Objective:To observe the effects of hyperbaric oxygen (HBO) at different courses of treatment on the proliferation of endogenous neural stem cells(NSCs) in cerebral ventricular subventricular zone (SVZ) and hippocampal dentate gyrus (DG) in rats with focal cerebral ischemia at different periods.Methods:The model of focal cerebral ischemia-reperfusion was performed by middle cerebral artery occlusion (MCAO). A total of 105 rats were divided by lottery into pseudo-surgery group(SS), ischemia-reperfusion group (IR group), HBO at 1 st day after ischemia-reperfusion group (IR1d+ HBO group), HBO at 7 th day after ischemia-reperfusion group (IR7d+ HBO group), HBO at 14 th day after ischemia-reperfusion group (IR14d+ HBO group), and HBO at 28 th day after ischemia-reperfusion group (IR28d+ HBO). The SVZ and DG-derived NSCs were detected by immunofluorescence BrdU/Nestin double labeling at the 2 nd, 4 th, 6 th, and 8 th week after modeling. Results:At the 2 nd week after modeling, the number of DG BrdU/Nestin positive cells was 21.20±2.58 in the SS group, 56.40±4.51 in the IR group, 82.80±7.19 in the IR1d+ HBO group, and 70.00±5.09 in the IR7d+ HBO group. At the 4 th week, it was 21.00±2.92 in the SS group, 37.20±3.27 in the IR group, 70.60±5.12 in the IR1d+ HBO group, 57.20±3.56 in the IR7d+ HBO group, 45.80±4.32 in the IR14d+ HBO group. At the 6 th week, it was 20.20±1.92 in the SS group, 26.40±2.74 in the IR group, 48.00±3.16 in the IR1d+ HBO group, 40.60±3.36 in the IR7d+ HBO group, 31.60±2.41 in the IR14d+ HBO group, 26.60±2.30 in the IR28d+ HBO group. The number of DG BrdU/Nestin positive cells was statistically significant among all subgroups during the same period ( P<0.01) except for that at the 8 th week. The pairwise comparison showed the numbers of DG BrdU/Nestin positive cells in the IR group at all time points were all higher than those in the SS group at the same time point ( P<0.05). Except for that at the 8 th week, all the numbers of DG BrdU/Nestin positive cells in the IR1d+ HBO group, the IR7d+ HBO group, and the IR14d+ HBO group at each time point were higher than those in the IR group ( P<0.05). In all the subgroups, the number of DG BrdU/Nestin positive cells reached the highest point at the 2 nd week/the initial measurement point ( P<0.05). At the 2 nd week after modeling, the number of SVZ BrdU/Nestin positive cells was 25.20±2.86 in the SS group, 66.40±2.96 in the IR group, 90.40±6.50 in the IR1d+ HBO group, 75.00±4.58 in the IR7d+ HBO group. At the 4 th week, it was 24.20±1.48 in the SS group, 49.80±4.32 in the IR group, 72.40±4.92 in the IR1d+ HBO group, 57.80±6.46 in the IR7d+ HBO group, 43.80±3.56 in the IR14d+ HBO group. At the 6 th week, it was 24.40±2.41 in the SS group, 28.80±2.77 in the IR group, 51.00±4.30 in the IR1d+ HBO group, 42.00±3.39 in the IR7d+ HBO group, 34.80±2.58 in the IR14d+ HBO group, 31.30±3.41 in the IR28d+ HBO group. The number of SVZ BrdU/Nestin positive cells was statistically significant among all subgroups during the same period ( P<0.05). The pairwise comparison showed the numbers of SVZ BrdU/Nestin positive cells in the IR group at all time points were all higher than those in the SS group at the same time point ( P<0.05) except for the 8 th week. The numbers of SVZ BrdU/Nestin positive cells in the IR1d+ HBO group at each time point were higher than that in the IR group( P<0.05). The numbers of SVZ BrdU/Nestin positive cells in the IR7d+ HBO group, the IR14d+ HBO group, and the IR28d+ HBO group at the 2 nd, 4 th, and 6 th week were higher than those in the IR group at the same time point ( P<0.05). In all the subgroups, the number of SVZ BrdU/Nestin positive cells reached the highest point at the 2 nd week/the initial measurement point ( P<0.05). Conclusion:The earlier HBO treatment on cerebral infarction starts, the better promotion of the proliferation of SVZ and DG-derived NSCs achieves. HBO treatment has almost no effect on the proliferation of endogenous NSCs at late cerebral infarction.

