GlpBio

Palmitic acid

目录号: GN10676纯度: >98.00%同义词: 棕榈酸
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。
Palmitic acid
Cas No.: 57-10-3
规格价格库存数量操作
10g¥380.00现货
1
10mM (in 1mL DMSO)¥450.00现货
1
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产品描述 Description

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]。

实验参考方法 Experimental Reference Method

Cell experiment [1]:

Cell lines

Saos-2 cells

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.

Reaction Conditions

0-800 µM Palmitic acid for 0-48 h

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]:

Animal models

Eight-week-old specific pathogen-free female BALB/c mice

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.

Dosage form

100 µL of Palmitic acid (800 µM) for 14days

Applications

Palmitic acid treatment in mice enhances resistance to Brucella infection and is accompanied by attenuated IL-10 induction during Brucella infection.

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.
[2]. 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.

产品文档 Product Documents

Purity:>98.00%

化学性质Chemical Properties

CAS 号
57-10-3
同义词
棕榈酸
化学名
hexadecanoic acid
SMILES
CCCCCCCCCCCCCCCC(=O)O
分子式
C16H32O2
分子量
256.42 g/mol
溶解性
≥ 51mg/mL in DMSO; ≥ 51mg/mL in Ethanol
保存条件
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°C，然后在超声波浴中震荡一段时间。
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。

计算工具摩尔浓度 / 稀释 / 分子量 / 单位换算 / 体内配方 / 溶解度

g/mol