Radiation encephalopathy is the main complication of cranial radiotherapy. It can cause necrosis of brain tissue and cognitive dysfunction. Our previous work had proved that a natural antioxidant shikonin possessed pr...Radiation encephalopathy is the main complication of cranial radiotherapy. It can cause necrosis of brain tissue and cognitive dysfunction. Our previous work had proved that a natural antioxidant shikonin possessed protective effect on cerebral ischemic injury. Here we investigated the effects of shikonin on carbon ion beam induced radiation brain injury in mice. Pretreatment with shikonin significantly increased the SOD and CAT activities and the ratio of GSH/GSSG in mouse brain tissues compared with irradiated group （P〈0.01）, while obviously reduced the MDA and PCO contents and the RO$ levels derived from of the brain mitochondria.展开更多
We have previously shown that the lipofuscin in the brain seems to have in-creased in amount in autopsy cases of epidemic hemorrhagic fever.The purpose of thisstudy was to testify if there is really such an increase.L...We have previously shown that the lipofuscin in the brain seems to have in-creased in amount in autopsy cases of epidemic hemorrhagic fever.The purpose of thisstudy was to testify if there is really such an increase.Lipfuscin in 10 sections from everybrain of 10 autopsy cases,stained with Sudan Ⅳ,Sudan black and H.E.,was carefully es-timated and found to be greatly increased as compared with the controls of the same agewithout brain disease.Animal experiment was also conducted on 15 sucking BALB/c miceby I.P.inoculation of 100 LD<sub>50</sub>（0.05ml）of strain Chen of hemorrhagic fever virus,andon 15 mice without inoculation as controls.No lipofuscin was detected in the controls.However,in the brains of experimental mice,lipofuscin was found to be markedly in-creased,especially in the necrotic cells.The findings suggest that the over-productionand deposition of lipofuscin may be a mild change caused by the virus and its related fac-tors,which might be enhanced by hypotension and shock.展开更多
To evaluate the long-term consequence of repetitive mild traumatic brain injury （mTBI） on bone, mTBI was induced in 10-week-old female C57BL/6J mice using a weight drop model, once per day for 4 consecutive days at ...To evaluate the long-term consequence of repetitive mild traumatic brain injury （mTBI） on bone, mTBI was induced in 10-week-old female C57BL/6J mice using a weight drop model, once per day for 4 consecutive days at different drop heights （0.5, 1 and 1.5 m） and the skeletal phenotype was evaluated at different time points after the impact. In vivo micro-CT （μ-CT） analysis of the tibial metaphysis at 2, 8 and 12 weeks after the impact revealed a 5%-32% reduction in trabecular bone mass. Histomorphometric analyses showed a reduced bone formation rate in the secondary spongiosa ofl.5 m impacted mice at 12 weeks post impact. Apparent modulus （bone strength）, was reduced by 30% （P 〈 0.05） at the proximal tibial metaphysis in the 1.5 m drop height group at 2 and 8 weeks post impact. Ex vivo μ-CT analysis of the fifth lumbar vertebra revealed a significant reduction in trabecular bone mass at 12 weeks of age in all three drop height groups. Serum levels of osteocalcin were decreased by 22%, 15%, and 19% in the 0.5, 1.0 and 1.5 m drop height groups, respectively, at 2 weeks post impact. Serum IGF-I levels were reduced by 18%-32% in mTBI mice compared to control mice at 2 weeks post impact. Serum osteocalcin and IGF-I levels correlated with trabecular BV/TV （r2 = 0.14 and 0.16, P 〈 0.05）. In conclusion, repetitive mTBI exerts significant negative effects on the trabecular bone microarchitecture and bone mechanical properties by influencing osteoblast function via reduced endocrine IGF-I actions.展开更多
