Sulfosuccinimidyl oleate sodium is a long-chain fatty acid that inhibits fatty acid transport into cells and is a potent and irreversible inhibitor of the mitochondrial respiratory chain and has anti-inflammatory properties without causing cytotoxic effects.

METHODS: BV2 cells were treated with Sulfosuccinimidyl oleate sodium (50μM) and exposed to 100 ng/ml LPS and 5 ng/ml IFNγ. The mRNA expression levels of IL-6, NOS2, Nrf2 and HO-1 were detected by qRT-PCR; WB detects the expression of NOS2, COX-2, HO-1, p-p38, t-p38 and β-actin in cells.
RESULTS Combined treatment with Sulfosuccinimidyl oleate sodium blocked the increase in the expression levels of IL-6 and NOS2; co-treatment with SSO allowed LPS + IFNγ to reduce the Nrf2 expression level back to the basal level; combined treatment with Sulfosuccinimidyl oleate sodium significantly reduced the expression level of Nrf2. Expression of NOS2 and COX-2 in BV2 cells induced by LPS + IFNγ; Sulfosuccinimidyl oleate sodium alone increased the basal protein level of HO-1, but did not change the level of HO-1 induced by LPS + IFNγ. [1]

METHODS: Sulfosuccinimidyl oleate sodium (50 mg/kg, oral) was treated in pMCAo mice and its therapeutic effect was tested; mice were analyzed for ischemia-induced cerebral microgliosis by immunohistochemical staining against Iba-1 3 days after stroke.
RESULTS Sulfosuccinimidyl oleate sodium significantly reduced the size of cortical ischemic infarcts, and significantly upregulated microgliosis was detected in the peri-ischemic area of ​​sulfosuccinimidyl oleate sodium-treated mice 3 days after stroke. A significant decrease in the degree of Iba-1 immunoreactivity was observed in the peri-ischemic area. [1]