Effect of acteoside on behavioral changes and endoplasmic reticulum stress in prefrontal cortex of depressive rats / 中国病理生理杂志

AIM:To explore the effect of acteoside on behavioral changes and endoplasmic reticulum stress(ERS)in prefrontal cortex of depressive rats.METHODS:Sprague-Dawley(SD)rats(n=108)were randomly divided into 6 groups:control group,model group,fluoxetine(20 mg/kg)group,low-dose(30 mg/kg)acteoside group,medium-dose(60 mg/kg)acteoside group and high-dose(120 mg/kg)acteoside group,with 18 rats in each group.The depres-sive-like rat model was established by chronic unpredictable mild stress(CUMS)combined with solitary way for 28 d.The rats in fluoxetine group and acteoside groups were treated with fluoxetine(20 mg/kg)or acteoside(30 mg/kg,60 mg/kg and 120 mg/kg)once daily by intragastric administration for 3 weeks.The rats in control group and model group were both given equal volume of saline by intragastric administration for 3 weeks.The behavioral changes were detected by the open-field test and sugar preference experiment.The protein expression of glucose-regulated protein 78(GRP78 )and C/EBP homologous protein(CHOP)was assessed by immunofluorescence and Western blot.The caspase-3 activity was measured by spectrophotometer.RESULTS:Compared with control group ,the total distance ,time spent in the center and sugar in-take were all decreased ,the expression of GRP78 and CHOP was increased ,and the activity of caspase-3 was increased in model group ,fluoxetine group and acteoside groups(P<0.05 ).Compared with model group ,the total distance ,time spent in the center and sugar intake were increased ,the expression of GRP78 and CHOP was reduced ,and the activity of caspase-3 was decreased(P<0.05)in fluoxetine group and acteoside groups.CONCLUSION:Acteoside improves de-pressive-like behaviors in depressive rats ,which may be related to the inhibition of ERS and neuronal apoptosis in prefron-tal cortex.

Neuroprotection of chloride channel blockers against NMDA-induced apoptosis of cultured rat hippocampal neurons / 南方医科大学学报

Activation of N-methyl-d-aspartic acid (NMDA) receptor plays an important role in neuronal apoptosis induced by cerebral ischemia but the underlying mechanisms are still unclear. The present study examined the neuroprotection of three chloride blockers in an in vitro cell model of cerebral ischemia established by treatment of cultured rat hippocampal neurons with NMDA. Hoechst 33258 staining and MTT assay were used to detect neuronal apoptosis and cell viability, respectively. The neuroprotective effects of chloride channel blockers on the cell viability and neuronal apoptosis were only observed when the blockers were applied before NMDA exposure. In comparison with DIDS, SITS showed more potent protective effect in a dose-dependent manner, whereas NPPB showed no significant neuroprotective effect. The results demonstrate that pretreatment with both SITS and DIDS have protective effect against neuronal apoptosis, which is achieved by blocking both NMDA receptor and chloride channel.

Expression of c-fos Protein in Hippocampus of Newborn Rats with Hypoxic-Ischemic Brain Damage and Its Significance / 实用儿科临床杂志

Objective To explore the relationship of c-fos protein and cell apoptosis by observing the expression of c-fos protein in hippocampus of newborn rat with hypoxic-ischemic brain damage(HIBD).Methods Forty-eight 7-day SD neonatal rats were randomly divided into control group(n=6) and experiment group(n=42).The models of HIBD were established in neonatal rats by inhaling the mixed gases of 920 mL/L N2 and 80 mL/L O2,and the animals were sacrificed by dislocation their heads at different time points(0.5,1,3,6,12,24,48,72 h),then the hippocampus were dissected by morphological analysis.Results The apoptotic cells appeared at the time point of 3 h,and reached the peak at 48 h,then decreased.The positive cell of c-fos protein increased from the time point of 30 min and reached the peak at 2 h and then decreased gradually,and there was a contrary tendency between the expression of c-fos protein and the number of damaged brain cells by HIBD(r=-0.57 P

Relationship between expression of bcl-2 gene and neuronal apoptosis in neonatal rats with hypoxic-ischemic brain damage / 实用儿科临床杂志

Objective To observe the expression of bcl-2 gene in cell apoptosis of neonatal rats followed by hypoxic-ischemic brain damage(HIBD) and investigate the mechanism of neuronal apoptosis after HIBD.Methods Fifty-four neonatal SD rats were used in 1 sham-operated group and 8 trial groups. The models of HIBD were established in neonatal rats by inhaling the mixed gases of 92 % N 2 and 8 % O 2, the animals were sacrificed by dislocation their heads at different time points(0.5,1,3,6,12,24,48,72 h), the hippocampus were dissected for morphological analysis. The neuronal apoptosis and the expression of bcl-2 gene in hippocampus were detected by the methods of immunohistochemistry. Results The apoptotic cells appeared at the time point of 3 h, and reached the peak at 48 h, then decreased. The positive cell of bcl-2 protein increased from the time point of 30 min and reached the peak at 6 h and then decreased gradually following HIBD. Conclusion The expression of bcl-2 gene plays a role in the process of neuronal apoptosis following HIBD.