Oxidative stress and NF-κB signaling plays a major role in pathogenesis of osteoarthritis. In the present study, we analyzed the potent role of carnosol against osteoarthritis in cells treated using monosodium iodoacetate (MIA) model through in vitro studies. MIA caused dose-dependent cell death and induced programmed cell death by increasing subG1 accumulation and caspase-3 expressions. MIA caused oxidative stress by increasing reactive oxygen species, lipid peroxidation and further induced NF-κB expression and down regulated Nrf-2 levels. Pre-treatment with carnosol significantly protected the cells by reducing the oxidative stress markers and improved the cell viability up to 98%. Further, carnosol down regulated NF-κB nuclear expression with a concomitant increase in Nrf-2 nuclear localization and up regulated the nuclear Nrf-2 levels. Carnosol also inhibited MIA-induced subG1 accumulation and caspase-3 activation. This study demonstrates that, carnosol might act as potent antioxidant and regulate MIA-induced oxidative stress, NF-κB signaling and programmed cell death by up regulating the Nrf-2 levels.

• MeSH
• antioxidancia metabolismus   MeSH
• apoptóza účinky léků   MeSH
• chondrocyty patologie   účinky léků   MeSH
• chrupavka MeSH
• diterpeny abietanové farmakologie   metabolismus   terapeutické užití   MeSH
• faktor 1 související s NF-E2 aplikace a dávkování   MeSH
• jodacetáty farmakologie   škodlivé účinky   MeSH
• kultivované buňky MeSH
• NF-kappa B antagonisté a inhibitory   MeSH
• osteoartróza * metabolismus   patofyziologie   MeSH
• oxidační stres účinky léků   MeSH
• potkani Sprague-Dawley MeSH
• reaktivní formy kyslíku antagonisté a inhibitory   MeSH
• zánět genetika   chemicky indukované   patofyziologie   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH