The Journal of surgical research
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High-mobility group box 1 (HMGB1) is a critical mediator in the pathogenesis of many inflammatory diseases. Penehyclidine hydrochloride (PHC) has been proven to reduce sepsis-related mortality and sepsis-induced pathological complications. These effects are because of the reduced expression and release of many inflammatory mediators, although it is not clear whether PHC affects the expression and release of HMGB1. In this study, we explored the effect of PHC on the release of HMGB1 in lipopolysaccharide (LPS)-activated RAW264.7 cells and cecal ligation and puncture (CLP)-induced septic mice. ⋯ Our study demonstrates that PHC inhibits the translocation of HMGB1 from the nucleus to the cytoplasm and the expression of HMGB1 messenger RNA in a dose-dependent manner. The mechanism responsible for these effects involves the NF-κB signaling pathway. Moreover, PHC can significantly protect important organs, such as the liver, kidney, and heart in mice with sepsis.
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Dexmedetomidine (DEX) has been shown to decrease ischemia-reperfusion (I/R) injury in kidney and brain tissues. In this study, the effects of DEX were evaluated in skeletal muscle during I/R injury. ⋯ We found that DEX exhibits protective effects against skeletal muscle I/R injury. These results underscore the necessity of human studies with DEX to determine if it is beneficial for preventing skeletal muscle I/R injury.