Palmitic acid (Cetylic acid) is a natural product, a common saturated fatty acid found in animals, plants and microorganisms. Palmitic acid has antitumor activity.

Colo-320-DM cells:0.35 µg/mL, Caco-2 cells:0.75 µg/mL, MCF-7 cells:0.55 µg/mL, WRL-68 cells:1 µg/mL

METHODS: Mouse microglia BV2 were treated with Palmitic acid (25-200 nM) for 6-48 h, and cell viability was measured by MTT.
RESULTS: Palmitic acid had concentration- and time-dependent inhibitory effects on microglia viability. [1]
METHODS: Monocyte-derived dendritic cells MoDC were treated with Palmitic acid (150 μM) for 12 h. The expression of DC co-stimulatory factors was measured by Flow Cytometry.
RESULTS: Palmitic acid induced the expression of CD86 and CD83, indicating that the activation and maturation of MoDC were induced simultaneously. [2]

METHODS: To investigate the effects on adverse biological behaviors in mice, Palmitic acid (0.3-30 μmol/mouse in castor oil) was administered as a single intraperitoneal injection to C57BL/6J mice, and biological behaviors were analyzed 2-24 h later.
RESULTS: In a dose-dependent manner, Palmitic acid rapidly reduced locomotor activity in mice through a mechanism dependent on fatty acid chain length. 24 h after Palmitic acid administration, mice exhibited anxiety-like behaviors, whereas there was no impairment of locomotion, food intake, depression-like behaviors, or spatial memory. [3]
METHODS: To investigate the effects on myocardial injury, Palmitic acid (5 mM in 500 μL solution) was injected intravenously into the tail of wild-type C57BL/6 (B6) and Md2-/- (KO) mice once a day for seven days.
RESULTS: Palmitic acid induced myocardial inflammatory injury via TLR4 accessory protein MD2 and protected Md2 knockout mice from myocardial injury induced by Palmitic acid and high-fat diet. [4]

As sources of PLA2, human recombinant sPLA2 (type IIA) is purified from CHO cells transfected with the PLA2 gene and rabbit recombinant platelet cPLA2 is obtained through its expression in baculovirus. The standard reaction mixture (200 μL) contained 100 mM Tris-HCl buffer (pH 9.0) with 6 mM CaCl2 and 20 nmol 1-acyl-[1-14C]-arachidonyl-sn-glycerophosphoethanolamine (2000 cpm/nmol) in the presence or absence of Tanshinone I. The reaction is started by adding 50 ng purified sPLA2 or cPLA2. After 20 min at 37°C, the free fatty acid generated is analysed. Under these standard conditions, the reaction mixture in the absence of Tanshinone I released approximately 10% of free fatty acid from the phospholipid substrate added[1].

Cell Experiment Solubilisation Formula:
1. Dissolve 1 mg of palmitic acid in 78 μL of anhydrous ethanol to obtain a 50 mM stock solution; if a higher concentration is required, dissolve 1 mg of palmitic acid in 39 μL of anhydrous ethanol to obtain a 100 mM stock solution.
2. Prepare a 10% BSA solution using culture medium (e.g., DMEM); BSA without fatty acids is preferable, with a concentration of 100 mg/mL.
3. For the solvent control group, prepare ethanol and BSA control solutions at the corresponding concentrations without lipids.
4. As an example of preparing 1 mL of a 0.25 mM working solution, mix 5 μL of 50 mM palmitic acid stock solution + 100 μL of 10% BSA solution + 895 μL of culture medium. The final solution will contain 1% BSA. The ethanol concentration should be controlled between 0.1%~0.5%.
5. Filter the working solution using a sterile filter membrane for use in cell processing.

DMSO: 100 mg/mL (389.99 mM), Sonication is recommended.

Ethanol: 40.83 mg/mL (159.23 mM), Sonication is recommended.

10% DMSO+40% PEG300+5% Tween 80+45% Saline: 0.26 mg/mL (1.01 mM), Solution.