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Chinese Journal of Trauma ; (12): 848-852, 2014.
Article in Chinese | WPRIM | ID: wpr-454077

ABSTRACT

Objective To investigate the role of aquaporin 4 (AQP4) in partial pathologic process of lung injury in rat models of fat embolism syndrome (FES).Methods A total of 120 healthy male C57BL/6J mice were assigned to control group and FES group which was subgrouped at 4,6,12,24,and 48 hours with 20 mice per group,according to the random number table.Allogeneic perinephric fat was injected to rat caudal veins in FES groups.Lung samples were harvested from each group to examine pathological morphology and lung weight to dry ratio (W/D) to verify the FES models and observe the pathologic process.Expression of AQP4 was detected by western blot and immunohistochemistry.Additional 36 C57BL/6J mice were divided into control group,DMSO group,FES 12-hour group,and AQP4 inhibitor group according to the random number table,with 9 mice per group.Pathologic process of FES-induced lung injury was detected after the inhibition of AQP4.Results Damage to lung tissues was notable in FES group compared with control group.Lung W/D value was 5.06 ± 1.23,5.22 ± 1.58,6.18 ± 1.65,and 5.07 ± 0.31 at 6,12,24,and 48 hours respectively,which was higher than 3.16 ± 1.58 in control group (F =3.62,P < 0.05).Expression of AQP4 was 1.71 ± 1.05 at 12 hours and 1.28 ± 0.68 at 24 hours in FES group,which showed significantly increase when compared with 0.65 ±0.08 in control group (F =4.12,P <0.01),whereas at 4 hours (0.76 ± 0.36),6 hours (1.17 ± 0.60),and 48 hours (0.85 ±0.45) in FES group,no statistical difference was observed when compared to control group.W/D value in FES 12-hour group (5.22 ± 1.17),DMSO group (4.96 ±1.66),and AQP4 inhibitor group (3.25 ± 1.19) was higher than 3.03 ± 1.68 in control group (F =3.69,P < 0.05).Meanwhile,there was no statistical difference between DMSO and FES 12-hour groups,but significantly lowered W/D value was observed in AQP4 inhibitor group than in FES 12-hour group.Conclusion AQP4 may be implicated in mitigating lung injury induced by FES.

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