We have previously reported that sequential common artery sectioning (SCAS) in mice produces a reproducible pattern of mortality, extensive brain damage and a wide range of measurable neurobehavioral alterations that ...We have previously reported that sequential common artery sectioning (SCAS) in mice produces a reproducible pattern of mortality, extensive brain damage and a wide range of measurable neurobehavioral alterations that include motor incoordination and forelimb flexion. The present study describes a comprehensive method to assess motor functional outcome after brain ischemia produced by SCAS using swimming behavior. We found that after the second artery occlusion the time for completion of the swimming task significantly increased and the swimming pattern alterations observed in the ischemic mice showed no evidence of recovery (up to 96 h). We view the swimming performance strategy described here as a sensitive, simple and economic procedure to assess motor performance after brain ischemia.展开更多
The persimmon leaf has been shown to improve cerebral ischemic outcomes; however, its mechanism of action remains unclear. In this study, mice were subjected to 10 minutes of ischemic preconditioning, and persimmon le...The persimmon leaf has been shown to improve cerebral ischemic outcomes; however, its mechanism of action remains unclear. In this study, mice were subjected to 10 minutes of ischemic preconditioning, and persimmon leaf flavonoid was orally administered for 5 days. Results showed that the persimmon leaf fiavonoid significantly improved the content of tissue type plasminogen activator and 6-keto prostaglandin-F1 a in the cerebral cortex, decreased the content of thromboxane B2, and reduced the content of plasminogen activator inhibitor-1 in mice. Following optical microscopy, persimmon leaf flavonoid was also shown to reduce cell swelling and nuclear hyperchromatism in the cerebral cortex and hippocampus of mice. These results suggested that persimmon leaf fiavonoid can effectively inhibit brain thrombosis, improve blood supply to the brain and relieve ischemia-induced pathological damage, resulting in brain ischemic tolerance.展开更多
目的探讨长链非编码RNA(lncRNA)-N1LR在脑缺血再灌注损伤后血脑屏障的作用机制。方法原代小鼠脑微血管内皮细胞常规培养,经氧糖剥夺/复糖复氧(OGD/R)处理模拟脑缺血再灌注损伤,实验分对照组、OGD组、lncRNA-N1LR过表达组(OGD处理后转染...目的探讨长链非编码RNA(lncRNA)-N1LR在脑缺血再灌注损伤后血脑屏障的作用机制。方法原代小鼠脑微血管内皮细胞常规培养,经氧糖剥夺/复糖复氧(OGD/R)处理模拟脑缺血再灌注损伤,实验分对照组、OGD组、lncRNA-N1LR过表达组(OGD处理后转染质粒lncRNA-N1LR过表达)、lncRNA-N1LR沉默组(OGD处理后转染质粒lncRNA-N1LR沉默)。采用逆转录聚合酶链反应检测各组中lncRNA-N1LR mRNA、紧密连接蛋白5(claudin-5)及闭合蛋白(occludin)mRNA表达水平;异硫氰酸荧光素-葡聚糖(FITC-dextran)渗透法检测血脑屏障通透性;免疫蛋白印迹法检测claudin-5、occludin蛋白表达。结果与对照组比较,OGD组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平下降(0.31±0.01 vs 1.00±0.10,0.42±0.03 vs 1.01±0.13,0.38±0.03 vs 1.00±0.15,P<0.05),血脑屏障FITC-dextran通透性明显升高(58.79±3.04 vs 8.87±0.63,P<0.01)。与OGD组比较,lncRNA-N1LR过表达组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平升高(0.67±0.07 vs 0.31±0.01,0.92±0.02 vs 0.42±0.03,0.70±0.08 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性降低(41.57±2.43 vs 58.79±3.04,P<0.05)。与OGD组比较,lncRNA-N1LR沉默组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平降低(0.21±0.02 vs 0.31±0.01,0.31±0.03 vs 0.42±0.03,0.22±0.02 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性升高(72.34±1.43 vs 58.79±3.04,P<0.05)。结论LncRNA-N1LR上调可能通过降低血脑屏障通透性发挥神经保护作用。展开更多
目的探究阿托伐他汀对高血糖诱导的小鼠脑缺血后出血转化(HT)的作用及机制。方法36只SPF级雄性C57BL/6小鼠随机分为假手术组、HT模型组和阿托伐他汀组,每组12只。比较各组小鼠神经功能评分、死亡率、HT发生率、HT分级评分,苏木精-伊红...目的探究阿托伐他汀对高血糖诱导的小鼠脑缺血后出血转化(HT)的作用及机制。方法36只SPF级雄性C57BL/6小鼠随机分为假手术组、HT模型组和阿托伐他汀组,每组12只。比较各组小鼠神经功能评分、死亡率、HT发生率、HT分级评分,苏木精-伊红染色观察脑组织出血情况,免疫荧光染色评估血脑屏障通透性,Western blot检测缺血半暗带脑组织免疫球蛋白G(IgG)、闭锁连接蛋白1(ZO-1)、闭合蛋白(occludin)、紧密连接蛋白5(claudin5)、基质金属蛋白酶(MMP)2和MMP-9的蛋白表达。结果与假手术组比较,HT模型组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度、IgG、MMP-2、MMP-9蛋白表达水平显著增高,ZO-1、occludin、claudin5蛋白表达水平明显降低(P<0.01)。与HT模型组比较,阿托伐他汀组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度及IgG、MMP-2、MMP-9蛋白表达水平显著降低[(2.73±1.19)分vs(3.91±0.94)分,16.7%vs 41.6%,58.3%vs 91.6%,(1.00±1.04)分vs(2.58±1.13)分,(504.30±105.52)a.u vs(859.91±153.28)a.u,4.55±1.40 vs 12.06±3.73,1.87±0.41 vs 2.95±0.68,1.47±0.24 vs 2.12±0.23,P<0.05,P<0.01],ZO-1、occludin、claduin5蛋白表达显著升高(1.55±0.20 vs 0.53±0.10,0.92±0.11 vs 0.35±0.07、0.58±0.04 vs 0.30±0.05,P<0.01)。结论阿托伐他汀可通过抑制MMP-2、MMP-9激活,上调ZO-1、occludin、claudin5表达,降低血脑屏障通透性,从而抑制高血糖诱导的脑缺血后HT。展开更多