Objective:To observe the differentiation of endogenous neural stem cells (NSCs) in the ischemic brain of rats with focal cerebral ischemia at different stages with various treatments.Methods:The model of focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO). A total of 105 rats were randomly divided into sham-surgery group (SS), ischemia-reperfusion group (IR), receiving hyperbaric oxygen (HBO) 1 day after modeling group (IR1d+ HBO), receiving HBO 7 days after modeling group (IR7d+ HBO group), receiving HBO 14 days after modeling group (IR14d+ HBO group), and receiving HBO 28 days after modeling group (IR28d+ HBO group). At the 2nd, 4th, 6th and 8th week after modeling, the cells of newly generated neurons and astrocyte in the ischemic area were positive in both immunofluorescence BrdU/β-tubulin and BrdU/glial fibrillary acidic protein (GFAP) test were detected.Results:Two weeks after modeling, the expressions of BrdU/β-tubulin were 11.40±1.52 in the SS group, 36.60±2.51 in the IR group, 48.60±3.21 in the IR1d+ HBO group, and 42.60±2.30 in the IR7d+ HBO group; four weeks after modeling, it was 12.20±1.92 in the SS group, 26.20±2.28 in the IR group, 39.80±2.17 in the IR1d+ HBO group, 33.20±1.92 in the IR7d+ HBO group, 29.20±1.48 in the IR14d+ HBO group. Six weeks after modeling, it was 12.40±1.67 in the SS group, 18.60±1.82 in the IR group, 30.20±2.49 in the IR1d+ HBO Group, 25.40±2.79 in the IR7d+ HBO group, 21.40±2.50 in the IR14d+ HBO group, 19.60±1.67 in the IR28d+ HBO group. Eight weeks after modeling, it was 11.80±1.64 in the SS group, 16.40±2.07 in the IR group, 24.40±1.95 in the IR1d+ HBO group, 21.20±1.48 in the IR7d+ HBO group, 18.40±1.67 in the IR14d+ HBO group, and 15.60±1.82 in the IR28d+ HBO group. The differences in the expressions of BrdU/β-tubulin between these groups were statistically significant ( P<0.01). Compared with the SS group, the expression of BrdU/β-tubulin increased in the IR group at each time point ( P<0.05). The expressions of BrdU/β-tubulin in the IR1d+ HBO and the IR7d+ HBO were higher than those in the IR group at each time point; while there were statistical differences comparing those in the IR14d+ HBO group and the IR28d+ HBO group with those in the IR group at each time point ( P>0.05). The expressions of BrdU/β-tubulin were at the highest level at the second week in all the groups except the SS group ( P<0.05). (2) Two weeks after modeling, the expression of BrdU/GFAP was 22.60±1.82 in the SS group, 59.00±3.67 in the IR group, 50.60±2.51 in the IR1d+ HBO group, and 55.20±2.58 in the IR7d+ HBO group. Four weeks after modeling, it was 22.20±1.48 in the SS group, 45.00±2.24 in the IR group, 35.80±1.64 in the IR1d+ HBO group, 40.20±2.16 in the IR7d+ HBO group, and 44.60±2.51 in the IR14d+ HBO group. Six weeks after modeling, it was 22.80±1.64 in the SS group, 26.68±1.78 in the IR group, 27.40±1.67 in the IR1d+ HBO group, 28.40±1.51 in the IR7d+ HBO group, 26.20±1.78 in the IR14d+ HBO group, and 26.20±1.48 in the IR28d+ HBO group. Eight weeks after modeling, it was 21.60±1.81 in the SS group, 21.40±1.14 in the IR group, 24.00±1.58 in the IR1d+ HBO group, 24.80±1.92 in the IR7d+ HBO group, 23.40±1.67 in the IR14d+ HBO group, and 22.20±1.30 in the IR28d+ HBO group. At each time point, the differences of BrdU/GFAP expression between each group were statistically significant ( P<0.05). Furthermore, the BrdU/GFAP expression in the IR group was higher than that in the SS group at each time point except the 8th week. The expressions of BrdU/GFAP in the IR1d+ HBO group and the IR7d+ HBO group were higher than those in the IR group at the 2nd and the 4th weeks ( P<0.05). There was no statistically significant difference in the expressions of BrdU/GFAP between the IR1d+ HBO group and the IR7d+ HBO group at the 6th and the 8th week( P>0.05). There was no statistically significance comparing the expressions of BrdU/GFAP in the IR14d+ HBO and the IR 28d+ HBO group respectively with those in the SS group( P>0.05) at each time point. All the expressions of BrdU/GFAP in each group reached the highest level at the 2nd week ( P<0.05). Conclusion:In the early and the recovery period, HBO can promote the differentiation of NSCs in the ischemic areas into neurons and inhibit its differentiation into astrocytes. An early long-term treatment of HBO can maintain NSCs differentiation in the ischemic area into neurons for a long time.

