| Summary: | 碩士 === 國立嘉義大學 === 生物科技研究所 === 92 === Traumatic brain injury (TBI) is one of the most prevalent causes of morbidity and mortality all over the world. It mainly affects young adults in their most productive stage of life and makes an enormous social and economical cost. However, there is no adequate treatment to reduce the cerebral damage following brain injury. This study assessed the effect of IL-1 on TBI-induced neuron damage. TBI model set up by the calibrated weight-drop device (450 g weight, 2 m height) and the rats were divided into sham operation and different time course after TBI (0 hr, 3 hr, 6 hr, 12 hr, 48 hr, 96 hr and 168 hr). The neuronal damage was verified by hematoxylin and eosin staining and microscopic examination. IL-1α and IL-1β mRNA expression were detected by RT-PCR and the protein expression was measured by Western blot. Blood brain barrier permeability during TBI was detected by β-galactosidase and immunofluorescent double labeling was used to elucidate the site of IL-1 release. In this study, we found that IL-1α mRNA expression peaked at 12 hr （increased 8-fold）and lasted for 168 hr, and IL-1β mRNA was significantly expressed after 12 hr（increased 4-fold）after TBI but only lasted for 96 hr. In the protein level, IL-1α and IL-1β level significantly elevated 3 hr（increased 2-fold）after TBI and lasted for 168 hr. The BBB permeability increased 3 hr after TBI and back to normal level about 1 week later. The possible intracellular signal transduction pathway of TBI is mediated by mitogen activated protein kinase phosphorylation. By the immunofluorescent double labeling, we found IL-1α was released from neuron and IL-1β was released from astrocyte. Moreover, administration of IL-1α and IL-1β antibodies significantly protects animals from TBI-induced neuronal loss. Theses results evidenced that IL-1 plays an essential roles in TBI-induced neuron damage and suggested that IL-1α and IL-1β elicited different effect during TBI.
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