Oleic acid (9-cis-Octadecenoic acid)
(Synonyms: 油酸; 9-cis-Octadecenoic acid; 9Z-Octadecenoic acid) 目录号 : GC30110
油酸（9-顺式-十八碳烯酸）是一种丰富的单不饱和脂肪酸。
Cas No.:112-80-1
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
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- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
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Cell lines |
HepG2 cell line |
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Preparation Method |
Effects of Oleic acid (9-cis-Octadecenoic acid) and EPA on PA-induced inhibition of HepG2 cell viability HepG2 cells were incubated for 12 h in the absence or presence of 0.5 mM PA and various concentrations (0 0.4 mM) of Oleic acid (9-cis-Octadecenoic acid) or EPA. |
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Reaction Conditions |
0 - 0.4 mM Oleic acid (9-cis-Octadecenoic acid) for 12 hrs |
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Applications |
Oleic acid (9-cis-Octadecenoic acid) attenuates PA-induced apoptosis through OA-activated autophagy. |
| Animal experiment [2]: | |
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Animal models |
Male Swiss mouse weighing about 25-30 grams |
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Preparation Method |
Mouse ear was topically treated after UVB irradiation with semisolid formulations (15 mg/ear inculding Oleic acid (9-cis-Octadecenoic acid)), with the aid of a spatula, according to the experimental groups. |
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Dosage form |
0.3%-3% Oleic acid (9-cis-Octadecenoic acid) in semisolid formulations for 24-72h |
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Applications |
Pemulen 3% Oleic acid (9-cis-Octadecenoic acid) and dexamethasone also reduced inflammatory cell infiltration. |
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References: [1]: Sun Y, Wang J, et,al.Oleic Acid and Eicosapentaenoic Acid Reverse Palmitic Acid-induced Insulin Resistance in Human HepG2 Cells via the Reactive Oxygen Species/JUN Pathway. Genomics Proteomics Bioinformatics. 2021 Oct;19(5):754-771. doi: 10.1016/j.gpb.2019.06.005. Epub 2021 Feb 23. PMID: 33631425; PMCID: PMC9170756. |
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Oleic acid (9-cis-Octadecenoic acid) is a monounsaturated Omega-9 fatty acid found in plants and animals[1]. It is a Na+/K+ ATPase activator[2].
Oleic acid (9-cis-Octadecenoic acid) or EPA treatment alone inhibited cell viability, similar to PA treatment, but PA and OA (PA+OA) or combined PA and EPA (PA+EPA) treatment increased cell viability in HepG2 cells compared with PA treatment alone PA+OA.The growth and proliferation effects of the treatment are consistent with previous observations that Oleic acid (9-cis-Octadecenoic acid) attenuates PA-induced apoptosis through OA-activated autophagy[4]. Oleic acid (9-cis-Octadecenoic acid) and palmitic acid can induce lipid deposition in HepG2 cells and increase expression of every component of mTOR/S6K1/SREBP-1c pathway[3]. Oleic acid (9-cis-Octadecenoic acid) caused a concentration- and time-dependent damage with typical apoptotic features in cortical and hippocampal cultures from embryonic and neonatal rats, respectively, as well as in human neuroblastoma SH-SY5Y cells[7].
Oleic acid (9-cis-Octadecenoic acid) in semisolids, especially Pemulen TR2-based ones, presented suitable characteristics for cutaneous administration and its anti-inflammatory activity seems to occur via glucocorticoid receptors. Oleic acid (9-cis-Octadecenoic acid) was also capable to reduce croton oil-induced skin inflammation. Besides, the ex vivo skin permeation study indicated that OA reaches the receptor medium, which correlates with a systemic absorption in vivo[5].In mice,the reduction of dopamine and oxidant effect during cytarabine treatment could result in brain injury but could be prevented by Oleic acid (9-cis-Octadecenoic acid)supplementation[6].
