Background
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]。
参考文献:
[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.
Protocol
| Cell experiment [1]: |
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Cell lines
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HepG2 cell line
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Preparation Method
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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
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0 - 0.4 mM Oleic acid (9-cis-Octadecenoic acid) for 12 hrs
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Applications
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Oleic acid (9-cis-Octadecenoic acid) attenuates PA-induced apoptosis through OA-activated autophagy.
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| Animal experiment [2]: |
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Animal models
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Male Swiss mouse weighing about 25-30 grams
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Preparation Method
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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
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0.3%-3% Oleic acid (9-cis-Octadecenoic acid) in semisolid formulations for 24-72h
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Applications
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Pemulen 3% Oleic acid (9-cis-Octadecenoic acid) and dexamethasone also reduced inflammatory cell infiltration.
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参考文献:
[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.
[2]: 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.
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