Induction of heat shock protein 27 by bicyclol attenuates d-galactosamine/lipopolysaccharide-induced liver injury.

摘要: Heat shock proteins (Hsps) are critical for cell survival under adverse environmental conditions. Bicyclol is a novel hepatoprotectant that has been shown to protect against liver injury by inducing Hsps, including Hsp27 and Hsp70. Although the role of Hsp70 in protecting acute hepatic failure clearly explored, precise function this setting poorly defined. This study was undertaken evaluate bicyclol-mediated hepatoprotection. Both primary hepatocytes bone marrow-derived macrophages were subjected bicyclol treatment, followed detection expression. Adenoviruses containing mouse coding sequence or shRNA interference targeting used manipulate expression before mice treated with and/or confronted D-galactosamine/lipopolysaccharide (Galn/LPS)-induced damage. Only increased their after treatment time course bicyclol-induced line vivo results. high-dose could without Hsp27, effect given at low dose dependent on induction. Adenovirus-mediated transduction protected damage partially replicated protective afforded bicyclol. These results demonstrated induced hepatocytes, which essential Overexpression confer remarkable protection