Selective inhibition of histone deacetylase 6 attenuates inflammation and improves long-term survival in a lethal septic model

regulated expression of cyclin D1, a downstream target of Wnt signaling. In contrast, Wnt agonist treatment restored beta-catenin and cyclin D1 levels in the lungs and liver. This was associated with a reduction of myeloperoxidase (MPO) activity and IL-6 mRNA in the lungs following treatment (Table), as well as an improvement in a lung histologic injury index. Also, Wnt agonist treatment increased Bcl-2 expression, while it inhibited the degradation of caspase-3 in the lungs.