RÉSUMÉ
Objective:To investigate the neuroprotective effect of ibuprofen, and influence of ibuprofen in hippocampal nod-like receptor protein 3 (NLRP3) inflammatome and its related products in chronic epilepsy rats models.Methods:Thirty male SD rats were randomly divided into 3 groups: control group, pentylenetetrazol (PTZ) group and PTZ+ibuprofen group ( n=10). Rats in the PTZ group were intraperitoneally injected with PTZ (35 mg/kg) once every one d, and rats in the PTZ+ibuprofen group were intraperitoneally injected with ibuprofen (30 mg/kg) once every one d 30 min before PTZ injection; rats in the control group were intraperitoneally injected with the same amount of normal saline every one d. Injection for 15 times was performed. After the last injection, the rats were observed for 10 min, and the latency, seizure level and complete ignition of the rats in each group were recorded. Electroencephalogram (EEG) was used to detect the abnormal brain discharge in rats. Four h after last injection, HE staining and Nissl staining were used to detect the proportion of damaged hippocampal neurons in each group. Immunohistochemical staining was used to detect the absorbance values of NLRP3 inflammasome, caspase-1 and interleukin (IL)-18 positive cells in the hippocampus of rats in each group; Western blotting was used to detect the protein expressions of NLRP3 inflammatome, caspase-1 and interleukin (IL)-18 in the hippocampus of each group. Results:(1) As compared with the PTZ group, rats in the PTZ+ibuprofen group had statistically lower incidence of complete ignition, significantly longer latency and significantly lower seizure level ( P<0.05). EEG showed spikes and high amplitude epileptic wave discharge in rats of the PTZ group; EEG showed low amplitude small spiny wave and slow spiny wave in rats of the PTZ+ibuprofen group. (2) As compared with the control group, the proportion of injured hippocampal neurons significantly increased in the PTZ group and PTZ+ibuprofen group ( P<0.05); and the proportion of injured hippocampal neurons in the PTZ+ibuprofen group signficantly decreased as compared with that in the PTZ group ( P<0.05). (3) As compared with those in the control group, the absorbance values of NLRP3 inflammatome, caspase-1 and IL-18 positive cells, and the protein expressions of NLRP3 inflammatome, caspase-1 and IL-18 in the hippocampus of the PTZ group and PTZ+ibuprofen group were all significantly increased ( P<0.05); as compared with the PTZ group, the the absorbance values of NLRP3 inflammatome, caspase-1 and IL-18 positive cells, and the protein expressions of NLRP3 inflammatome, caspase-1 and IL-18 in the hippocampus in the PTZ+ibuprofen group were all significantly decreased ( P<0.05). Conclusion:Ibuprofen can inhibit the expressions of NLRP3 inflammatome, caspase-1 and IL-18, reduce the intensity of seizures, and play a neuroprotective role.
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Objective To investigate the mechanism of neural protection of mouse nerve growth factor combined with sub-hypothermia in the treatment of patients with severe traumatic brain injury. Methods 90 cases of severe traumatic brain injury were randomly divided into study group and control group with 45 cases of each group, the control group were given routine treatment; the study group were given on the basis of routine treatment of mouse nerve growth factor combined with sub-hypothermia treatment, with 2 weeks treatment, the clinical indicators and corresponding nerve injury, inflammation, oxidative stress indexes, clinical effect and complications were compared after 2 weeks treatment. Results Compared with before treatment or control group, scores of Glasgow coma scale (GCS) and Glasgow outcome scale (GOS) and montreal cognitive assessment (MoCA) in study group after the treatment increased, National Institute of Health stroke scale (NIHSS) score decreased(P<0.05), neuronspecific enolase (NSE), myelin basic protein (MBP) and S100 beta levels decreased(P<0.05), the serum tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6), IL-10 levels decreased (P<0.05), the malondialdehyde (MDA) decreased, the glutathione peroxidase (GPx) and oxidation resistance (AOA) levels increased (P<0.05). The control group efficiency was 73.33%, the study group efficiency was 91.11%, there was significant difference (P<0.05). All patients were followed up, no case off, there was no significant difference in adverse drug reaction rate between two groups. Conclusion Mouse nerve growth factor and sub-hypothermia has the significant neural protection for patients with severe traumatic brain injury, and its mechanism may be related to reduce nerve injury indicators and improve inflammatory factor and oxidative stress response.
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Objective To investigate the effect of sulforaphane synergistic with lithium chloride on neuroprotective of rats with traumatic brain injury. Methods According to feeney method free fall production models of traumatic brain injury induced injury models, and rats were divided into control group, model group, SFN group and collaborative group, each group 15 rats, control group without impact experiment, after operation the SFN group received daily intraperitoneal injection of sulforaphane, collaborative group were given sulforaphane and chloride lithium intraperitoneal injection, the model group received daily intraperitoneal injection of saline, the degree of nerve function impairment score (mNSS) in rats of each group postoperative 1 d, 3 d, 5 d and 7 d, and brain tissue of rats, the water content of brain tissue, HE staining of brain tissue and activity of SOD, IL-6, TNF-alpha, the level of MDA in each group postoperative 7 d were compared. Results Compared with the control group, mNSS scores in the model group, SFN group, collaborative group at each time point were significantly increased (P<0.05); After 5 d, 7 d of operation, synergy scores in SFN group and mNSS group rats were significantly lower than those in the model group (P<0.05), and mNSS score in collaborative group was significantly lower than that of SFN group(P<0.05); After 7 d of operation, the brain tissue water content in control group of rats was (69.29±2.06)%, the model group was(75.40±1.73)%, SFN group was (73.08±1.06)%, collaborative group was (71.27±1.52)%; Brain tissue HE staining results showed that the nerve cell injury of rats in SFN group and cooperative group was obviously alleviated than those in the model group, necrotic cells decreased, and the collaborative group relieve neuronal injury was the most remarkable; The SOD in model group, SFN group, collaborative group decreased significantly compared with the control group (P<0.05), IL-6, TNF-alpha, MDA levels increased significantly(P<0.05);The activity of SOD in SFN group and collaborative group increased significantly compared with the model group(P<0.05), IL-6, TNF-alpha, MDA levels decreased significantly (P<0.05), and collaborative TNF-alpha and IL-6 levels were significantly lower than that of SFN group (P<0.05). Conclusion Sulforaphane in combination with lithium chloride have remarkable neuroprotection on traumatic brain injury in rats, its mechanism may be related with the reduction of brain edema in rats, nerve cell damage, inhibition of oxidative stress and related to the release of inflammatory factors.
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Objective To study the relation between chronic stressful, the neural changes in prefrontal cortex and depression. Methods Adapt chronic unpredictable stress with separate model to make depression model rats. After 22 days all the rats were killed and use immunohistochemistry method and computer image analysis to detect BDNF. To analysis the date with SPSS11.5 software. Results After 21 days stress, body weight ( t =2.915, P < 0.05), ambulation ( t = 6. 245, P < 0. 01 ), rearing( t = 2.693, P < 0. 05 ) and grooming ( t = 2. 685, P<0.05) decreased and stopping time in center( t=2. 388, P<0. 05) ,defecation( t =3. 846, P<0. 01 ) increased in experimental group. BDNF expressed obviously in control group and the prefrontal cortex expressed highly than that of the experimental group. BDNF expressions of experimental group were lower than that in control group ( P< 0.01 ) especially in right prefrontal cortex. Conclusion There was no difference of BDNF distribution in prefrontal cortex between both groups ,but after 21 days stress ,the BDNF levels of experimental rats obviously descent,especially in right prefrontal cortex.