Ghrelin Reduces S100B in Brain Tissue and Tumor Necrosis Factor-α in Intestinal Tissue of Mice after Traumatic Brain Injury
Blow, Chelsea A.
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Traumatic brain injury (TBI) is a serious medical problem; millions of cases occur in the United States each year and many have long-term, debilitating effects. TBI causes substantial changes in physiologic homeostasis which has an important impact on the human body. Over-production of pro-inflammatory mediators directly affects the brain by causing intracranial pressure, formation of brain edema, neurological deficit and apoptosis in neurons. In some cases of TBI, pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), are amplified throughout the entire body which, when unchecked, can lead to systemic inflammatory response syndrome (SIRS). This can be followed by increased intestinal permeability, bacterial translocation, sepsis, and multiple organ failure (MOF). Ghrelin is a hormone that has recently been discovered to have potent neuroprotective and anti-inflammatory effects in intestinal tissue of mice with sepsis. In this study, mice were subjected to a weight drop model of TBI to determine effects of ghrelin on brain tissue and intestinal tissue post-injury. S100B is an accepted determinant of TBI severity; low levels indicate mild TBI while high levels indicate more severe TBI. We performed a Western blot to determine whether ghrelin reduced S100B after TBI. TNF-α is a pro-inflammatory cytokine that has been recognized as one of the causes of increased intestinal permeability. To determine if ghrelin inhibited TNF-α, we quantified concentrations of TNF-α after TBI using an enzyme-linked imunosorbent assay (ELISA). We confirmed that ghrelin reduced S100B in brain tissue as well as TNF-α in intestinal tissue following TBI. To our knowledge, our study is the first suggesting ghrelin as a possible treatment for neuronal damage in the brain and inflammation in the gastrointestinal tract following TBI.
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