BACKGROUND： It has been confirmed that brain-derived neurotrophic factor （BDNF） can promote the proliferation of neural stem cells （NSCs） and protect neuron-like cells in vitro. However, its effect on endogenous ...BACKGROUND： It has been confirmed that brain-derived neurotrophic factor （BDNF） can promote the proliferation of neural stem cells （NSCs） and protect neuron-like cells in vitro. However, its effect on endogenous NSCs in vivo is still unclear. OBJECTIVE： To evaluate whether BDNF can induce the endogenous NSCs to proliferate and differentiate into the neurons in the mice model of cerebral infarction. DESIGN： A synchronal controlled observation. SETTINGS： Department of Neurology, Microbiology Division of the Department of Laboratory, Tianjin First Central Hospital; Howard Florey Institute, Medical College, the University of Melbourne. MATERIALS： Twenty-four pure breed C57BL/6J mice at the age of 10 weeks old （12 males and 12 females） were divided into saline control group and BDNF-treated group, 6 males and 6 females in each group. METHODS： The experiments were performed at the University of Melbourne from July 2004 to February 2005. ① The left middle cerebral artery （MCA） was ligated in both groups to establish models of cerebral infarction and the Matsushita measuring method was used to monitor the blood flow of the lesioned region supplied by MCA. 75% reduction of blood flow should be reached in the lesioned region. ② At 24 hours after infarction, mice in the BDNF-treated group were administrated with BDNF, which was slowly delivered using an ALZET osmium pump design. BDNF was dissolved in saline at the dosage of 500 mg/kg and injected into the pump, which could release the solution consistently in the following 28 days. The mice in the saline control group accepted the same volume of saline at 24 hours after infarction. ③ The Rotarod function test began at 1 week preoperatively, the time stayed on Rotarod was recorded. The mice were tested once a day till the end of the experiment. At 4 weeks post cerebral infarction, double labeling of Nestin and GFAP, BIH tubulin and CNPase immunostaining was performed to observe the differentiation directions of the re-expressed endogenous NSCs, and the percentages of the cells differentiated into astrocytes, neurons and oligodendrocytes were calculated. MAIN OUTCOME MEASURES： ① The differentiation directions of the re-expressed endogenous NSCs, and the percentage of the cells differentiated into astrocytes, neurons and oligodendrocytes.② Comparison of motor function between the two groups. RESULTS： All the 24 pure C57BL/6J mice were involved in the analysis of results. ①Positively expressed endogenous NSCs appeared in the mice of both groups, and they mainly distributed around the focus of lesion, as well as the contralateral side. The expressed cells in the BDNF-treated group were obviously more than those in the saline control group. ②Activations of endogenous NSCs： At 4 weeks after infarction, re-expressions of endogenous NSCs appeared in both groups. The number of the re-expressed cells in the BDNF-treated group was about 4.2 times higher than that in the saline control group. The percentage of the cells differentiated into neurons in the BDNF-treated group was significantly higher than that in the saline control group （36%, 15%）, the percentage of the cells differentiated into astrocytes was lower than that in the saline control group （54%, 77%）, whereas the percentage of the cells differentiated into oligodendrocytes was similar to that in the saline control group （10%, 8%）. ③ Results of motor functional test： Compared with before cerebral infarction, the mice in both groups manifested as obvious decrease in motor function at 1 week after infarction, whereas the recovery of motor function in the BDNF-treated group was significantly superior to that in the saline control group at 2, 3 and 4 weeks （P 〈 0.01）. CONCLUSION： BDNF can promote the proliferation of endogenous NSCs in the brain of mice with cerebral infarction, it can decrease the differentiation rate of astrocytes, and increase the differentiation rate of neurons. BDNF has small influence on the differentiation of endogenous NSCs into oligodendrocytes, which was not benefit for the recovery of neural axon. Endogenous NSCs may improve the motor function of mice through the above pathways.展开更多
基金supported by Key Program of National Natural Science Foundation of China(U1432248)National Natural Science Foundation of China(11175222,11305226)
