Palmitic acid
(Synonyms: 棕榈酸) 目录号 : GN10676
棕榈酸 (PA) 是人体中最常见的饱和脂肪酸，可以从饮食中提供，也可以从其他脂肪酸、碳水化合物和氨基酸内源合成。
Cas No.:57-10-3
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
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- Datasheet
| Cell experiment [1]: | |
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Cell lines |
Saos-2 cells |
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Preparation Method |
When the cells reached 70 -80% confluence, they were treated with different concentrations (0-800 µM) of Palmitic acid. At various times (0-48 h) during the treatment, cells were collected and processed for further experiments. In other experiments, Saos-2 were exposed to 200 µM Palmitic acid in the presence or absence of 500 nM 4-PBA, 5 mM 3-MA, 5 µM AY-22989, or 500 nM TG for 24 h. |
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Reaction Conditions |
0-800 µM Palmitic acid for 0-48 h |
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Applications |
Palmitic acid treatment decreased cell viability in a dose-dependent manner, and the minimum effective dose was 100 µM Palmitic acid. |
| Animal experiment [2]: | |
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Animal models |
Eight-week-old specific pathogen-free female BALB/c mice |
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Preparation Method |
Prior to infection, mice were treated orally using a gavage needle with 100 L of Palmitic acid (800 uM) or vehicle (PBS containing 0.1% ethanol and 0.1% BSA) for 3 d. Oral treatment was continued for 14 d post-infection. |
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Dosage form |
100 µL of Palmitic acid (800 µM) for 14days |
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Applications |
Palmitic acid treatment in mice enhances resistance to Brucella infection and is accompanied by attenuated IL-10 induction during Brucella infection. |
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References: [1]. Yang L, Guan G, et,al. Palmitic acid induces human osteoblast-like Saos-2 cell apoptosis via endoplasmic reticulum stress and autophagy. Cell Stress Chaperones. 2018 Nov;23(6):1283-1294. doi: 10.1007/s12192-018-0936-8. Epub 2018 Sep 7. PMID: 30194633; PMCID: PMC6237680. |
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Palmitic acid (PA) is the most common saturated fatty acid found in the human body and can be provided in the diet or synthesized endogenously from other fatty acids, carbohydrates and amino acids[9].
Palmitic acid treatment decreased cell viability in a dose-dependent manner, and the minimum effective dose was 100 μM Palmitic acid. Palmitic acid treatment increased the percentage of apoptotic Saos-2 cells in a dose-dependent manner, IC50 value is about 200 μM[3]. Obesity-related neurodegenerative diseases are associated with elevated saturated fatty acids (SFAs) in the brain. Palmitic acid induces significant neuron cell cycle arrest in the G2/M phase in SH-SY5Y cells[2]. Palmitic acid was able to cause an increase in autophagic flux. PA-induced autophagy was found to be independent of mTOR regulation. Inhibition of autophagy sensitized the cells to Palmitic acid-induced apoptosis, suggesting the pro-survival function of autophagy induced by Palmitic acid [4]. Treatment of SMMC-7721 cells with Palmitic acid increased LC3-II expression in time- and dose-dependent manners, whereas the unsaturated fatty acid oleic acid had no effect[5]. Palmitic acid can induce the expression of glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP) in in mouse granulosa cells[1].
Transient higher levels of Palmitic acid exposure in pregnant mice activates NLRP3 inflammasome and induces placental inflammation, resulting in the incidence of absorption[6]. In a dose-dependent fashion, palmitic acid rapidly reduced mouse locomotor activity by a mechanism that did not rely on TLR4, MyD88, IL-1, IL-6 or TNFα but was dependent on fatty acid chain length. Twenty-four hours after palmitic acid administration mice exhibited anxiety-like behavior without impairment in locomotion, food intake, depressive-like behavior or spatial memory. Additionally, the serotonin metabolite 5-HIAA was increased by 33% in the amygdala 24h after palmitic acid treatment[7]. Palmitic acid treatment in mice enhances resistance to Brucella infection and is accompanied by attenuated IL-10 induction during Brucella infection[8].
References:
[1]. Harada H, Yamashita U, et,al. Antitumor activity of palmitic acid found as a selective cytotoxic substance in a marine red alga. Anticancer Res. 2002 Sep-Oct;22(5):2587-90. PMID: 12529968.
[2]. Hsiao YH, Lin CI, et,al.Palmitic acid-induced neuron cell cycle G2/M arrest and endoplasmic reticular stress through protein palmitoylation in SH-SY5Y human neuroblastoma cells. Int J Mol Sci. 2014 Nov 13;15(11):20876-99. doi: 10.3390/ijms151120876. PMID: 25402647; PMCID: PMC4264201.
