Xue Feng1, Yu-jia Yao. 1. Department of Pediatrics, West China Second Hospital, Sichuan University, Chengdu 610041, China.
Abstract
OBJECTIVE: To observe the expressions of mRNA and protein for the CCR2 in cerebral tissue with experimental hypoxic-ischemic brain damage (HIBD) to newborn rat. METHODS: The HIBD model of SD rat was set up by ligating the right carotid artery and exposing the animals to 8% oxygen for 2.5 h. The dynamic change of CCR2 mRNA level was studied by using quantitative, real-time, fluorescence PCR assay (TaqMan), and the change of CCR2 protein was detected by SDS-PAGE assay. RESULTS: The highest expression of CCR2 mRNA was showing at 24 h after HIBD, of which the level was significantly higher in hypoxic-ischemic (HI) cerebral hemisphere than in control (P < 0.05). The CCR2 mRNA level of 72 h after HIBD was still higher than that of control (P > 0.05) but had no difference on 7 d after HIBD when compared with control (P > 0.05). The increased expression of CCR2 protein was detected at 12 h after HIBD and peaked at 24 h after HIBD. The significant increase of CCR2 protein persisted in HI hemisphere up to 3 d after HIBD. CONCLUSION: The expressions of CCR2 mRNA and protein increase significantly in cerebral tissue of newborn rat with HIBD. The dynamic change of CCR2 expression is consistent with the process of HIBD, which suggests that CCR2 expression after HIBD may play an important role in the mechanism of brain damage.
OBJECTIVE: To observe the expressions of mRNA and protein for the CCR2 in cerebral tissue with experimental hypoxic-ischemic brain damage (HIBD) to newborn rat. METHODS: The HIBD model of SD rat was set up by ligating the right carotid artery and exposing the animals to 8% oxygen for 2.5 h. The dynamic change of CCR2 mRNA level was studied by using quantitative, real-time, fluorescence PCR assay (TaqMan), and the change of CCR2 protein was detected by SDS-PAGE assay. RESULTS: The highest expression of CCR2 mRNA was showing at 24 h after HIBD, of which the level was significantly higher in hypoxic-ischemic (HI) cerebral hemisphere than in control (P < 0.05). The CCR2 mRNA level of 72 h after HIBD was still higher than that of control (P > 0.05) but had no difference on 7 d after HIBD when compared with control (P > 0.05). The increased expression of CCR2 protein was detected at 12 h after HIBD and peaked at 24 h after HIBD. The significant increase of CCR2 protein persisted in HI hemisphere up to 3 d after HIBD. CONCLUSION: The expressions of CCR2 mRNA and protein increase significantly in cerebral tissue of newborn rat with HIBD. The dynamic change of CCR2 expression is consistent with the process of HIBD, which suggests that CCR2 expression after HIBD may play an important role in the mechanism of brain damage.