文摘Radiation encephalopathy is the main complication of cranial radiotherapy. It can cause necrosis of brain tissue and cognitive dysfunction. Our previous work had proved that a natural antioxidant shikonin possessed protective effect on cerebral ischemic injury. Here we investigated the effects of shikonin on carbon ion beam induced radiation brain injury in mice. Pretreatment with shikonin significantly increased the SOD and CAT activities and the ratio of GSH/GSSG in mouse brain tissues compared with irradiated group （P〈0.01）, while obviously reduced the MDA and PCO contents and the RO$ levels derived from of the brain mitochondria.
基金Project was supported by the National Natural Science Foundation of China No.38 970 335
文摘We have previously shown that the lipofuscin in the brain seems to have in-creased in amount in autopsy cases of epidemic hemorrhagic fever.The purpose of thisstudy was to testify if there is really such an increase.Lipfuscin in 10 sections from everybrain of 10 autopsy cases,stained with Sudan Ⅳ,Sudan black and H.E.,was carefully es-timated and found to be greatly increased as compared with the controls of the same agewithout brain disease.Animal experiment was also conducted on 15 sucking BALB/c miceby I.P.inoculation of 100 LD<sub>50</sub>（0.05ml）of strain Chen of hemorrhagic fever virus,andon 15 mice without inoculation as controls.No lipofuscin was detected in the controls.However,in the brains of experimental mice,lipofuscin was found to be markedly in-creased,especially in the necrotic cells.The findings suggest that the over-productionand deposition of lipofuscin may be a mild change caused by the virus and its related fac-tors,which might be enhanced by hypotension and shock.
基金supported by funding from a Veterans Administration BLR&D merit review grant 1–101-BX-002717 to Dr Subburaman Mohan
文摘To evaluate the long-term consequence of repetitive mild traumatic brain injury （mTBI） on bone, mTBI was induced in 10-week-old female C57BL/6J mice using a weight drop model, once per day for 4 consecutive days at different drop heights （0.5, 1 and 1.5 m） and the skeletal phenotype was evaluated at different time points after the impact. In vivo micro-CT （μ-CT） analysis of the tibial metaphysis at 2, 8 and 12 weeks after the impact revealed a 5%-32% reduction in trabecular bone mass. Histomorphometric analyses showed a reduced bone formation rate in the secondary spongiosa ofl.5 m impacted mice at 12 weeks post impact. Apparent modulus （bone strength）, was reduced by 30% （P 〈 0.05） at the proximal tibial metaphysis in the 1.5 m drop height group at 2 and 8 weeks post impact. Ex vivo μ-CT analysis of the fifth lumbar vertebra revealed a significant reduction in trabecular bone mass at 12 weeks of age in all three drop height groups. Serum levels of osteocalcin were decreased by 22%, 15%, and 19% in the 0.5, 1.0 and 1.5 m drop height groups, respectively, at 2 weeks post impact. Serum IGF-I levels were reduced by 18%-32% in mTBI mice compared to control mice at 2 weeks post impact. Serum osteocalcin and IGF-I levels correlated with trabecular BV/TV （r2 = 0.14 and 0.16, P 〈 0.05）. In conclusion, repetitive mTBI exerts significant negative effects on the trabecular bone microarchitecture and bone mechanical properties by influencing osteoblast function via reduced endocrine IGF-I actions.
文摘We have previously reported that sequential common artery sectioning (SCAS) in mice produces a reproducible pattern of mortality, extensive brain damage and a wide range of measurable neurobehavioral alterations that include motor incoordination and forelimb flexion. The present study describes a comprehensive method to assess motor functional outcome after brain ischemia produced by SCAS using swimming behavior. We found that after the second artery occlusion the time for completion of the swimming task significantly increased and the swimming pattern alterations observed in the ischemic mice showed no evidence of recovery (up to 96 h). We view the swimming performance strategy described here as a sensitive, simple and economic procedure to assess motor performance after brain ischemia.