[3]. Yang L, Guan G, et,al.Palmitic acid induces human osteoblast-like Saos-2 cell apoptosis via endoplasmic reticulum stress and autophagy. Cell Stress Chaperones. 2018 Nov;23(6):1283-1294. doi: 10.1007/s12192-018-0936-8. Epub 2018 Sep 7. PMID: 30194633; PMCID: PMC6237680.
[4]. Tan SH, Shui G, et,al. Induction of autophagy by palmitic acid via protein kinase C-mediated signaling pathway independent of mTOR (mammalian target of rapamycin). J Biol Chem. 2012 Apr 27;287(18):14364-76. doi: 10.1074/jbc.M111.294157. Epub 2012 Mar 9. Erratum in: J Biol Chem. 2014 Apr 4;289(14):9501. PMID: 22408252; PMCID: PMC3340233.
[5]. Tu QQ, Zheng RY, et,al.Palmitic acid induces autophagy in hepatocytes via JNK2 activation. Acta Pharmacol Sin. 2014 Apr;35(4):504-12. doi: 10.1038/aps.2013.170. Epub 2014 Mar 10. PMID: 24608675; PMCID: PMC4813717.
[6]. Sano M, Shimazaki S, et,al. Palmitic acid activates NLRP3 inflammasome and induces placental inflammation during pregnancy in mice. J Reprod Dev. 2020 Jun 12;66(3):241-248. doi: 10.1262/jrd.2020-007. Epub 2020 Feb 27. PMID: 32101829; PMCID: PMC7297640.
[7]. Moon ML, Joesting JJ, et,al.The saturated fatty acid, palmitic acid, induces anxiety-like behavior in mice. Metabolism. 2014 Sep;63(9):1131-40. doi: 10.1016/j.metabol.2014.06.002. Epub 2014 Jun 9. PMID: 25016520; PMCID: PMC4151238.
[8]. Reyes AWB, Huy TXN,et,al. Protection of palmitic acid treatment in RAW264.7 cells and BALB/c mice during Brucella abortus 544 infection. J Vet Sci. 2021 Mar;22(2):e18. doi: 10.4142/jvs.2021.22.e18. PMID: 33774934; PMCID: PMC8007444.
[9].Carta G, Murru E, Banni S, Manca C. Palmitic Acid: Physiological Role, Metabolism and Nutritional Implications. Front Physiol. 2017 Nov 8;8:902. doi: 10.3389/fphys.2017.00902. PMID: 29167646; PMCID: PMC5682332.
棕榈酸 (PA) 是人体中最常见的饱和脂肪酸，可以从饮食中提供，也可以从其他脂肪酸、碳水化合物和氨基酸内源合成[9]。
棕榈酸处理以剂量依赖性方式降低细胞活力，最低有效剂量为 100 μM 棕榈酸。棕榈酸处理以剂量依赖的方式增加凋亡的Saos-2细胞的百分比，IC50值约为200 μM[3]。肥胖相关的神经退行性疾病与大脑中饱和脂肪酸 (SFA) 升高有关。棕榈酸在 SH-SY5Y 细胞中诱导显着的 G2/M 期神经元细胞周期阻滞[2]。棕榈酸能够引起自噬通量的增加。发现 PA 诱导的自噬独立于 mTOR 调节。自噬的抑制使细胞对棕榈酸诱导的细胞凋亡敏感，表明棕榈酸诱导的自噬具有促生存作用[4]。用棕榈酸处理 SMMC-7721 细胞后，LC3-II 的表达呈时间和剂量依赖性增加，而不饱和脂肪酸油酸没有影响[5]。棕榈酸可诱导小鼠颗粒细胞葡萄糖调节蛋白78（GRP78）和CCAAT/增强子结合蛋白同源蛋白（CHOP）的表达[1]。
怀孕小鼠短暂接触较高水平的棕榈酸会激活 NLRP3 炎性体并诱发胎盘炎症，从而导致吸收发生[6]。以剂量依赖的方式，棕榈酸通过一种不依赖于 TLR4、MyD88、IL-1、IL-6 或 TNFα 但依赖于脂肪酸链长度的机制迅速降低小鼠的运动活性。给予棕榈酸 24 小时后，小鼠表现出焦虑样行为，而运动、食物摄入、抑郁样行为或空间记忆没有受损。此外，棕榈酸处理 24 小时后杏仁核中的血清素代谢物 5-HIAA 增加了 33%[7]。小鼠的棕榈酸治疗增强了对布鲁氏菌感染的抵抗力，并伴随着布鲁氏菌感染期间 IL-10 的减弱[8]。
| Cas No. | 57-10-3 | SDF | |
| 别名 | 棕榈酸 | ||
| 化学名 | hexadecanoic acid | ||
| Canonical SMILES | CCCCCCCCCCCCCCCC(=O)O | ||
| 分子式 | C16H32O2 | 分子量 | 256.42 |
| 溶解度 | ≥ 51mg/mL in DMSO; ≥ 51mg/mL in Ethanol | 储存条件 | Store at -20°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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.8999 mL | 19.4993 mL | 38.9985 mL |
| 5 mM | 0.78 mL | 3.8999 mL | 7.7997 mL |
| 10 mM | 0.39 mL | 1.9499 mL | 3.8999 mL |
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| 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 |
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Palmitic acid induces human osteoblast-like Saos-2 cell apoptosis via endoplasmic reticulum stress and autophagy
