Study on cerebral edema in the rat model with closed craniocerebral injury and its relationship with apoptosis, inflammatory factor generation and AQPs expression

• Main Authors: Yong-Fu Li, Yan-Jun Chen
• Format: Article
• Language: English
• Published: Editorial Board of Journal of Hainan Medical University 2018-02-01
• Series: Journal of Hainan Medical University
• Subjects: Craniocerebral injury; Cerebral edema; Apoptosis; Inflammatory factor; Aquaporins
• Online Access: http://www.hnykdxxb.com/PDF/201802/01.pdf

Objective: To study the relationship of cerebral edema with apoptosis, inflammatory factor generation and AQPs expression in the rat model with closed craniocerebral injury. Methods: Male SD rats were selected as experimental animals and divided into model group and control group. Model group were established into the closed craniocerebral injury models and control group received sham operation. The water content of damaged brain tissue as well as the expression of apoptosis molecules, the generation of inflammatory factors and the expression of aquaporins (AQPs) molecules were measured 7 d after model establishment. Results: The water content of brain tissue of model group was significantly higher than that of control group; Homer1a, Pim-3, Bcl-2, AQP1, AQP4 and AQP9 mRNA expression in brain tissue of model group were significantly lower than those of control group while Cdk5, FasL and Caspase-3 mRNA expression as well as NF-kB, TNF-α, IL-1β, IL-6 and p-JNK generation were significantly higher than those of control group. Homer1a, Pim-3, Bcl-2, AQP1, AQP4 and AQP9 mRNA expression in brain tissue of model group were negatively correlated with water content while Cdk5, FasL and Caspase-3 mRNA expression as well as NF-kB, TNF-α, IL-1β, IL-6 and p-JNK generation were positively correlated with water content. Conclusion: The excessive apoptosis, increased inflammatory factor generation and decreased AQPs expression are closely related to the occurrence of cerebral edema in the process of closed craniocerebral injury.