| Popis: |
Objective To explore the mechanisms by which Dexras1 promotes inflammation and participates in white matter damage (WMD) after subarachnoid hemorrhage (SAH). Methods Ninety healthy adult male SD rats were randomly divided into control group (sham group), SAH group, SAH time ponits group, SAH+LV-Scramble group, SAH+LV-Dexras1+ group, and SAH+LV-Dexras1- group, with 12 rats in each group. Intravascular puncture was used to establish a rat model of intracranial hemorrhage under subarachnoid. Immunofluorescence assay and Luxol fast blue staining were used to detect myelin changes in each group; Neurobehavioral scores were used to evaluate the changes in neurological function; Western blot analysis was used to detect the expression of Dexras1, TNF-α, IL-1β and myelin basic protein (MBP) in each group. Results Compared with the sham group, Dexras1, TNF-α, and IL-1β were significantly increased in the brain tissue (P < 0.01), MBP was significantly reduced (P < 0.01), and obvious neurological deficits, cerebral edema, myelin sheath injury and inflammatory cell infiltration were observed in the SAH group. Compared with the SAH+LV-Scramble group, Dexras1, TNF-α, and IL-1β in the brain tissue of the SAH+LV-Dexras1+ group continued to increase (P < 0.01), MBP was further reduced (P < 0.05), and neurological deficits, cerebral edema, and myelin sheath damage were significantly aggravated, and inflammatory cell infiltration was also significantly increased in the group. However, Dexras1, TNF-α, and IL-1β in the brain tissue were significantly reduced (P < 0.01), MBP was increased (P < 0.05), and neurological deficits, cerebral edema and myelin sheath damage were obviously improved, inflammatory cell infiltration was significantly reduced in the SAH+LV-Dexras1- group. Conclusion Dexras1 can promote the inflammatory response, and thereby participate in white matter damage after SAH. |
