The Journal of surgical research
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Epidemiologic data has shown that metformin confers a survival advantage in patients with cardiovascular disease. Although the underlying cardioprotective mechanism is unclear, it appears to be independent of metformin's insulin-sensitizing effect. The purpose of this study was to evaluate the effect of metformin on the apoptosis pathway in the ischemic and nonischemic cardiac tissue in a swine model of metabolic syndrome. ⋯ Metformin selectively alters the apoptosis pathway by inhibiting FOXO3 and decreasing the active form of caspase 3, cleaved caspase 3. Metformin also upregulates mitogen-activated kinase proteins p38 and extracellular signal-regulated protein kinases 1 and 2, which are considered cardioprotective during ischemic preconditioning. Perhaps, the altered activation of the apoptosis pathway in ischemic myocardium is one mechanism by which metformin is cardioprotective.
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We have shown previously that vagal nerve stimulation (VNS) protects against burn-induced acute lung injury (ALI). Although the mobilization and activation of immune cells is central to tissue injury caused by the systemic inflammatory response, the specific inflammatory cell populations that are modulated by VNS have yet to be fully defined. The purpose of this study was to assess whether VNS alters inflammatory cell recruitment to the lung after severe burn injury. ⋯ VNS is an effective method to limit pulmonary DC recruitment to the lung and prevent ALI after burn injury. Identifying strategies to limit inflammatory cell recruitment to the lung may have clinical utility in preventing ALI in severely burned patients.