Mitochondria of damaged brain tissues following traumatic brain injury and immersion in rat models

WANG Juan; QIAN Lingjia; XIE Fang; CHENG Gang; WANG Yaming; LI Zhichao; ZHANG Leiming; ZHANG Jianning

Abstract：Objective The mild and moderate traumatic brain injury (TBI) model with seawater immersion was set up and the pathogenesis of seawater on mitochondria of damaged brain tissues was investigated.Methods Fifty-five adult Sprague-Dawley (SD) rats were used in the study and divided into sham group (n=5), TBI group (n=25), and TBI +seawater group (n=25), respectively.TBI was produced by a modified weight-drop model.TBI and TBI +seawater were divided into five subgroups according to different time points after injury (6 h, 12 h, 1 d, 3 d, 5 d ).The damage of neuron was observed by Nepalˊs staining.Apoptosis was observed by terminal dexynucleotidyl transferase (TdT)-mediated 2ˊ-Deoxyuridine 5ˊ-Triphosphate (dUTP) Nick-End labeling (TUNEL). Mitochondrial membrane potential (MMP), H+-ATPase activity and adenosine triphosphate (ATP) content were measured by multifunctional enzyme-labeled instrument.Pyruvate dehydrogenase (PDH), succinate dehydrogenase (SDH) and nicotinamide adenine dinucleotide (NADH) activity were measured by microplate reader.Results TBI group showed that the injury in brain tissues was the most severe at 3 d.In TBI+seawater group the injury in brain tissues was the most severe at 1 d and the mitochondrial function was worse than that of TBI group at different time points (P<0.05).Conclusion Seawater can promote neuronal apoptosis and aggravate brain damage in a short period.These could provide the experimental basis for mechanism of brain protection after seawater immersion.