Association of genetic polymorphisms of GALNT3 and VDR with osteoporosis in postmenopausal women.

The correlation of genetic polymorphisms of GALNT3 and vitamin D receptor (VDR) with osteoporosis in postmenopausal women was investigated. A total of 1,212 cases of postmenopausal patients diagnosed with osteoporosis (observation group) and 404 cases of postmenopausal women without osteoporosis (control group) were selected. Dual-energy X-ray absorptiometry was used for measurement of bone mineral density (BMD) of lumbar vertebrae L2-4, proximal femoral neck and total hip, and classifications were made. TaqMan genotyping technology was employed to examine tag single-nucleotide polymorphism (tagSNP) of GALNT3 and VDR and the correlation of tagSNP with bone turnover markers (BTMs) and serum calcium and phosphorous levels was analyzed. The multiple logistic regression analysis was used to screen risk factors for osteoporosis. A comparison of age and menopause time of the two groups, yielded no statistical significance difference (P>0.05). BMD and T values of the lumbar vertebrae, femoral neck and total hip in the observation group were significantly lower than those in the control group, and the differences were statistically significant (P<0.05). A comparison of the degree of osteoporosis, yielded statistically significant differences (P<0.05). The proportion of tagSNP of 5 loci in GALNT3 and 3 loci in VDR in the observation group was significantly higher than that in the control group, and the differences were of statistical significance (P<0.05). Levels of 25-OHD3, ß-CTX, P1NP and serum calcium in the observation group were lower than those in the control group and the level of serum phosphorus in the observation group was higher than that in the control group, and all of these results were statistically significant (P<0.05). The result of the correlation analysis revealed that rs1425000 and rs757343 were negatively correlated with BTM and serum calcium and phosphorus levels (P<0.05). The result of the regression analysis revealed that 8 tagSNPs were independent risk factors for osteoporosis. Genetic polymorphisms of GALNT3 and VDR were closely associated with osteoporosis in postmenopausal women.

[The expression of bFGF, GAP-43 and neurogenesis after cerebral ischemia/reperfusion in rats].

OBJECTIVE: To observe time points of the expressions of basic fibroblast growth factor (bFGF), growth associated protein-43 (GAP-43) and neurogenesis after cerebral ischemia/reperfusion in rats and explore its possible mechanism of neurogenesis. METHODS: Models of middle cerebral artery occlusion (MCAO) were established in SD rats which were divided into 3 d, 7 d, 14 d and 28 d groups (n = 6). The neurological severity was evaluated by neurological severity scores (NSS) and scores of motor test (SMT). Neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Nissl staining; The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blot and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively. RESULTS: It showed up neurologic impairment and motor dysfunction after cerebral ischemia/reperfusion in rats at 3 d, the numbers of neuron apoptosis also peaked at 3d, the protein levels of bFGF and GAP-43 were significantly increased in time-dependent manner, peaked at 7 d and then decreased gradually, meanwhile, Brdu and NeuN double fluorescence staining displayed scattered Brdu-and NeuN-positive cells in the boundary zone of the infarction area. CONCLUSION: These results suggest that the upregulation of bFGF and GAP-43 may contribute to the neurogenesis after cerebral ischemia/reperfusion.

[Influence of ilexonin A on the expression of bFGF, GAP-43 and neurogenesis after cerebral ischemia-reperfusion in rats].

This study is to observe the effect of ilexonin A (IA) on the expression of basic fibroblast growth factor (bFGF) and growth associated protein-43 (GAP-43), and neurogenesis after cerebral ischemia-reperfusion in rats and explore its possible mechanism of protecting neuronal injury. Models of middle cerebral artery occlusion (MCAO) were established in SD rats. Before and after two hours ischemia-reperfusion, IA (20 and 40 mg x kg(-1)) was injected immediately and on 3, 7, 14, and 28 d once a day. The neurological severity was evaluated by neurological severity scores (NSS); neuronal injury in the boundary zone of the infarction area was evaluated by TUNEL and Niss1 staining. The expressions of bFGF and GAP-43 and neurogenesis were evaluated by Western blotting and 5-bromodeoxyuridine (Brdu) fluorescence staining, respectively. After treatment with IA, the NSS of treatment groups were lower than that of the models (3 and 7 d). The number of TUNEL positive neurons decreased and Nissl positive neurons increased at the same time (3 d). The expressions of bFGF and GAP-43 increased significantly in the boundary zone of the infarction area when compared to model group. Moreover, IA markedly enhanced the neurogenesis in the brain after ischemia-reperfusion, which revealed an increase of Brdu/NeuN positive cells in the boundary zone of the infarction area. The possible mechanism of protecting neuronal injury of IA may be related to inhibition on neuronal apoptosis, upregulation of bFGF and GAP-43, and neurogenesis in boundary zone of infarction after cerebral ischemia-reperfusion.