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.

Objective To investigate the correlation of insulin resistance (IR) and benign prostate hyperplasia (BPH). Methods The 200 health examination men were divided into three groups according to the prostate volume (PV). There were 100 healthy subjects as control group (PV≤20 ml), 50 cases in BPH1 group (20 ml＜PV＜50 ml) and 50 cases in BPH2 group (PV≥50 ml).The fasting blood glucose (FBG) and fasting serum insulin (FSI) were determined using hexokinase method and radioimmunoassy, respectively. The IR index (IRI) and body mass index (BMI) were calculated according to the formula in HOMA model. Results There were no statistical differences between BPHl group and healthy control group in IRI (1.10±0. 18 vs. 1.18±0.21) and BMI (22. 0±3.0vs. 21.8±2.7) (t=0.74, 0.18, both P＞0. 05), but the IRI (1.31±0.19) and BMI (24. 8±3.29) increased in BPH2 group (P=0. 01, 0.03). The percentage of hyperglycosemia was higher in BPH patients than in normal controls (25% vs. 5%, P = 0. 00). Of them, the percentage of hyperglycosemia was the highest in BPH2 group (36%, P = 0. 01 ), their IRI ( 1.47 ± 0.21 ) was higher than in euglycemia patients (t=3.92, P=0.00), but the BM1 was unchanged compared with the control group ( 25.8 ± 4.3 vs. 24.3 ± 2.71, P = 0. 95 ). Conclusions There is a positive correlation of IR and hyperglycosemia with severe BPH, and the IR in severe BPH is independent of BMI.