油酸（9-顺式-十八碳烯酸）是一种单不饱和的Omega-9脂肪酸，存在于植物和动物中。它可以激活Na+/K+ ATPase。
单独使用油酸（9-顺式-十八碳烯酸）或EPA处理会抑制细胞的存活能力，与PA处理类似。但是，PA和OA（PA+OA）或联合使用PA和EPA（PA+EPA）处理相比于仅使用PA处理时可以增加HepG2细胞的存活能力。这种治疗对生长和增殖的影响与之前观察到的油酸通过激活自噬减轻了由PA引起的细胞凋亡一致[4]。油酸和棕榈酸可以诱导HepG2细胞中脂质沉积，并增加mTOR/S6K1/SREBP-1c通路每个组分的表达[3]。浓度依赖性地、具有典型凋亡特征地损害了来自大鼠胚胎和新生儿海马及皮层培养以及人神经母细胞瘤SH-SY5Y 细胞中发现了油酸所致[7]。
在半固态物中，特别是基于Pemulen TR2的物质中，油酸（9-顺式-十八碳烯酸）表现出适合皮肤给药的特性，并且其抗炎作用似乎是通过糖皮质激素受体发挥的。油酸（9-顺式-十八碳烯酸）还能够减少蓖麻油引起的皮肤炎症。此外，离体皮肤渗透实验表明OA可以到达受体介质，这与 vivo 中的系统吸收相关[5]。在小鼠中，在紫杉醇治疗期间降低多巴胺和氧化剂效应可能导致脑损伤，但可以通过补充油酸（9-顺式-十八碳烯酸）来预防[6]。
References:
[1]: Jack-Hays MG, Xie Z, et,al. Activation of Na+/K(+)-ATPase by fatty acids, acylglycerols, and related amphiphiles: structure-activity relationship. Biochim Biophys Acta. 1996 Feb 21;1279(1):43-8. doi: 10.1016/0005-2736(95)00245-6. PMID: 8624359.
[2]: Li S, Zhou T, et,al.High metastaticgastric and breast cancer cells consume oleic acid in an AMPK dependent manner. PLoS One. 2014 May 13;9(5):e97330. doi: 10.1371/journal.pone.0097330. PMID: 24823908; PMCID: PMC4019637.
[3]: Zhou YP, Wu R, et,al. [Comparison of effects of oleic acid and palmitic acid on lipid deposition and mTOR / S6K1 / SREBP-1c pathway in HepG2 cells]. Zhonghua Gan Zang Bing Za Zhi. 2018 Jun 20;26(6):451-456. Chinese. doi: 10.3760/cma.j.issn.1007-3418.2018.06.012. PMID: 30317760.
[4]: Sun Y, Wang J, et,al.Oleic Acid and Eicosapentaenoic Acid Reverse Palmitic Acid-induced Insulin Resistance in Human HepG2 Cells via the Reactive Oxygen Species/JUN Pathway. Genomics Proteomics Bioinformatics. 2021 Oct;19(5):754-771. doi: 10.1016/j.gpb.2019.06.005. Epub 2021 Feb 23. PMID: 33631425; PMCID: PMC9170756.
[5]: Pegoraro NS, Camponogara C, et,al.Oleic acid-containing semisolid dosage forms exhibit in vivo anti-inflammatory effect via glucocorticoid receptor in a UVB radiation-induced skin inflammation model. Inflammopharmacology. 2020 Jun;28(3):773-786. doi: 10.1007/s10787-019-00675-5. Epub 2019 Dec 4. PMID: 31802387.
[6]: GuzmÁn DC, Brizuela NO, et,al. Oleic Acid Protects Against Oxidative Stress Exacerbated by Cytarabine and Doxorubicin in Rat Brain. Anticancer Agents Med Chem. 2016;16(11):1491-1495. doi: 10.2174/1871520615666160504093652. PMID: 27141883.
[7]: Zhu Y, Schwarz S, et,al.Oleic acid causes apoptosis and dephosphorylates Bad. Neurochem Int. 2005 Jan;46(2):127-35. doi: 10.1016/j.neuint.2004.08.003. PMID: 15627513.