Cell Stress Chaperones2018 Nov;23(6):1283-1294.PMID: 30194633DOI: 10.1007/s12192-018-0936-8
Palmitic acid (PA) is the most common saturated long-chain fatty acid in food that causes cell apoptosis. However, little is known about the molecular mechanisms of PA toxicity. In this study, we explore the effects of PA on proliferation and apoptosis in human osteoblast-like Saos-2 cells and uncover the signaling pathways involved in the process. Our study showed that endoplasmic reticulum (ER) stress and autophagy are involved in PA-induced Saos-2 cell apoptosis. We found that PA inhibited the viability of Saos-2 cells in a dose- and time-dependent manner. At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux. Inhibiting ER stress with 4-PBA diminished the PA-induced cell apoptosis, activated autophagy, and increased the expression of Caspase 3 and BAX. Inhibiting autophagy with 3-MA attenuated the PA and ER stress-induced cell apoptosis and the apoptosis-related gene expression (Caspase 3 and BAX), but seemed to have no obvious effects on ER stress, although the CHOP expression was downregulated. Taken together, our results suggest that PA-induced Saos-2 cell apoptosis is activated via ER stress and autophagy, and the activation of autophagy depends on the ER stress during this process.
Palmitic Acid-Rich High-Fat Diet Exacerbates Experimental Pulmonary Fibrosis by Modulating Endoplasmic Reticulum Stress
Am J Respir Cell Mol Biol2019 Dec;61(6):737-746.PMID: 31461627DOI: 10.1165/rcmb.2018-0324OC
The impact of lipotoxicity on the development of lung fibrosis is unclear. Saturated fatty acids, such as palmitic acid (PA), activate endoplasmic reticulum (ER) stress, a cellular stress response associated with the development of idiopathic pulmonary fibrosis (IPF). We tested the hypothesis that PA increases susceptibility to lung epithelial cell death and experimental fibrosis by modulating ER stress. Total liquid chromatography and mass spectrometry were used to measure fatty acid content in IPF lungs. Wild-type mice were fed a high-fat diet (HFD) rich in PA or a standard diet and subjected to bleomycin-induced lung injury. Lung fibrosis was determined by hydroxyproline content. Mouse lung epithelial cells were treated with PA. ER stress and cell death were assessed by Western blotting, TUNEL staining, and cell viability assays. IPF lungs had a higher level of PA compared with controls. Bleomycin-exposed mice fed an HFD had significantly increased pulmonary fibrosis associated with increased cell death and ER stress compared with those fed a standard diet. PA increased apoptosis and activation of the unfolded protein response in lung epithelial cells. This was attenuated by genetic deletion and chemical inhibition of CD36, a fatty acid transporter. In conclusion, consumption of an HFD rich in saturated fat increases susceptibility to lung fibrosis and ER stress, and PA mediates lung epithelial cell death and ER stress via CD36. These findings demonstrate that lipotoxicity may have a significant impact on the development of lung injury and fibrosis by enhancing pro-death ER stress pathways.
