ABSTRACT
Objective:To investigate the effect of total saponins of Panax notoginseng (TSPN) on learning and memory of post-stroke depression (PSD) rats and its mechanism.Methods:Four-vessel occlusion method was used to build the rat stroke model and 7 days later these rats were given solitary breeding with chronic unpredictable mild stress (CUMS) to make depression model. Rats were randomly divided into Sham group ( n=10), Model group ( n=10), PSD group ( n=10) and TSPN group ( n=10). The rats in the Model group and PSD group were injected administered with equal volume of 0.9% saline 30 min post-brain ischemia, one injection per day for 30 days. while TSPN group were treated with TSPN. The dose of TSPN (75 mg/kg) was dissolved in 0.9% saline 10 g/L, once per day for 30 days. Then the learning and memory of rats were tested by Morris water maze.The protein levels of DCX and Nestin in the hippocampus were detected by Western blot. Furthermore, the DCX/Ki67 co-labeled cells in the SGZ of hippocampus were observed by the immunofluorescence. Results:The escape latency at the fifth day of PSD group((31.8±3.8)s) was longer than that in the Sham group((10.4±3.2)s) and Model group((19.8±3.7)s) ( t=9.23, 5.15; both P<0.05). The escape latency ((14.2±2.8)s) of TSPN group was shortened significantly than PSD group ( t=8.56, P<0.05). The times across the platform in the Sham group was (10.3±1.7), and the PSD group was (4.1±1.1), difference was statistically significant between two groups( t=11.24, P<0.05). The times across the platform (8.4±1.6) of TSPN group statistically increased compared with PSD group ( t=5.77, P<0.05). The protein levels of DCX and Nestin in the PSD group were (0.60±0.02), (0.58±0.03) respectively, and in the TSPN group were (1.07±0.07), (0.95±0.11) correspondingly, there were significant differences of the DCX, Nestin protein level between the two groups( t=20.22, 7.68, both P<0.01). Moreover, there was significant difference in the number of the DCX/Ki67cells in the hippocampus SGZ between the PSD group((16.2±2.8) /mm 2) and TSPN group ((21.2±3.1) /mm 2)( t=2.42, P<0.05). Conclusion:TSPN could improve the learning and memory of the rats with post-stroke depression through enhancing the hippocampus neurogenesis.
ABSTRACT
Objective To explore the effect of the total saponins of panax notoginseng ( TSPN) on depression-like behavior following global cerebral ischemia depression in rats and its mechanism. Method-s Using four-vessel occlusion method to build the global cerebral ischemia model,then the cerebral ischemi-a rats were given solitary breeding with chronic unpredictable mild stress ( CUMS) to prepare depression model. Seventy rats were divided into sham group (n=10),model group ( n=20),PSD group ( n=20) and TSPN group (n=20). The rats in the TSPN group were administered TSPN intraperitoneally 30 min post-brain ischemia. The dose of TSPN (75mg/kg) was suspended in 0. 9% saline 10g/L,once per day for 30 days after reperfusion. While rats in the vehicle group and PSD group was treated with equal volume of 0. 9% saline,one injection per day until the rats were sacrificed at 30 days after brain ischemia. The BrdU,dou-blecortin (DCX) expression in the hippocampus was assessed by immunohistochemistry. Results In com-parison with the model group,the sucrose preference percentage in the PSD group was significantly lower ((46. 2±9. 2)%,(61. 2±7. 6)%;t=3. 18,P<0. 05),then the PSD rats were administered TSPN intraperito-neally,the sucrose preference percentage increased significantly ((62. 4±3. 4)%,(46. 2±9. 2)%;t=3. 43, P<0. 05). During the forced swimming test,the immobility time of PSD group was significantly increased compared with the model group ((119. 4±9. 7)s,(88. 0±15. 6)s ;t=4. 30,P<0. 01),while after PSD rats administering TSPN intraperitoneally,the immobility time was shorten remarkably ((97. 4±6. 7)s,(119. 4± 9. 7)s;t=3. 01,P<0. 05). Compared with the Model group( BrdU+:( 12. 6± 2. 2)/mm2,DCX+:( 38. 6± 4. 2)/mm2),the number of BrdU+ and DCX+ cells in the SGZ of hippocampus in PSD group decreased (BrdU+:(8. 8±1. 5)/mm2,DCX+:(27. 2±2. 8)/mm2;t=3. 25,4. 29,both P<0. 01). And compared with PSD group,the number of BrdU+ and DCX+ cells in the SGZ of hippocampus in TSPN group increased sig-nificantly (BrdU+:(14. 8±2. 8)/mm2,DCX+:(37. 0±3. 3)/mm2;t=4. 68,3. 69,both P<0. 05). Conclu-sion TSPN can improve the depression-like behavior of rats following global cerebral ischemia,which may be related with promoting hippocampal nerve regeneration.
ABSTRACT
Aim Pharmacological intervention is one of important strategies to deal with spinal cord injury.The effect of Pharmacological intervention has highly differentiated features because of complex physiopathology mechanisms in SCI.Moreover contraindications,complications having different features,it is constantly the focal point in the selection of pharmacological intervention to protect spinal cord,attenuate secondary injury and promote injuried neuron regeneration.At present only several of those have been applied in clinic and the majority are still being carried out in clinic trial stage,even preclinical animal experiment stage.This paper made a particular review of the current situation in pharmacological intervention for spinal cord injury.