| Cas No. | 112-80-1 | SDF | |
| 别名 | 油酸; 9-cis-Octadecenoic acid; 9Z-Octadecenoic acid | ||
| Canonical SMILES | CCCCCCCC/C=C\CCCCCCCC(O)=O | ||
| 分子式 | C18H34O2 | 分子量 | 282.46 |
| 溶解度 | DMSO : ≥ 62.5 mg/mL (221.27 mM) | 储存条件 | Store at 2-8°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 | 3.5403 mL | 17.7016 mL | 35.4032 mL |
| 5 mM | 0.7081 mL | 3.5403 mL | 7.0806 mL |
| 10 mM | 0.354 mL | 1.7702 mL | 3.5403 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。
Role of Oleic acid in the Gut-Liver Axis: From Diet to the Regulation of Its Synthesis via Stearoyl-CoA Desaturase 1 (SCD1)
Nutrients 2019 Sep 24;11(10):2283.31554181 PMC6835877
The consumption of an olive oil rich diet has been associated with the diminished incidence of cardiovascular disease and cancer. Several studies have attributed these beneficial effects to Oleic acid (C18 n-9), the predominant fatty acid principal component of olive oil. Oleic acid is not an essential fatty acid since it can be endogenously synthesized in humans. Stearoyl-CoA desaturase 1 (SCD1) is the enzyme responsible for Oleic acid production and, more generally, for the synthesis of monounsaturated fatty acids (MUFA). The saturated to monounsaturated fatty acid ratio affects the regulation of cell growth and differentiation, and alteration in this ratio has been implicated in a variety of diseases, such as liver dysfunction and intestinal inflammation. In this review, we discuss our current understanding of the impact of gene-nutrient interactions in liver and gut diseases, by taking advantage of the role of SCD1 and its product Oleic acid in the modulation of different hepatic and intestinal metabolic pathways.
An overview of the modulatory effects of Oleic acid in health and disease
Mini Rev Med Chem 2013 Feb;13(2):201-10.23278117
Evidences in the last years have showed the effects of Oleic acid (OA) in human health and disease. Olive oil, rich in Oleic acid, is supposed to present modulatory effects in a wide physiological functions, while some studies also suggest a beneficial effect on cancer, autoimmune and inflammatory diseases, besides its ability to facilitate wound healing. Although the OA role in immune responses are still controversial, the administration of olive oil containing diets may improve the immune response associated to a more successful elimination of pathogens such as bacteria and fungi, by interfering in many components of this system such as macrophages, lymphocytes and neutrophils. Then, novel putative therapies for inflammatory and infectious diseases could be developed based on the characteristics presented by unsaturated fatty acids like OA. Finally, the purpose of this work was to review some of the modulatory effects of OA on inflammatory diseases and health, aiming at high lightening its potential role on the future establishment of novel therapeutic approaches for infections, inflammatory, immune, cardiovascular diseases or skin repair based on this fatty acid mainly found in the Mediterranean diet.
Triglyceride accumulation protects against fatty acid-induced lipotoxicity
Proc Natl Acad Sci U S A 2003 Mar 18;100(6):3077-82.12629214 PMC152249
Excess lipid accumulation in non-adipose tissues is associated with insulin resistance, pancreatic beta-cell apoptosis and heart failure. Here, we demonstrate in cultured cells that the relative toxicity of two common dietary long chain fatty acids is related to channeling of these lipids to distinct cellular metabolic fates. Oleic acid supplementation leads to triglyceride accumulation and is well tolerated, whereas excess palmitic acid is poorly incorporated into triglyceride and causes apoptosis. Unsaturated fatty acids rescue palmitate-induced apoptosis by channeling palmitate into triglyceride pools and away from pathways leading to apoptosis. Moreover, in the setting of impaired triglyceride synthesis, oleate induces lipotoxicity. Our findings support a model of cellular lipid metabolism in which unsaturated fatty acids serve a protective function against lipotoxicity though promotion of triglyceride accumulation.
