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Objective@#To observe the effect of electroacupuncture on the volume of cerebral infarction, apoptosis of cerebral cells and the expression of protein kinase A (PKA) in the cerebral cortex of rats after ischemia and reperfusion so as to explore how electroacupuncture stimulates brain protection.@*Methods@#One hundred and twenty healthy, adult, male Sprague-Dawley rats were randomly divided into a sham operation group, a model group, an electroacupuncture group and an electroacupuncture with pre-stimulation group. All except the rats in the sham operation group received occulusion of the left middle cerebral artery using the intraluminal thread method for 2h and then reperfusion. Before the operation, the rats in the electroacupuncture with pre-stimulation group were given 30 minutes of electroacupuncture at the baihui, dazhui and right neiguan points every day for 5 days. After the operation both the electroacupuncture group and the pre-stimulated group were given that same electroacupuncture regimen. The other two groups received no special treatment. Garcia scoring was used to evaluate the neurological deficits of all of the rats 5 and 10 days after the intervention. Meanwhile, the ischemic volume, apoptosis of cortical cells and PKA-positive cells were determined using flow cytometry and immunohistochemistry after triphenyltetrazolium chloride (TTC) staining.@*Results@#The neurological function of the injured rats was severely impaired, while no neurological deficit was found in the sham operation group. The average Garcia score, cerebral infarction volume, cerebral apoptosis rate and PKA-positive cell expression rate of the electroacupuncture and electroacupuncture with pre-stimulation groups were all significantly better than those of the model group at the same time points. The averages of the electroacupuncture with pre-stimulation group were all significantly superior to those of the electroacupuncture group at the same time points.@*Conclusions@#Pre-stimulation using electroacupuncture can promote the recovery of injured nerves after cerebral ischemia and reperfusion, at least in rats. Electroacupuncture′s protective mechanism may be related to its reducing the infarcted volume, inhibiting apoptosis of brain cells and promoting PKA expression.
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Objective To explore the clinical effect of targeted soft channel intracranial hematoma drainage combined with urokinase and autologous serum on hypertensive cerebral hemorrhage.Methods Form October 2016 to October 2017,120 patients with hypertensive cerebral hemorrhage were selected as the research objects in Handan First Hospital.In accordance with the principle of random number rule,they were divided into two groups,60 cases in each group,the study group was given directional soft channel with autologous serum treatment,the control group was given directional soft channel joint urokinase for treatment of intracranial hematoma drainage,and then nerve function,clinical curative effect,inflammatory factors and endothelial function of two groups were compared.Results Before treatment,the National Institutes of HealthStroke Scale (NIHSS) score of the study group and the control group were (4.70±0.99) and (4.71 ± 1.02),after treatment were (9.57± 1.54) and (6.63 ± 1.35),respectively.The difference between the two groups before treatment was not statistically significant (t =0.054,P =0.957).After treatment,the NIHSS scores of patients in both groups were significantly higher than those before treatment (Study group t =20.605,P=0.000,Control group t =8.790,P =0.000),The NIHSS score of the study group was significantly higher than that of the control group and the difference was statistically significant (t=11.120,P=0.000).Before treatment,Interleukin-6 (I1-6) in the study group and the control group were(45.61 ±4.13) ng/L and (44.98±2.19) ng/L,after treatment were (13.72±2.19) ng/L and (26.17±2.51) ng/L,respectively,and the two groups before treatment showed no significant difference (t =0.065,P =0.948).After treatment,IL-6 in both the study group and the control group decreased significantly (Studygroup t =52.841,P =0.000,Control group t =43.740,P =0.000),and IL-6 in the study group was significantly lower than that in the control group (t =28.951,P=0.000).Before treatment,the Tumor necrosis factor-α (TNF-αt) of the study group and the control group were (63.01 ± 4.22) μg/L and (62.96 ± ±4.21) μg/L,after treatment were (40.92 ± 3.12) μg/L and (55.67.4.02) μg/L,respectively.The difference between the two groups before treatment was not statistically significant (t =0.065,P =0.948).TNF-α in both the study group and the control group significantly decreased after treatment (Study group t=32.604,P=0.000,Control group t=9.933,P=0.000).TNF-α in the study group was significantly lower than the control group (t =22.453,P=0.000).Before treatment,the nitric oxide of the study group and the control group were (33.46±4.27) μmol/L and(32.97±4.25) μmol/L,after treatment were(54.15±3.11) μmoL/L and (43.17± 3.22) μmol/L.No statistically significant difference was observed between the two groups before treatment (t =0.630,P =0.530).After treatment,nitric oxide was significantly increased in both the study group and the control group (Study group t =30.339,P =0.000,Control group t =14.818,P =0.000).Nitric oxide in the study group was significantly higher than that in the control group (t =18.999,P=0.000).Before treatment,the Endothelin-1 of the study group and the control group before and after treatment were (84.43±4.22) μg/L and (84.51±4.26) μg/L,after treatment were(57.47±5.07) μg/L and (70.14±5.12) μg/L.There was no statistically significant difference between the two groups before the treatment (t =0.335,P =0.738).After the treatment,endothelin-1 in both the study group and the control group was significantly reduced (Study group t =22.889,P =0.000,Control groupt =10.662,P =0.000),and endothelin-1 in the study group was significantly lower than that in the control group (t =9.226,P =0.000).The total effective rate of the study group after treatment was 88.33％ (53/60),significantlyhigher than that of the control group (73.33％) (44/60).The difference between the two groups was statistically significant (x2 =4.357,P =0.037).Conclusion Targeted soft channel intracranial hematoma drainage combined with autologous serum was effective in the treatment of hypertensive cerebral hemorrhage,which is worthy of clinical application.
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Objective To observe the influence of swimming training on the expression of nerve growth factor (NGF) and neurotrophins-3 (NT-3) in rats with cerebral infarction,and to explore the underlying neuroprotection mechanism of exercise training on cerebral infarction.Methods Forty-five healthy male Sprague-Dawley rats were randomly divided into a sham-operation group,a control group and a training group,with 15 rats in each group.Each group was further divided into a 3-day,7-day and 14-day subgroups,which amounts to 9 groups.To establish animal model of cerebral ischemia-reperfusion in rats,the intraluminal thread method was applied to cause left middle cerebral artery occlusion (MCAO) for 2 h before reperfusion.The rats of the training group were given swimming training for 10 min,once daily,while those of the sham-operation and control groups were not given any training.Neurological deficits were assessed using Bederson scores.The expression of NGF mRNA and NT-3 mRNA in the ischemiareperfusion pallium was examined using reverse transcription-polymerase chain reaction (RT-PCR).Results The rats of the sham-operation group showed no neurological deficits.At the same time points,the average Bederson scores of the training group were significantly lower than the control group,but significantly higher than the sham group.Moreover,the 14 d training group had the lowest Bederson score (1.20 ±0.45),compared to the value 3 and 7 days after modeling.The expression of NGF mRNA and NT-3 mRNA of ischemic cerebral cortex in the training group was significantly improved when compared to the sham-operation group or the control group.On day 14,the expression of the NGF mRNA (0.66 ± 0.07),and the NT-3 mRNA (0.79 ± 0.06),were significantly higher than those on day 3 and 7.Conclusions Swimming training could increase the expressions of NGF mRNA and NT-3 mRNA in the ischemic cerebral cortex.It might be one of the key mechanisms that exercise training could promote the recovery of damaged neurological function in rats with cerebral infarction.