Sulfosuccinimidyl oleate (Synonyms: Sulfo-N-succinimidyl oleate)

Sulfosuccinimidyl oleate is a long chain fatty acid that inhibits fatty acid transport into cells. Sulfosuccinimidyl oleate binds the CD36 receptor on the surface of microglia. Anti-inflammatory effect[1].

Sulfosuccinimidyl oleate (20 μM and 50 μM, 24 hours) alone does not alter the cellular viability. Exposure to 100 ng/ml LPS+5 ng/mL IFNγ modestly, yet significantly reduces the viability of the BV2 cells. Co-treatment with Sulfosuccinimidyl oleate prevents the LPS+IFNγ-induced reduction in the cell viability[1]. Sulfosuccinimidyl oleate (50 μM, 24 hours) co-treatment significantly reduces the LPS+IFNγ-induced expression of NOS2 and COX-2 in BV2 cells. Western blot analysis reveals a significant LPS/IFNγ-induced upregulation in the phosphorylated form of the p38, which is prevented by co-treatment with Sulfosuccinimidyl oleate (50 μM, 24 hours)[1].|| Cell Viability Assay[1]||Cell Line:|BV2 cells|Concentration:|20 μM and 50 μM|Incubation Time:|24 hours|Result:|Did not alter the viability of BV2 cells alone. Exposure of BV2 cells to 100 ng/mL LPS and 5 ng/mL IFNγ significantly reduced the viability of BV2 cells while simultaneous treatment with Sulfosuccinimidyl oleate prevented it.|| Western Blot Analysis[1]||Cell Line:|BV2 cells|Concentration:|50 μM |Incubation Time:|24 hours|Result:|Drastically increased the levels of NOS2, COX-2, and P-p38/T-p38.

Sulfosuccinimidyl oleate (50 mg/kg; administered once by single oral gavage) significantly reduces the cortical ischemic infarct size compared to vehicle-treated controls in male BALB/cABom mice with pMCAo model. In addition, Sulfosuccinimidyl oleate at 50 mg/kg is suitable to see a beneficial effect after stroke[1].|| Animal Model:|4-month-old male BALB/cABom mice with pMCAo model[1]|Dosage:|50 mg/kg|Administration:|Administered once by single oral gavage|Result:|Reduced brain damage following ischemia. Attenuated infarct size.

[1]. Dhungana H, et al. Sulfosuccinimidyl oleate sodium is neuroprotective and alleviates stroke-induced neuroinflammation. J Neuroinflammation. 2017 Dec 4;14(1):237.