescence ratio was calibrated to the appropriate pH using nigericin (2 μM; Glpbio,Shanghai, China)/high K+-solutions at different pH values.
Vet Microbiol 289 (2024): 109916. PMID: 38159369 IF: 3.3 -
Related Biological Data
Vitamin K3 Suppresses Pyroptosis in THP-1 Cells. Vitamin K3 (0, 5, 10, 20, and 30 μM) was used to pretreat THP-1 cells for 1 h before LPS plus nigericin (Nig) induced pyroptosis. (A) Cell viability and (B) supernatant LDH levels were quantified.
Briefly, 1 × 106/mL cells were cultured with RPMI 1640 medium containing 2% FBS overnight and then treated with 1 μg/mL LPS for 3 h, followed by 8 μg/mL Nigericin (GlpBio) treatment for 1 h.
Biol Pharm Bull 46.1 (2023): 52-60. PMID: 36288961 IF: 2.2641
Quality Control & SDS
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- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Nigericin is an antibiotic derived from S. hygroscopicus that acts as a potassium ionophore promoting K+/H+ exchange across mitochondrial membranes. Nigericin can be used as a research tool to disrupt intracellular H+ and K+ concentration, thus altering pH, membrane potential, and cell volume.1,2,3 At 10 μM, nigericin induces egress of T. gondii parasites by inducing efflux of K+.4
Nigericin是一种来源于吸湿链霉菌的抗生素，作为K+/H+离子载体，促进线粒体膜上K+/H+[1]的交换。Nigericin可以是一种NLRP3激活剂，以NALP3依赖的方式诱导IL-1β的释放[2]。Nigericin引发丹毒，这种作用与ROS的形成平行，部分原因是氧化应激的诱导。Nigericin触发细胞凋亡[3]。
[1]. Zotova L, et al. Novel components of an active mitochondrial K(+)/H(+) exchange. J Biol Chem. 2010 May 7;285(19):14399-414.
[2]. Mariathasan S, et al.Cryopyrin activates the inflammasome in response to toxins and ATP.Nature. 2006 Mar 9;440(7081):228-32.
[3]. Bissinger R, et al. Triggering of Suicidal Erythrocyte Death by the Antibiotic Ionophore Nigericin. Basic Clin Pharmacol Toxicol. 2016 May;118(5):381-9.
| Cas No. | 28380-24-7 | SDF | |
| 别名 | 尼日利亚霉素 | ||
| Canonical SMILES | C[C@H]1[C@](O[C@@H]2C[C@](CC[C@@H]3C)([H])O[C@@]3([H])[C@@H](C)C(O)=O)([C@@H]([C@H](OC)C2)C)O[C@](C)([C@]4([H])O[C@](C)([C@]5([H])O[C@]([C@@]([C@H](C[C@H]6C)C)([H])O[C@@]6(O)CO)([H])C[C@@H]5C)CC4)C1 | ||
| 分子式 | C40H68O11 | 分子量 | 724.96 |
| 溶解度 | 1.2mg/mL in DMF, 20mg/mL in Ethanol | 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 | 1.3794 mL | 6.8969 mL | 13.7939 mL |
| 5 mM | 0.2759 mL | 1.3794 mL | 2.7588 mL |
| 10 mM | 0.1379 mL | 0.6897 mL | 1.3794 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。
Nigericin exerts anticancer effects through inhibition of the SRC/STAT3/BCL-2 in osteosarcoma
Biochem Pharmacol 2022 Apr;198:114938.PMID:35114189DOI:10.1016/j.bcp.2022.114938.