[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 Zhi2018 Jun 20;26(6):451-456.PMID: 30317760DOI: 10.3760/cma.j.issn.1007-3418.2018.06.012
Objective: To explore the effects of oleic acid and palmitic acid on lipid deposition and mTOR/S6K1/SREBP-1c pathways in HepG2 cells. Methods: The model of steatosis was established with induction of oleic acid and palmitic acid and was intervened by rapamycin. The changes in lipid droplets were observed after staining the cells with oil Red O. Intracellular triglyceride (TG) contents in cells were measured by TG kit. mTOR, S6K1, and SREBP-1c mRNA expression levels were detected using QRT-PCR. Western blot was used to determine protein expression levels of mTOR, S6K1 and SREBP-1c. Results: Both fatty acids increased lipid droplets in HepG2 cells. Fatty degeneration with elevated TG occurred with significant changes in oleic acid group lipids. Rapamycin alleviated lipid deposition caused by oleic acid and palmitic acid and inhibited their induction of increased expression of mTOR, S6K1, and SREBP-1c. QRT-PCR and Western blot results showed that mRNA and protein expressions of mTOR, S6K1, and SREBP-1c in oleic acid and palmitic acid group were significantly higher than the control group (P < 0.05). The increase was more pronounced in the palmitic acid group (P < 0.05); however, after rapamycin intervention, the expression of mRNA and protein in the three groups were significantly lower (P < 0.05), and the change in palmitic acid group was more pronounced (P < 0.05). Conclusion: Oleic acid and palmitic acid can induce lipid deposition in HepG2 cells and increase expression of every component of mTOR/S6K1/SREBP-1c pathway; however, Oleic acid-induced lipid deposition is more pronounced, and the mTOR, S6K1, and SREBP-1c pathway change is more obvious in palmitic acid. Rapamycin has high potent inhibitory effect on palmitic acid-induced lipid deposition. These results specify that lipid synthesis involved in the mTOR/S6K1/SREBP-1c pathways are mainly associated to palmitic acid in HepG2 cells, whereas other signaling pathway may mediate oleic acid-induced lipid synthesis.
Palmitic acid promotes resistin-induced insulin resistance and inflammation in SH-SY5Y human neuroblastoma
Sci Rep2021 Mar 8;11(1):5427.PMID: 33686181DOI: 10.1038/s41598-021-85018-7
Saturated fatty acids such as palmitic acid promote inflammation and insulin resistance in peripheral tissues, contrasting with the protective action of polyunsaturated fatty acids such docosahexaenoic acid. Palmitic acid effects have been in part attributed to its potential action through Toll-like receptor 4. Beside, resistin, an adipokine, also promotes inflammation and insulin resistance via TLR4. In the brain, palmitic acid and resistin trigger neuroinflammation and insulin resistance, but their link at the neuronal level is unknown. Using human SH-SY5Yneuroblastoma cell line we show that palmitic acid treatment impaired insulin-dependent Akt and Erk phosphorylation whereas DHA preserved insulin action. Palmitic acid up-regulated TLR4 as well as pro-inflammatory cytokines IL6 and TNF¦Á contrasting with DHA effect. Similarly to palmitic acid, resistin treatment induced the up-regulation of IL6 and TNF¦Á as well as NF¦ʂ activation. Importantly, palmitic acid potentiated the resistin-dependent NFkB activation whereas DHA abolished it. The recruitment of TLR4 to membrane lipid rafts was increased by palmitic acid treatment; this is concomitant with the augmentation of resistin-induced TLR4/MYD88/TIRAP complex formation mandatory for TLR4 signaling. In conclusion, palmitic acid increased TLR4 expression promoting resistin signaling through TLR4 up-regulation and its recruitment to membrane lipid rafts.
Palmitic Acid Lipotoxicity in Microglia Cells Is Ameliorated by Unsaturated Fatty Acids
Int J Mol Sci2021 Aug 23;22(16):9093.PMID: 34445796DOI: 10.3390/ijms22169093
Obesity and metabolic syndrome are associated with cognitive decline and dementia. Palmitic acid (PA) is increased in the cerebrospinal fluid of obese patients with cognitive impairment. This study was therefore designed to examine fatty acid (FA) lipotoxicity in BV2 microglia cells. We found that PA induced time- and dose-dependent decrease in cell viability and increase in cell death without affecting the cell cycle profile and that PA lipotoxicity did not depend on cell surface free fatty acid receptors but rather on FA uptake. Treatment with sulfosuccinimidyl oleate (SSO), an irreversible inhibitor of fatty acid translocase CD36, significantly inhibited FA uptake in BSA- and PA-treated cells and blocked PA-induced decrease in cell viability. Inhibition of ER stress or treatment with N-acetylcysteine was not able to rescue PA lipotoxicity. Our study also showed that unsaturated fatty acids (UFAs), such as linoleic acid (LA), oleic acid (OA), ¦Á-linolenic acid (ALA), and docosahexaenoic acid (DHA), were not lipotoxic but instead protected microglia against PA-induced decrease in cell viability. Co-treatment of PA with LA, OA, and DHA significantly inhibited FA uptake in PA-treated cells. All UFAs tested induced the incorporation of FAs into and the amount of neutral lipids, while PA did not significantly affect the amount of neutral lipids compared with BSA control.