| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10g | 电议 |
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.
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 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. |
| 产品描述 | 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: |
m.cnreagent.com