Objective:To observe the differentiation of endogenous neural stem cells (NSCs) in the ischemic brain of rats with focal cerebral ischemia at different stages with various treatments.Methods:The model of focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO). A total of 105 rats were randomly divided into sham-surgery group (SS), ischemia-reperfusion group (IR), receiving hyperbaric oxygen (HBO) 1 day after modeling group (IR1d+ HBO), receiving HBO 7 days after modeling group (IR7d+ HBO group), receiving HBO 14 days after modeling group (IR14d+ HBO group), and receiving HBO 28 days after modeling group (IR28d+ HBO group). At the 2nd, 4th, 6th and 8th week after modeling, the cells of newly generated neurons and astrocyte in the ischemic area were positive in both immunofluorescence BrdU/β-tubulin and BrdU/glial fibrillary acidic protein (GFAP) test were detected.Results:Two weeks after modeling, the expressions of BrdU/β-tubulin were 11.40±1.52 in the SS group, 36.60±2.51 in the IR group, 48.60±3.21 in the IR1d+ HBO group, and 42.60±2.30 in the IR7d+ HBO group; four weeks after modeling, it was 12.20±1.92 in the SS group, 26.20±2.28 in the IR group, 39.80±2.17 in the IR1d+ HBO group, 33.20±1.92 in the IR7d+ HBO group, 29.20±1.48 in the IR14d+ HBO group. Six weeks after modeling, it was 12.40±1.67 in the SS group, 18.60±1.82 in the IR group, 30.20±2.49 in the IR1d+ HBO Group, 25.40±2.79 in the IR7d+ HBO group, 21.40±2.50 in the IR14d+ HBO group, 19.60±1.67 in the IR28d+ HBO group. Eight weeks after modeling, it was 11.80±1.64 in the SS group, 16.40±2.07 in the IR group, 24.40±1.95 in the IR1d+ HBO group, 21.20±1.48 in the IR7d+ HBO group, 18.40±1.67 in the IR14d+ HBO group, and 15.60±1.82 in the IR28d+ HBO group. The differences in the expressions of BrdU/β-tubulin between these groups were statistically significant ( P<0.01). Compared with the SS group, the expression of BrdU/β-tubulin increased in the IR group at each time point ( P<0.05). The expressions of BrdU/β-tubulin in the IR1d+ HBO and the IR7d+ HBO were higher than those in the IR group at each time point; while there were statistical differences comparing those in the IR14d+ HBO group and the IR28d+ HBO group with those in the IR group at each time point ( P>0.05). The expressions of BrdU/β-tubulin were at the highest level at the second week in all the groups except the SS group ( P<0.05). (2) Two weeks after modeling, the expression of BrdU/GFAP was 22.60±1.82 in the SS group, 59.00±3.67 in the IR group, 50.60±2.51 in the IR1d+ HBO group, and 55.20±2.58 in the IR7d+ HBO group. Four weeks after modeling, it was 22.20±1.48 in the SS group, 45.00±2.24 in the IR group, 35.80±1.64 in the IR1d+ HBO group, 40.20±2.16 in the IR7d+ HBO group, and 44.60±2.51 in the IR14d+ HBO group. Six weeks after modeling, it was 22.80±1.64 in the SS group, 26.68±1.78 in the IR group, 27.40±1.67 in the IR1d+ HBO group, 28.40±1.51 in the IR7d+ HBO group, 26.20±1.78 in the IR14d+ HBO group, and 26.20±1.48 in the IR28d+ HBO group. Eight weeks after modeling, it was 21.60±1.81 in the SS group, 21.40±1.14 in the IR group, 24.00±1.58 in the IR1d+ HBO group, 24.80±1.92 in the IR7d+ HBO group, 23.40±1.67 in the IR14d+ HBO group, and 22.20±1.30 in the IR28d+ HBO group. At each time point, the differences of BrdU/GFAP expression between each group were statistically significant ( P<0.05). Furthermore, the BrdU/GFAP expression in the IR group was higher than that in the SS group at each time point except the 8th week. The expressions of BrdU/GFAP in the IR1d+ HBO group and the IR7d+ HBO group were higher than those in the IR group at the 2nd and the 4th weeks ( P<0.05). There was no statistically significant difference in the expressions of BrdU/GFAP between the IR1d+ HBO group and the IR7d+ HBO group at the 6th and the 8th week( P>0.05). There was no statistically significance comparing the expressions of BrdU/GFAP in the IR14d+ HBO and the IR 28d+ HBO group respectively with those in the SS group( P>0.05) at each time point. All the expressions of BrdU/GFAP in each group reached the highest level at the 2nd week ( P<0.05). Conclusion:In the early and the recovery period, HBO can promote the differentiation of NSCs in the ischemic areas into neurons and inhibit its differentiation into astrocytes. An early long-term treatment of HBO can maintain NSCs differentiation in the ischemic area into neurons for a long time.

