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- W2041044801 abstract "Sepsis continues to be a challenge in clinic. The rates of mortality in sepsis patients remain high. The present study aimed to investigate the effects and the underlying mechanisms of carbon monoxide-releasing molecules II (CORM-2)-liberated CO on suppressing inflammatory response in sepsis. It was shown that treatment of septic mice with CORM-2 attenuated PMN accumulation, downregulated cytokines production, inhibited expressions of iNOS and NF-κB activity in the lung and liver. In parallel, CORM-2 prevented activation of NF-κB in LPS-stimulated HUVEC. This was accompanied by a decrease in ROS and NO production, expression of ICAM-1 and subsequent PMN adhesion to HUVEC. These findings demonstrated that CORM-released CO attenuates inflammatory responses by interfering with NF-κB activation and therefore decreasing the expression of ICAM-1 and NO production, attenuating the oxidative stress and inflammation in sepsis." @default.
- W2041044801 created "2016-06-24" @default.
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- W2041044801 date "2013-10-07" @default.
- W2041044801 modified "2023-10-16" @default.
- W2041044801 title "Effect of Carbon Monoxide-Releasing Molecules II-liberated CO on Suppressing Inflammatory Response in Sepsis by Interfering with Nuclear Factor Kappa B Activation" @default.
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- W2041044801 doi "https://doi.org/10.1371/journal.pone.0075840" @default.
- W2041044801 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3792130" @default.
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