• Inflammation · Feb 2012

    Vagal stimulation modulates inflammation through a ghrelin mediated mechanism in traumatic brain injury.

    • Vishal Bansal, Seok Yong Ryu, Nicole Lopez, Sarah Allexan, Michael Krzyzaniak, Brian Eliceiri, Andrew Baird, and Raul Coimbra.
    • Department of Surgery, Division of Trauma, Surgical Critical Care and Burns, University of California San Diego, 200 W. Arbor Drive #8896, San Diego, CA 92103, USA. v3bansal@ucsd.edu
    • Inflammation. 2012 Feb 1;35(1):214-20.

    AbstractTraumatic brain injury (TBI) releases a cascade of inflammatory cytokines. Vagal nerve stimulation (VNS) and ghrelin have known anti-inflammatory effects; furthermore, ghrelin release is stimulated by acetylcholine. We hypothesized VNS decreases post-TBI inflammation through a ghrelin-mediated mechanism. TBI was created in five groups of mice: sham, TBI, TBI/ghrelin, TBI/VNS, and TBI/VNS/ghrelin receptor antagonist (GRa). Serum and tissue ghrelin, and serum TNF-α were measured. Ghrelin increased following VNS 2 h post-TBI compared to sham or TBI. At 6 h, TBI and TBI/VNS/GRa had increased TNF-α compared to sham while TBI/VNS and TBI/ghrelin had TNF-α level comparable to sham. The highest ghrelin was measured in stomach where TBI decreased ghrelin in contrast to an increase by VNS. In conclusion, VNS increased serum ghrelin and decreased TNF-α following TBI. This was abrogated with GRa. Our data suggests that ghrelin plays an important role in the anti-inflammatory effects of VNS following TBI.

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