Effect of Oxymatrine on Neuronal Cell Apoptosis and Its Mechanisms after Traumatic Brain Injury

OBJECTIVE To investigate the effect of oxymatrine on neuronal cell apoptosis, oxidative injury and inflammatory reaction and furthermore discuss possible mechanism of oxymatrine suppressing neuronal cell apoptosis. METHODS All of 140 male Wistar rats were randomly divided into sham operation group, brain trauma group, as well as oxymatrine of 60 mg·kg^-1 and 120 mg·kg^-1 treatment group. The rat model of traumatic brain injury was induced by a modi?cation of Feeney’s weight-drop model. Oxymatrine was given to rats in the oxymatrine of 60 mg·kg^-1 and 120 mg·kg^-1 treatment groups via intraperitoneal injection (60 and 120 mg·kg^-1) after trauma, and then once a day till day 5. The rats in the brain trauma and sham operation groups received an intraperitoneal administration of 1 mL of saline after trauma or procedures. Animals were sacrificed by decapitation at hour 2, 6 and 12, as well as day 1, 2, 3, and 5 after trauma. Brains were removed and blood was collected. Neuronal cell apoptosis was measured using terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling; superoxide dismutase activity in serum, was determined by xanthine oxidase method; serum malondialdehyde level, was analyzed by thiobarbituric acid reactive substance assay; interleukin-1beta, tumor necrosis factor-beta, and interleukin-6 levels in serum, were measured by enzyme linked immunosorbent assay. Statistical analysis was performed. RESULTS At hour 2, 6 and 12, as well as day 1, 2, 3, and 5 after trauma, the differences between the number of apoptotic neuronal cell, superoxide dismutase activity in serum, as well as serum malondialdehyde, interleukin-1beta, tumor necrosis factor-beta and interleukin-6 levels in the oxymatrine of 60 mg·kg^-1 treatment group and brain trauma group were not significant statistically (P>0.05). At hour 12, as well as day 1, 2, 3, and 5 after trauma, the number of apoptotic neuronal cell, superoxide dismutase activity in serum, as well as serum malondialdehyde, interleukin-1beta, tumor necrosis factor-beta and interleukin-6 levels in the oxymatrine of 120 mg·kg^-1 treatment group were significantly lower than those in the brain trauma group (P<0.05), but at hour 2 and 6, these differences were not significant (P>0.05). CONLCUSION Oxymatrine may suppress neuronal cell apoptosis via inhibition of free radical and inflammatory reactions after traumatic brain injury.