ABSTRACT
Objective To investigate the effect of curcumin on brain glucose metabolism in rat models of intracerebral hemorrhage ( ICH), and evaluate the therapeutic effect of curcumin. Methods Twenty-four healthy adult male SD rats were randomly divided into 4 groups ( 6 rats/group) by simple random sampling method:normal group ( group A) , ICH+curcumin group ( group B) , ICH +vehicle group ( group C) , and sham operated group (group D). ICH model was made by injecting collagenase (2 μl) into the right cau-date nucleus of rat. 18F-FDG with a dose of (17.8±0.4) MBq was injected through caudal vein at 6 h, 24 h, 48 h, 3 d, 5 d, 7 d, 14 d after the model was built successfully. 18F-FDG microPET/CT was performed 30 min post injection at each time point. ROI in the hematoma and peri-hematoma brain tissue was drawn, and its volume and SUVmean were measured and analyzed. Meanwhile, each rat was evaluated by neurological severi-ty scores ( NSS) . Analysis of variance for repeated measurement data and Pearson correlation analysis were used. Results NSS in group B were lower than those in group C from 6 h to 5 d (F=183.26, P<0. 01). MicroPET/CT showed decreased glucose uptake in the hematoma and peri-hematoma brain tissue after cere-bral hemorrhage. In group B, the 18 F-FDG uptake in peri-hematoma brain tissue of ICH decreased after 6 h, and reached the minimum at 24 h (1.20±0.08), and then increased. The glucose metabolism in group B was significantly lower than that in group D at each time point (F=7306.74, P<0.01), and significantly higher than that in group C ( F=471.50, P<0.01) . SUVmean within ROI had a significantly negative correla-tion with both ROI volume and NSS in group B at each time point( r values:-0.672 and -0.727, both P<0. 05) . Conclusions MicroPET/CT might visualize decreased glucose uptake of hematoma and peri-hema-toma brain tissue after cerebral hemorrhage. Curcumin might have a neuroprotective effect on ICH, and im-prove the glucose uptake in hematoma and peri-hematoma brain tissue.
ABSTRACT
Objective To investigate the effect of curcumin on brain glucose metabolism in rat models of intracerebral hemorrhage ( ICH), and evaluate the therapeutic effect of curcumin. Methods Twenty-four healthy adult male SD rats were randomly divided into 4 groups ( 6 rats/group) by simple random sampling method:normal group ( group A) , ICH+curcumin group ( group B) , ICH +vehicle group ( group C) , and sham operated group (group D). ICH model was made by injecting collagenase (2 μl) into the right cau-date nucleus of rat. 18F-FDG with a dose of (17.8±0.4) MBq was injected through caudal vein at 6 h, 24 h, 48 h, 3 d, 5 d, 7 d, 14 d after the model was built successfully. 18F-FDG microPET/CT was performed 30 min post injection at each time point. ROI in the hematoma and peri-hematoma brain tissue was drawn, and its volume and SUVmean were measured and analyzed. Meanwhile, each rat was evaluated by neurological severi-ty scores ( NSS) . Analysis of variance for repeated measurement data and Pearson correlation analysis were used. Results NSS in group B were lower than those in group C from 6 h to 5 d (F=183.26, P<0. 01). MicroPET/CT showed decreased glucose uptake in the hematoma and peri-hematoma brain tissue after cere-bral hemorrhage. In group B, the 18 F-FDG uptake in peri-hematoma brain tissue of ICH decreased after 6 h, and reached the minimum at 24 h (1.20±0.08), and then increased. The glucose metabolism in group B was significantly lower than that in group D at each time point (F=7306.74, P<0.01), and significantly higher than that in group C ( F=471.50, P<0.01) . SUVmean within ROI had a significantly negative correla-tion with both ROI volume and NSS in group B at each time point( r values:-0.672 and -0.727, both P<0. 05) . Conclusions MicroPET/CT might visualize decreased glucose uptake of hematoma and peri-hema-toma brain tissue after cerebral hemorrhage. Curcumin might have a neuroprotective effect on ICH, and im-prove the glucose uptake in hematoma and peri-hematoma brain tissue.
ABSTRACT
The incidence of thyroid carcinoma is associated with a variety of factors.Radiation is the clear risk factor,the relationship between iodine intake and thyroid carcinoma remains controversial.Researches show that the genetic and epigenetic changes of many signaling pathways are the key of molecular pathogenetic mechanism of thyroid carcinoma.In addition,thyroid stimulating hormone,body mass index and chronic lymphocytic thyroiditis are also associated with thyroid carcinoma.