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Carnosol ameliorates monosodium iodoacetate-induced osteoarthritis by targeting NF-κB and Nrf-2 in primary rat chondrocytes
Jun Wang, Guang Yang, Yong-Xin Hua, Tao Sun, Chen Gao, Qing Xia, Bin Li
Language English Country Czech Republic
- MeSH
- Antioxidants metabolism MeSH
- Apoptosis drug effects MeSH
- Chondrocytes pathology drug effects MeSH
- Cartilage MeSH
- Abietanes pharmacology metabolism therapeutic use MeSH
- NF-E2-Related Factor 1 administration & dosage MeSH
- Iodoacetates pharmacology adverse effects MeSH
- Cells, Cultured MeSH
- NF-kappa B antagonists & inhibitors MeSH
- Osteoarthritis * metabolism physiopathology MeSH
- Oxidative Stress drug effects MeSH
- Rats, Sprague-Dawley MeSH
- Reactive Oxygen Species antagonists & inhibitors MeSH
- Inflammation genetics chemically induced physiopathology MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
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.
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Literatura
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- $a Wang, Jun $u Department of Joint Surgery, Weifang People's Hospital, Shandong Province 261041, China
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- $a 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.
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