ABSTRACT
Objective To explore the long-term effects of bubble baths on seizure-induced neurobehavior deficits and the expression of apoptotic/autophagic marker B cell lymphoma/leukemia-2 ( Bcl-2 ),Beclin-1,and plasticity-related gene-1 ( PRG-1 ) in newborn rats. MethodsSixty rats aged 6 days were randomly divided into 4 groups:a control group (CON),a control hydrotherapy group (HCON),a recurrent-seizure group (RS) and a recurrent-seizure hydrotherapy group (HRS),with 15 in each group.Flurothyl was used to induce 30 min of seizures daily for 6 consecutive days in the RS and HRS groups.Rats in the CON and HCON groups were placed in the same container for equal duration without exposure to flurothyl.Rats in the HCON and HRS groups were given bubble baths for 28 consecutive days after the end of the last seizure.Neurobehavioral damage was observed using open field behavior at postnatal day 26 (P26) and Morris water maze performance at postnatal day 43 to 49 (P43-P49) and a single-blind method.PRG-1,Bcl-2 and Beclin-1 protein levels in the hippocampus were detected by Western blotting at postnatal day 50 (P50). Results①The average open field test scores of the RS rats decreased significantly compared with those of the CON and HRS rats at P26.②In the Morris water maze test the average latencies of all rats decreased gradually from the 1st to 5th days (d1 to d5) after establishment of seizure model.The average escape latency was significantly longer for rats of the RS group than for CON group rats at the 4th and 5th days ( d4 and d5 ) after establishment of seizure model.The escape latency was significantly shorter for rats of the HRS group than for RS group rats at d4.③The level of Bcl-2 protein in the hippocampus was much lower in the RS group than in the HRS and control groups.In addition,the expression of PRG-1 in the RS group was significantly higher than in the CON group. ConclusionsRecurrent prolonged seizures cause long-term neurobehavior deficits,which might be associated with the down-regulated expression of Bcl-2 and up-regulated expression of PRG-1 in the hippocampus.Bubble baths can improve the neurobehavioral sequelae from seizures,perhaps through up-regulation of hippocampal Bcl-2 expression.
ABSTRACT
Objective To observe the effects of passive movement on the functional outcome after occlusion of the middle artery in the brain and reperfusion, and to explore the molecular mechanisms involved. Methods Cerebral infarction models were established in rats using left middle cerebral artery occlusion ( MCAO). The survivors were randomly divided into a passive movement group and a natural recovery group. There was also a sham-operated group and a normal group. Passive movement treatment (twice a day, twenty min per time) was started at different times after reperfusion. The expression of brain-derived neurotrophic factor (BDNF) and B cell lymphoma/leukemia-2 gene (Bcl-2) were determined using real-time PCRs. Results Expression of BDNF and Bcl-2 was detected a-round the infarction area in both groups. The expression of BDNF and Bcl-2 was highest in the sub-groups where passive movement was begun 24 or 48 h after the operation. Conclusions The expression of BDNF and Bcl-2 in the brain peaks when daily, moderate intensity passive movement is administered beginning 24 to 48 h after reperfusion. Passive movement might have a protective and rehabilitative effect after cerebral infarction.
ABSTRACT
Objective To study the effect of electroacupuncture (EA) combined with transcranial magnetic stimulation (TMS) on the expression of the B-cell lymphoma/leukemia-2 gene (Bcl-2) and brain derived neurotrophic factor (BDNF) after cerebral infarction. Methods One hundred Sprague-Dawley rats were randomly and equally divided into a normal group, a sham-operated control group, a model group and an EA plus TMS group. A cerebral infarction model was established in the latter two groups using left middle cerebral artery occlusion (MCAO). Five-member subgroups of the EA plus TMS group were then treated at 6, 12, 24,48 and 72 hours after reperfusion. Sham EA plus TMS was given to similar sub-groups from the other groups at the same time points. The expression of Bcl-2 mRNA and BDNF mRNA were measured using a RT-PCR at the 14th day. Results Positive expression of Bcl-2 mRNA and BDNF mRNA was detected around the infarction in all groups. The average expression of both was significantly higher in the EA plus TMS group than in the model group. Bcl-2 mRNA peaked when the therapy was administered at 24 hours and BDNF mRNA at 48 hours.Conclusions The expression of Bcl-2 mRNA and BDNF mRNA is maximized when EA plus TMS is administered 24-48 hours after cerebral infarction. EA plus TMS does have protective and rehabilitative effects on rats after cerebral infarction.
ABSTRACT
Objective To study the effect of transcranial magnetic stimulation (TMS) on the rehabilitation of rats with cerebral infarction. Methods One hundred Sprague-Dawley rats were randomly divided into a normal group, a sham-operated control group, a model group and a TMS group with 25 rats in each group. A cerebral infarction model was established in the latter two groups by left middle cerebral artery occlusion (MCAO). TMS was started at either 12 or 24 hours after reperfusion, and sham-TMS was given to the first two groups at the same time points. The expression of Bcl-2 mRNA and BDNF mRNA were measured by RT-PCR after 14 days. Results Bcl-2 mRNA and BDNF mRNA were detected in all groups. The expression of Bcl-2 mRNA in the TMS-12 h group, and that of BDNF mRNA in the TMS-24 h group were significantly higher than in the other groups. Conclusions The expression of Bcl-2 mRNA and BDNF mRNA in the brains of rats after cerebral infarction peak when TMS is administered 12 h and 24 h after reperfusion, respectively. TMS might have protective and rehabilitative effects on rats after cere-bral infarct.