Hyperbaric Oxygen Ameliorated Acute Pancreatitis in Rats via the Mitochondrial Pathway

Acute pancreatitis (AP) is a common disease of the digestive system. The mechanism of hyperbaric oxygen (HBO) therapy for AP is not completely clear.

This study investigated the effects of HBO in AP and whether it acts through the mitochondria-mediated apoptosis pathway.

Eighty male Sprague-Dawley rats were randomly assigned to four groups: control (8 rats), sham (24 rats), AP (24 rats), or AP + HBO (24 rats). AP was induced by ligating the pancreatic duct. The AP + HBO group was given HBO therapy starting at 6 h postinduction. Eight rats in each group were killed on days 1, 2, and 3 postinduction to assess pancreatic injury, mitochondrial membrane potential, ATP level, and expression levels of BAX, Bcl-2, caspase-3, caspase-9, and PARP in pancreatic tissue and blood levels of amylase, lipase, and pro-inflammatory cytokines.

HBO therapy alleviated the severity of AP and decreased histopathological scores and levels of serum amylase, lipase, and pro-inflammatory cytokines. Compared to AP induction alone, HBO therapy increased expression of the apoptotic protein BAX, caspase-3, caspase-9, and PARP and ATP levels in tissues and decreased antiapoptotic protein Bcl-2 expression levels and the mitochondrial membrane potential on the first day; the results on the second day were partly consistent with those on the first day, while there was no obvious difference on the third day.

HBO therapy could induce caspase-dependent apoptosis in AP rats to alleviate pancreatitis, which was possibly triggered by mitochondrial apoptosis pathway regulation of Bcl-2 family members.