基金funded by the State "Major New Drug Creation" Science and Technology Major Special Project Foundation, No. 2009ZX09103-324a grant from the Henan Province Science and Technology Innovation Team in University, No. 2012IRTSTHN011
文摘The persimmon leaf has been shown to improve cerebral ischemic outcomes; however, its mechanism of action remains unclear. In this study, mice were subjected to 10 minutes of ischemic preconditioning, and persimmon leaf flavonoid was orally administered for 5 days. Results showed that the persimmon leaf fiavonoid significantly improved the content of tissue type plasminogen activator and 6-keto prostaglandin-F1 a in the cerebral cortex, decreased the content of thromboxane B2, and reduced the content of plasminogen activator inhibitor-1 in mice. Following optical microscopy, persimmon leaf flavonoid was also shown to reduce cell swelling and nuclear hyperchromatism in the cerebral cortex and hippocampus of mice. These results suggested that persimmon leaf fiavonoid can effectively inhibit brain thrombosis, improve blood supply to the brain and relieve ischemia-induced pathological damage, resulting in brain ischemic tolerance.
文摘目的探讨长链非编码RNA(lncRNA)-N1LR在脑缺血再灌注损伤后血脑屏障的作用机制。方法原代小鼠脑微血管内皮细胞常规培养,经氧糖剥夺/复糖复氧(OGD/R)处理模拟脑缺血再灌注损伤,实验分对照组、OGD组、lncRNA-N1LR过表达组(OGD处理后转染质粒lncRNA-N1LR过表达)、lncRNA-N1LR沉默组(OGD处理后转染质粒lncRNA-N1LR沉默)。采用逆转录聚合酶链反应检测各组中lncRNA-N1LR mRNA、紧密连接蛋白5(claudin-5)及闭合蛋白(occludin)mRNA表达水平;异硫氰酸荧光素-葡聚糖(FITC-dextran)渗透法检测血脑屏障通透性;免疫蛋白印迹法检测claudin-5、occludin蛋白表达。结果与对照组比较,OGD组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平下降(0.31±0.01 vs 1.00±0.10,0.42±0.03 vs 1.01±0.13,0.38±0.03 vs 1.00±0.15,P<0.05),血脑屏障FITC-dextran通透性明显升高(58.79±3.04 vs 8.87±0.63,P<0.01)。与OGD组比较,lncRNA-N1LR过表达组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平升高(0.67±0.07 vs 0.31±0.01,0.92±0.02 vs 0.42±0.03,0.70±0.08 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性降低(41.57±2.43 vs 58.79±3.04,P<0.05)。与OGD组比较,lncRNA-N1LR沉默组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平降低(0.21±0.02 vs 0.31±0.01,0.31±0.03 vs 0.42±0.03,0.22±0.02 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性升高(72.34±1.43 vs 58.79±3.04,P<0.05)。结论LncRNA-N1LR上调可能通过降低血脑屏障通透性发挥神经保护作用。
文摘目的探究阿托伐他汀对高血糖诱导的小鼠脑缺血后出血转化(HT)的作用及机制。方法36只SPF级雄性C57BL/6小鼠随机分为假手术组、HT模型组和阿托伐他汀组,每组12只。比较各组小鼠神经功能评分、死亡率、HT发生率、HT分级评分,苏木精-伊红染色观察脑组织出血情况,免疫荧光染色评估血脑屏障通透性,Western blot检测缺血半暗带脑组织免疫球蛋白G(IgG)、闭锁连接蛋白1(ZO-1)、闭合蛋白(occludin)、紧密连接蛋白5(claudin5)、基质金属蛋白酶(MMP)2和MMP-9的蛋白表达。结果与假手术组比较,HT模型组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度、IgG、MMP-2、MMP-9蛋白表达水平显著增高,ZO-1、occludin、claudin5蛋白表达水平明显降低(P<0.01)。与HT模型组比较,阿托伐他汀组神经功能评分、死亡率、HT发生率、HT评分、IgG荧光强度及IgG、MMP-2、MMP-9蛋白表达水平显著降低[(2.73±1.19)分vs(3.91±0.94)分,16.7%vs 41.6%,58.3%vs 91.6%,(1.00±1.04)分vs(2.58±1.13)分,(504.30±105.52)a.u vs(859.91±153.28)a.u,4.55±1.40 vs 12.06±3.73,1.87±0.41 vs 2.95±0.68,1.47±0.24 vs 2.12±0.23,P<0.05,P<0.01],ZO-1、occludin、claduin5蛋白表达显著升高(1.55±0.20 vs 0.53±0.10,0.92±0.11 vs 0.35±0.07、0.58±0.04 vs 0.30±0.05,P<0.01)。结论阿托伐他汀可通过抑制MMP-2、MMP-9激活,上调ZO-1、occludin、claudin5表达,降低血脑屏障通透性,从而抑制高血糖诱导的脑缺血后HT。
文摘BACKGROUND： It has been confirmed that brain-derived neurotrophic factor （BDNF） can promote the proliferation of neural stem cells （NSCs） and protect neuron-like cells in vitro. However, its effect on endogenous NSCs in vivo is still unclear. OBJECTIVE： To evaluate whether BDNF can induce the endogenous NSCs to proliferate and differentiate into the neurons in the mice model of cerebral infarction. DESIGN： A synchronal controlled observation. SETTINGS： Department of Neurology, Microbiology Division of the Department of Laboratory, Tianjin First