Objective:To observe the effects of hyperbaric oxygen (HBO) at different courses of treatment on the proliferation of endogenous neural stem cells(NSCs) in cerebral ventricular subventricular zone (SVZ) and hippocampal dentate gyrus (DG) in rats with focal cerebral ischemia at different periods.Methods:The model of focal cerebral ischemia-reperfusion was performed by middle cerebral artery occlusion (MCAO). A total of 105 rats were divided by lottery into pseudo-surgery group(SS), ischemia-reperfusion group (IR group), HBO at 1 st day after ischemia-reperfusion group (IR1d+ HBO group), HBO at 7 th day after ischemia-reperfusion group (IR7d+ HBO group), HBO at 14 th day after ischemia-reperfusion group (IR14d+ HBO group), and HBO at 28 th day after ischemia-reperfusion group (IR28d+ HBO). The SVZ and DG-derived NSCs were detected by immunofluorescence BrdU/Nestin double labeling at the 2 nd, 4 th, 6 th, and 8 th week after modeling. Results:At the 2 nd week after modeling, the number of DG BrdU/Nestin positive cells was 21.20±2.58 in the SS group, 56.40±4.51 in the IR group, 82.80±7.19 in the IR1d+ HBO group, and 70.00±5.09 in the IR7d+ HBO group. At the 4 th week, it was 21.00±2.92 in the SS group, 37.20±3.27 in the IR group, 70.60±5.12 in the IR1d+ HBO group, 57.20±3.56 in the IR7d+ HBO group, 45.80±4.32 in the IR14d+ HBO group. At the 6 th week, it was 20.20±1.92 in the SS group, 26.40±2.74 in the IR group, 48.00±3.16 in the IR1d+ HBO group, 40.60±3.36 in the IR7d+ HBO group, 31.60±2.41 in the IR14d+ HBO group, 26.60±2.30 in the IR28d+ HBO group. The number of DG BrdU/Nestin positive cells was statistically significant among all subgroups during the same period ( P<0.01) except for that at the 8 th week. The pairwise comparison showed the numbers of DG BrdU/Nestin positive cells in the IR group at all time points were all higher than those in the SS group at the same time point ( P<0.05). Except for that at the 8 th week, all the numbers of DG BrdU/Nestin positive cells in the IR1d+ HBO group, the IR7d+ HBO group, and the IR14d+ HBO group at each time point were higher than those in the IR group ( P<0.05). In all the subgroups, the number of DG BrdU/Nestin positive cells reached the highest point at the 2 nd week/the initial measurement point ( P<0.05). At the 2 nd week after modeling, the number of SVZ BrdU/Nestin positive cells was 25.20±2.86 in the SS group, 66.40±2.96 in the IR group, 90.40±6.50 in the IR1d+ HBO group, 75.00±4.58 in the IR7d+ HBO group. At the 4 th week, it was 24.20±1.48 in the SS group, 49.80±4.32 in the IR group, 72.40±4.92 in the IR1d+ HBO group, 57.80±6.46 in the IR7d+ HBO group, 43.80±3.56 in the IR14d+ HBO group. At the 6 th week, it was 24.40±2.41 in the SS group, 28.80±2.77 in the IR group, 51.00±4.30 in the IR1d+ HBO group, 42.00±3.39 in the IR7d+ HBO group, 34.80±2.58 in the IR14d+ HBO group, 31.30±3.41 in the IR28d+ HBO group. The number of SVZ BrdU/Nestin positive cells was statistically significant among all subgroups during the same period ( P<0.05). The pairwise comparison showed the numbers of SVZ BrdU/Nestin positive cells in the IR group at all time points were all higher than those in the SS group at the same time point ( P<0.05) except for the 8 th week. The numbers of SVZ BrdU/Nestin positive cells in the IR1d+ HBO group at each time point were higher than that in the IR group( P<0.05). The numbers of SVZ BrdU/Nestin positive cells in the IR7d+ HBO group, the IR14d+ HBO group, and the IR28d+ HBO group at the 2 nd, 4 th, and 6 th week were higher than those in the IR group at the same time point ( P<0.05). In all the subgroups, the number of SVZ BrdU/Nestin positive cells reached the highest point at the 2 nd week/the initial measurement point ( P<0.05). Conclusion:The earlier HBO treatment on cerebral infarction starts, the better promotion of the proliferation of SVZ and DG-derived NSCs achieves. HBO treatment has almost no effect on the proliferation of endogenous NSCs at late cerebral infarction.

