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October 12, 2014
10:00 AM - 12:00 PM
Room Hall B1-Area D
Earlier M2 Microglia Activation Promotes the Recovery in Developing Brain After Traumatic Brain Injury
Shiyu Shu, Ph.D.
Children's Hospital of Chongqing Medical University, Chongqing, China
Objectives: Microglial/macrophage activation and neuro-inflammation play a significant role in neuronal injury after pediatric traumatic brain injury (TBI). A better understanding of the role of microglial polarization and its regulation in developing brain will help in determining the optimal time of targeting therapies for attenuation of secondary inflammatory injury while promoting repair and regeneration.

Methods: Male newborn Sprague Dawley rats of postnatal day (PND) 9-10(n=10) and PND 29-30(n=10) and were used to perform controlled cortical impact (CCI) injury. Brain damage was induced by round impact tip (speed 5.0-5.5 m/s) with 3 mm diameter and the impact depth was 1.5 mm. Rats were perfused on 3d and 7 d after TBI. Brain was isolated and cut into 25 μm thick coronal section. The brain lesion volume was measured with Image J. Iba-1 was used to investigate the microglial activation by immunohistochemisty. M1 macrophages (co-localization of CD68 ) and M2 macrophages (co-localization of CD68 and CD206) was assayed by immunofluorescence and immunohistochemistry. M1 microglia markers (IL-1β,TNF-α,IL-12p35,IL-12p40) and M2 microglia markers (IL-4 , IL-10) were measured with real-time PCR.

Results: Compared with 7d after TBI, the brain lesion volume percentage of PND 9-10 was smaller than that of PND 30 on 3d after TBI. IL-4 and IL-10 were higher than that of PND30 on 3d after TBI. The percentage of M2 macrophages was more than that of M1 macrophages on 3d. IL-1 β and TNF-α increased substantially on TBI 3d. IL4 and IL-10 increased significantly on 3d in PND 9-10.But the other inflammation factors had no major variation, especially on 7d.

Conclusion: More rapid transition to an M2 state of microglia may help promote the recovery of developing brain after TBI.

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