Central Hospital; Howard Florey Institute, Medical College, the University of Melbourne. MATERIALS： Twenty-four pure breed C57BL/6J mice at the age of 10 weeks old （12 males and 12 females） were divided into saline control group and BDNF-treated group, 6 males and 6 females in each group. METHODS： The experiments were performed at the University of Melbourne from July 2004 to February 2005. ① The left middle cerebral artery （MCA） was ligated in both groups to establish models of cerebral infarction and the Matsushita measuring method was used to monitor the blood flow of the lesioned region supplied by MCA. 75% reduction of blood flow should be reached in the lesioned region. ② At 24 hours after infarction, mice in the BDNF-treated group were administrated with BDNF, which was slowly delivered using an ALZET osmium pump design. BDNF was dissolved in saline at the dosage of 500 mg/kg and injected into the pump, which could release the solution consistently in the following 28 days. The mice in the saline control group accepted the same volume of saline at 24 hours after infarction. ③ The Rotarod function test began at 1 week preoperatively, the time stayed on Rotarod was recorded. The mice were tested once a day till the end of the experiment. At 4 weeks post cerebral infarction, double labeling of Nestin and GFAP, BIH tubulin and CNPase immunostaining was performed to observe the differentiation directions of the re-expressed endogenous NSCs, and the percentages of the cells differentiated into astrocytes, neurons and oligodendrocytes were calculated. MAIN OUTCOME MEASURES： ① The differentiation directions of the re-expressed endogenous NSCs, and the percentage of the cells differentiated into astrocytes, neurons and oligodendrocytes.② Comparison of motor function between the two groups. RESULTS： All the 24 pure C57BL/6J mice were involved in the analysis of results. ①Positively expressed endogenous NSCs appeared in the mice of both groups, and they mainly distributed around the focus of lesion, as well as the contralateral side. The expressed cells in the BDNF-treated group were obviously more than those in the saline control group. ②Activations of endogenous NSCs： At 4 weeks after infarction, re-expressions of endogenous NSCs appeared in both groups. The number of the re-expressed cells in the BDNF-treated group was about 4.2 times higher than that in the saline control group. The percentage of the cells differentiated into neurons in the BDNF-treated group was significantly higher than that in the saline control group （36%, 15%）, the percentage of the cells differentiated into astrocytes was lower than that in the saline control group （54%, 77%）, whereas the percentage of the cells differentiated into oligodendrocytes was similar to that in the saline control group （10%, 8%）. ③ Results of motor functional test： Compared with before cerebral infarction, the mice in both groups manifested as obvious decrease in motor function at 1 week after infarction, whereas the recovery of motor function in the BDNF-treated group was significantly superior to that in the saline control group at 2, 3 and 4 weeks （P 〈 0.01）. CONCLUSION： BDNF can promote the proliferation of endogenous NSCs in the brain of mice with cerebral infarction, it can decrease the differentiation rate of astrocytes, and increase the differentiation rate of neurons. BDNF has small influence on the differentiation of endogenous NSCs into oligodendrocytes, which was not benefit for the recovery of neural axon. Endogenous NSCs may improve the motor function of mice through the above pathways.
