KMID : 1147920230060010032
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Medical Biological Science and Engineering 2023 Volume.6 No. 1 p.32 ~ p.41
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¥á-MSH suppresses neuroinflammation and improves neurobehavioral outcomes after traumatic brain injury in mice
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Jin Baoyuan
Kim Hye-Hyun Jeong Seong-Tae
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Abstract
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Traumatic brain injury (TBI) leads to a cascade of neuroinflammation and subsequent long-term cognitive deficits. Alpha melanocyte stimulating hormone (¥á-MSH) is a neuropeptide that protects against TBI. In this study, we aimed to evaluate the effect of ¥á-MSH on TBI induced brain inflammation. ¥á-MSH improved rotarod latencies during the first 3 days and water maze latencies over 29-32 days. Here, ¥á-MSH-treated mice had significantly lower tumor necrosis factor- alpha (TNF-¥á) concentrations in the cortex at 30 min and 1 h. The mitogen-activated protein kinase (MAPK) isoforms JNK, ERK, and p38 decreased following administration of ¥á-MSH. The inhibitor of nuclear factor-¥êB (I¥êB) kinase (IKK)/Nuclear factor-¥êB (NF¥êB) signaling system is a key regulator of inflammation. Phosphorylation of IKK/NF¥êB increased after TBI but decreased significantly in response to ¥á-MSH. Strongly immunoreactive microglia increased and were observed throughout the hippocampus in the TBI model, whereas ¥á-MSH-treated mice showed less activation. TNF-¥á concentrations tended to decrease in the hippocampus. These data indicate that ¥á-MSH might attenuate inflammation in a TBI mouse model.
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KEYWORD
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Alpha melanocyte stimulating hormone, Inflammation, Microglia, Mitogen-activated protein kinase, Traumatic brain injury
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