Obstructive sleep apnea (OSA) has been demonstrated to be
implicated in disorder of insulin secretion and diabetes mellitus.
In this study, we aimed to evaluate the protective role of tempol,
a powerful antioxidant, in chronic intermittent hypoxia
(IH)-induced pancreatic injury. The rat model of OSA was
established by IH exposure. The pathological changes, increased
blood-glucose level, and raised proinsulin/insulin ratio in
pancreatic tissues of rats received IH were effectively relieved
by tempol delivery. In addition, the enhanced levels of
pro-inflammatory cytokines, TNF-α, IL-1β, IL-6, and inflammatory
mediators, PGE2, cyclooxygenase-2 (COX-2), NO, and inducible
nitric oxide synthase (iNOS) in pancreatic tissue were suppressed
by tempol. Moreover, tempol inhibited IH-induced apoptosis in
pancreatic tissue as evidenced by upregulated Bcl-2 level, and
downregulated Bax and cleaved caspase-3 levels. Finally, the
abnormal activation of mitogen-activated protein kinase (MAPK)
and nuclear factor kappa-light-chain-enhancer of activated B cells
(NF-κB) signaling pathways induced by IH was restrained by
tempol administration. In summary, our study demonstrates that
tempol relieves IH-induced pancreatic injury by inhibiting
inflammatory response and apoptosis, which provides theoretical
basis for tempol as an effective treatment for OSA-induced
pancreatic injury.