Objective :To explore influence of intra—arterial thrombolysis combined hyperbaric oxygen on serum levels of soluble intercellular adhesion molecule—1 (sICAM—1) and calcitonin gene related peptide (CGRP) in patients with severe ischemic stroke .Methods : A total of 96 patients with severe ischemic stroke in our hospital were randomly and equally divided into thrombolysis group and combined treatment group (received intra—arterial thrombolysis +hyperbaric oxygen therapy ).United States National Institutes of Health Stroke score (NIHSS) was used to assess neurological function recovery , and modified Rankin rating score (mRS) was used to assess recovery of clinical symptoms.After two—week treatment ,clinical therapeutic effect etc .were compared between two groups .Results :Compared with thrombolysis group after treatment ,there was significant rise in total effective rate (77.08% vs. 93. 75%, P＝0.021) ;significant reductions in scores of NIHSS [ (8.10 ± 3.45) scores vs .(5.36 ± 2.11) scores] and mRS [ (2.58 ± 0. 80) scores vs .(1.81 ± 0.76) scores] ;significant reduction in serum sICAM—1 level [ (237.31 ± 18. 04) ng／ml vs.(220.25 ± 16.40) ng／ml] ,and significant rise in serum CGRP level [ (27.02 ± 6.06) pg／ml vs. (35.24 ± 6.13) pg／ml] in combined treatment group , P＝0.001 all.There was no significant difference in revascu—larization within two weeks between two groups , P＝0.551. Conclusion : Intra—arterial thrombolysis combined hy—perbaric oxygen possesses significant therapeutic effect on patients with severe ischemic stroke .It can relieve clinical symptoms ,recover cognitive function ,improve revascularization rate in these patients .

Objective To investigate the proliferation,apoptosis and cell cycle and possible mechanisms of different breast cell lines by difluoromethylorithine (DMFO).Methods The growth of breast cancer MDA-435 (ODC GG) cell lines and SK-br3 (ODC AA) cell lines treated with DFMO were observed.The apoptosis and cell cycle were detected by flow cytometry.PCR was applied to detect the changes of A and G alleles of ODC G316A in MCF-7 cells treated with DFMO.Results The growth inhibition rates of MDA-435 and SK-br3 cells treated with 10 mmol/L and 20 mmol/L DFMO after 48 h were 24.1％ and 33.6 ％,46.3 ％ and 53.5 ％,respectively,and there was statistical significance (t =2.134,P =0.021,t =2.213,P =0.019).The growth inhibition rates of MDA-435 and SK-br3 treated with 10 mmol/L and 20 mmol/L DFMO after 72 h were 28.9 ％ and 35.7 ％,54.3 ％ and 65.4 ％,respectively,and there was statistical significance (t =2.434,P =0.015,t =2.489,P =0.013).The apoptosis rates of MDA-435 (ODC GG) and SK-br3 (ODC AA) cells both dealt with 20 mmol/L of DFMO after 24 h,48 h and 72 h were (7.58± 2.06) ％ and (13.88±3.45) ％ (t =2.047,P =0.041),(43.28±14.28) ％ and (59.96±16.42) ％ (t =3.680,P =0.000),(77.87±30.25) ％ and (93.08±32.15) ％ (t =3.293,P =0.000 1),respectively.The proportions of S stage cells MDA-435 (ODC GG) and SK-br3 (ODC AA) cells under the same condition after 24 h,48 h and 72 h were (13.25±2.38) ％ and (12.89±2.21) ％ (P ＞ 0.05),(21.43±3.12) ％ and (12.24±3.55) ％ (t =2.638,P =0.012),(16.32±3.23) ％ and (15.24±3.01) ％ (P ＞ 0.05),respectively.After the treatment by DFMO,the expression of ODC G316A allele A in breast cancer cell line MCF-7 (ODC AG) was reduced (t =3.708,P =0.000),and the expression of G had no significant changes.Conclusion The proliferation inhibition and apoptosis in breast cancer cells treated by DFMO is different in breast cancer cells with different genetic type of ODC G316A.DFMO can inhibit the activity of ODC,and the mechanism may be that DFMO could selectively bind to ODC G316A allele A.