The treatment of osteosarcoma has reached a bottleneck period in recent 30 years, there is an urgent need to find new drugs and treatment methods. Nigericin, an antibiotic derived from Streptomyces hygroscopicus, has exerted promising antitumoral effect in various tumors. The anticancer effect of Nigericin in human osteosarcoma has never been reported. In the present study, we explored the anticancer effects of Nigericin in osteosarcoma in vitro and in vivo. Our results showed that Nigericin treatment significantly reduced tumor cell proliferation in dose-dependent and time-dependent in human osteosarcoma cells. Nigericin can inhibit cell growth of osteosarcoma cells, in addition to S-phase cycle arrest, the Nigericin induces apoptosis. Furthermore, bioinformatics predicted that Nigericin exerts anticancer effects through inhibiting SRC/STAT3 signaling pathway in osteosarcoma. The direct binding between SRC and activator of transcription 3 (STAT3) was confirmed by Western blot. Nigericin can down regulate STAT3 and Bcl-2. In order to further elucidate the inhibitory effect of Nigericin on SRC/STAT3/Bcl-2 signal transduction mechanism, we established human osteosarcoma cancer cells stably expressing STAT3. Western blot confirmed that Nigericin exerts anticancer effects on human osteosarcoma cancer cells by directly targeting STAT3. In addition, Nigericin can significantly inhibit tumor migration and invasion. Finally, Nigericin inhibits tumor growth in a mouse osteosarcoma model. The Nigericin targeting the SRC/STAT3/BCL-2 signaling pathway may provide new insights into the molecular mechanism of Nigericin on cancer cells and suggest its possible clinical application in osteosarcoma.
Dehydroepiandrosterone exacerbates nigericin-induced abnormal autophagy and pyroptosis via GPER activation in LPS-primed macrophages
Cell Death Dis 2022 Apr 19;13(4):372.PMID:35440074DOI:10.1038/s41419-022-04841-6.
As a widely acknowledged FDA-approved dietary supplement or over-the-counter medicines, dehydroepiandrosterone (DHEA) exerts anti-inflammatory and immunomodulatory function. Pyroptosis is an important form of programmed cell death (PCD), and which acts a key role in the body's anti-infection and inflammatory responses. But the effects and mechanisms of DHEA on pyroptosis remain unclear. Here, we found that DHEA inhibited the NLRP3 inflammasome components expression by blocking inflammatory signals in lipopolysaccharide (LPS)-primed macrophages, and prevented the bacterial toxin Nigericin (Nig)-induced NLRP3 inflammasome assembly. However, DHEA exacerbated NLRP3-independent cell death in Nig-treated inflammatory macrophages. During this process, DHEA induced the abnormal autophagy, which reflected as the blocking of autophagic flux and the accumulation of autophagy receptor p62 (SQSTM1) protein. In addition, DHEA caused a burst of reactive oxygen species (ROS) and activated extracellular signal-regulated kinase (ERK) phosphorylation in LPS plus Nig-stimulated macrophages but not in LPS-treated macrophages. Mechanistically, the present study certified that the activation of G protein-coupled estrogen receptor (GPER) signal mediated the cell death induced by DHEA in Nig-stimulated inflammatory macrophages, as GPER specific inhibitor G15 alleviated the abnormal autophagy and ultimately prevented the gasdermin D (GSDMD)-mediated pyroptosis induced by DHEA. Collectively, DHEA can exacerbate Nig-induced abnormal autophagy and pyroptosis via activation of GPER in LPS-primed macrophages, which prompts us the potential application value of DHEA in anti-infection or anti-tumor immunity.
Evidence of Nigericin as a potential therapeutic candidate for cancers: A review
Biomed Pharmacother 2021 May;137:111262.PMID:33508621DOI:10.1016/j.biopha.2021.111262.