Oleic acid and Eicosapentaenoic Acid Reverse Palmitic Acid-induced Insulin Resistance in Human HepG2 Cells via the Reactive Oxygen Species/JUN Pathway
Genomics Proteomics Bioinformatics 2021 Oct;19(5):754-771.33631425 PMC9170756
Oleic acid (OA), a monounsaturated fatty acid (MUFA), has previously been shown to reverse saturated fatty acid palmitic acid (PA)-induced hepatic insulin resistance (IR). However, its underlying molecular mechanism is unclear. In addition, previous studies have shown that eicosapentaenoic acid (EPA), a ω-3 polyunsaturated fatty acid (PUFA), reverses PA-induced muscle IR, but whether EPA plays the same role in hepatic IR and its possible mechanism involved need to be further clarified. Here, we confirmed that EPA reversed PA-induced IR in HepG2 cells and compared the proteomic changes in HepG2 cells after treatment with different free fatty acids (FFAs). A total of 234 proteins were determined to be differentially expressed after PA+OA treatment. Their functions were mainly related to responses to stress and endogenous stimuli, lipid metabolic process, and protein binding. For PA+EPA treatment, the PA-induced expression changes of 1326 proteins could be reversed by EPA, 415 of which were mitochondrial proteins, with most of the functional proteins involved in oxidative phosphorylation (OXPHOS) and tricarboxylic acid (TCA) cycle. Mechanistic studies revealed that the protein encoded by JUN and reactive oxygen species (ROS) play a role in OA- and EPA-reversed PA-induced IR, respectively. EPA and OA alleviated PA-induced abnormal adenosine triphosphate (ATP) production, ROS generation, and calcium (Ca2+) content. Importantly, H2O2-activated production of ROS increased the protein expression of JUN, further resulting in IR in HepG2 cells. Taken together, we demonstrate that ROS/JUN is a common response pathway employed by HepG2 cells toward FFA-regulated IR.
Walnuts and Vegetable Oils Containing Oleic acid Differentially Affect the Gut Microbiota and Associations with Cardiovascular Risk Factors: Follow-up of a Randomized, Controlled, Feeding Trial in Adults at Risk for Cardiovascular Disease
J Nutr 2020 Apr 1;150(4):806-817.31848609 PMC7138683
Background: It is unclear whether the favorable effects of walnuts on the gut microbiota are attributable to the fatty acids, including α-linolenic acid (ALA), and/or the bioactive compounds and fiber. Objective: This study examined between-diet gut bacterial differences in individuals at increased cardiovascular risk following diets that replace SFAs with walnuts or vegetable oils. Methods: Forty-two adults at cardiovascular risk were included in a randomized, crossover, controlled-feeding trial that provided a 2-wk standard Western diet (SWD) run-in and three 6-wk isocaloric study diets: a diet containing whole walnuts (WD; 57-99 g/d walnuts; 2.7% ALA), a fatty acid-matched diet devoid of walnuts (walnut fatty acid-matched diet; WFMD; 2.6% ALA), and a diet replacing ALA with Oleic acid without walnuts (Oleic acid replaces ALA diet; ORAD; 0.4% ALA). Fecal samples were collected following the run-in and study diets to assess gut microbiota with 16S rRNA sequencing and Qiime2 for amplicon sequence variant picking. Results: Subjects had elevated BMI (30 ± 1 kg/m2), blood pressure (121 ± 2/77 ± 1 mmHg), and LDL cholesterol (120 ± 5 mg/dL). Following the WD, Roseburia [relative abundance (RA) = 4.2%, linear discriminant analysis (LDA) = 4], Eubacterium eligensgroup (RA = 1.4%, LDA = 4), LachnospiraceaeUCG001 (RA = 1.2%, LDA = 3.2), Lachnospiraceae UCG004 (RA = 1.0%, LDA = 3), and Leuconostocaceae (RA = 0.03%, LDA = 2.8) were most abundant relative to taxa in the SWD (P ≿0.05 for all). The WD was also enriched in Gordonibacter relative to the WFMD. Roseburia (3.6%, LDA = 4) and Eubacterium eligensgroup (RA = 1.5%, LDA = 3.4) were abundant following the WFMD, and Clostridialesvadin BB60group (RA = 0.3%, LDA = 2) and gutmetagenome (RA = 0.2%, LDA = 2) were most abundant following the ORAD relative to the SWD (P ≿0.05 for all). Lachnospiraceae were inversely correlated with blood pressure and lipid/lipoprotein measurements following the WD. Conclusions: The results indicate similar enrichment of Roseburia following the WD and WFMD, which could be explained by the fatty acid composition. Gordonibacter enrichment and the inverse association between Lachnospiraceae and cardiovascular risk factors following the WD suggest that the gut microbiota may contribute to the health benefits of walnut consumption in adults at cardiovascular risk. This trial was registered at clinicaltrials.gov as NCT02210767.