BACKGROUND:Previous studies have shown that bone marrow mesenchymal stem cels in the treatment of neurological diseases have achieved some success, which can promote neurological alterations; however, there is no breakthrough on gene and drug regulation. OBJECTIVE:To investigate the influence of ginsenosides-induced differentiation of bone marrow mesenchymal stem cels on nerve regeneration after traumatic brain injury. METHODS: A traumatic brain injury model was built in rats using hydraulic shock method, and then rat models were randomly divided into model group (traumatic brain injury group), bone marrow mesenchymal stem cel group, ginsenosides group (ginsenosides induced differentiation of bone marrow mesenchymal stem cels). At 2 weeks after transplantation, western blot assay was used to detect protein expression levels of nerve growth factor and brain-derived neurotrophic factor, immunohistochemistry assay used to detect the number of BrdU-positive cels. At 1, 3 days and 1, 2 weeks after transplantation, modified neurological severity scores were recorded. RESULTS AND CONCLUSION: The expression levels of nerve growth factor and brain-derived neurotrophic factor protein were significantly higher in the ginsenosides group than the bone marrow mesenchymal stem cel group and model group (P < 0.05). The number of BrdU positive nerve cels was also higher in the ginsenosides group than the bone marrow mesenchymal stem cel group and model group (P < 0.05). At 3 days and 1, 2 weeks after transplantation, the modified neurological severity scores in the ginsenosides group were lower than those in the bone marrow mesenchymal stem cel group and model group (P< 0.05). These findings indicate that ginsenoside-induced bone marrow mesenchymal stem cel transplantation can promote nerve regeneration in rats with traumatic brain injury, which has better outcomes than bone marrow mesenchymal stem cel transplantation alone.

BACKGROUND:Bone marrow mesenchymal stem cels (BMSCs) can promote nerve regeneration, but there are no better results because of the limitations of treatment methods. BMSC transplantation alone is not enough to achieve desired therapeutic effects. OBJECTIVE:To investigate the effect of fibroblast growth factor (FGF)-modified BMSC transplantation on functional recovery and expression of glial fibrilary acidic protein after traumatic brain injury. METHODS:Animal models of traumatic brain injury were established in Sprague-Dawley rats using hydraulic shock method, and then randomized into control group (traumatic brain injury group), BMSC group and FGF-BMSC group (FGF-modified BMSC group). After isolation and culture, BMSCs were modified by adenovirus vector-mediated FGF gene. Western blot assay was used to detect transfection efficiency and glial fibrilary acidic protein expression; immunohistochemical detection was used to detect distribution and number of BrdU positive cels in the brain; Longa score was used to evaluate the neurologic function of rats at 1, 3 days, 1, 2 weeks after transplantation; TUNEL assay was used to detect cel apoptosis in the brain. RESULTS AND CONCLUSION:Western blot results showed that FGF gene was successfuly transferred to the adenovirus vector, and capable of expressing in BMSCs; moreover, the glial fibrilary acidic protein expression of FGF-BMSC group was significantly higher than that in the other two groups (P < 0.05). The number of BrdU positive cels in the brain was significantly higher in the FGF-BMSC group than the other two groups (P < 0.05). Two weeks after transplantation, the Longa scores in the FGF-BMSC group were significantly lower than those in the other two groups (P < 0.05). TUNEL results showed that the number of apoptotic cels in the FGF-BMSC group was significantly lower than that in the other two groups (P < 0.05). These findings indicate that FGF-modified BMSCs transplantation is able to improve neurological damage after traumatic brain injury and promote neurological recovery, which is better than BMSC transplantation alone.