Emerging studies have shown that Nigericin, an H+, K+ and Pb2+ ionophore, has exhibited a promising anti-cancer activity in various cancers. However, its anti-cancer mechanisms have not been fully elucidated. In this review, the recent progresses on the use of Nigericin in human cancers have been summarized. By exchanging H+ and K+ across cell membranes, Nigericin shows promising anti-cancer activities in in vitro and in vivo as a single agent or in combination with other anti-cancer drugs through decreasing intracellular pH (pHi). The underlying mechanisms of Nigericin also include the inactivation of Wnt/β-catenin signals, blockade of Androgen Receptor (AR) signaling, and activation of Stress-Activated Protein Kinase/c-Jun N-terminal Kinase (SAPK/JNK) signaling pathways. In many cancers, Nigericin is proved to specifically target putative Cancer Stem Cells (CSCs), and its synergistic effects on photodynamic therapy are also reported. Other mechanisms of Nigericin including influencing the mitochondrial membrane potentials, inducing an increase in drug accumulation and autophagy, controlling insulin accumulation in nuclei, and increasing the cytotoxic activity of liposome-entrapped drugs, are also discussed. Notably, the potential adverse effects such as teratogenic effects, insulin resistance and eryptosis shall not be ignored. Taken together, these reports suggest that treatment of cancer cells with Nigericin may offer a novel therapeutic strategy and future potential of translation to clinics.
Nigericin is effective against multidrug resistant gram-positive bacteria, persisters, and biofilms
Front Cell Infect Microbiol 2022 Dec 20;12:1055929.PMID:36605124DOI:10.3389/fcimb.2022.1055929.
Multidrug-resistant (MDR) bacteria pose a significant clinical threat to human health, but the development of antibiotics cannot meet the urgent need for effective agents, especially those that can kill persisters and biofilms. Here, we reported that Nigericin showed potent bactericidal activity against various clinical MDR Gram-positive bacteria, persisters and biofilms, with low frequencies of resistance development. Moreover, Nigericin exhibited favorable in vivo efficacy in deep-seated mouse biofilm, murine skin and bloodstream infection models. With Staphylococcus aureus, Nigericin disrupted ATP production and electron transport chain; cell death was associated with altered membrane structure and permeability. Obtaining nigericin-resistant/tolerant mutants required multiple rounds of challenge, and, cross-resistance to members of several antimicrobial classes was absent, probably due to distinct Nigericin action with the GraSR two-component regulatory system. Thus, our work reveals that Nigericin is a promising antibiotic candidate for the treatment of chronic or recurrent infections caused by Gram-positive bacteria.
Bavachin enhances NLRP3 inflammasome activation induced by ATP or Nigericin and causes idiosyncratic hepatotoxicity
Front Med 2021 Aug;15(4):594-607.PMID:33909257DOI:10.1007/s11684-020-0809-2.
Psoraleae Fructus (PF) is a well-known traditional herbal medicine in China, and it is widely used for osteoporosis, vitiligo, and other diseases in clinical settings. However, liver injury caused by PF and its preparations has been frequently reported in recent years. Our previous studies have demonstrated that PF could cause idiosyncratic drug-induced liver injury (IDILI), but the mechanism underlying its hepatotoxicity remains unclear. This paper reports that bavachin isolated from PF enhances the specific stimuli-induced activation of the NLRP3 inflammasome and leads to hepatotoxicity. Bavachin boosts the secretion of IL-1β and caspase-1 caused by ATP or Nigericin but not those induced by poly(I:C), monosodium urate crystal, or intracellular lipopolysaccharide. Bavachin does not affect AIM2 or NLRC4 inflammasome activation. Mechanistically, bavachin specifically increases the production of nigericin-induced mitochondrial reactive oxygen species among the most important upstream events in the activation of the NLRP3 inflammasome. Bavachin increases the levels of aspartate transaminase and alanine aminotransferase in serum and hepatocyte injury accompanied by the secretion of IL-1β via a mouse model of lipopolysaccharide-mediated susceptibility to IDILI. These results suggest that bavachin specifically enhances the ATP- or nigericin-induced activation of the NLRP3 inflammasome. Bavachin also potentially contributes to PF-induced idiosyncratic hepatotoxicity. Moreover, bavachin and PF should be evaded among patients with diseases linked to the ATP- or nigericin-mediated activation of the NLRP3 inflammasome, which may be a dangerous factor for liver injury.