Objective: To investigate the colocalization of Somatostatin (SOM ) and NADPH--diaphorase (NADPHd ) of the neurons in raphe nuclei innervating pharyngeal muscles in the rats. Methods: After PRV was injected into the p...Objective: To investigate the colocalization of Somatostatin (SOM ) and NADPH--diaphorase (NADPHd ) of the neurons in raphe nuclei innervating pharyngeal muscles in the rats. Methods: After PRV was injected into the pharyngeal muscles. PRV and SOM immunofluorescence double labeling procedure was completed at first,then proceeded NADPH -d histochemistry. Results: PRV and SOM double--labled cells were present mainly in the nucleus raphe magnus. but some PRV and SOM double labled neurons were found in the other raphe nuclei as well, such as nucleus raphe pallidus. nucleus raphe obsurus, median raphe nucleus and dorsal raphe nucleus.NADPH -d positive neurons were also observed in the raphe nuclei. PRV. SOM and NADPH-d triple labeling neurons were found in the nucleus raphe magnus. Conclusion: It is suggested that the colocalization of SOM and NADPH--d of the neurons in the raphe nuclei innervating pharyngeal muscles may play an important role in the coordination of the pharyngeal motility.展开更多
Mitochondrial DNA(mtDNA) common deletion(CD) plays a significant role in aging and age-related diseases.In this study,we used D-galactose(D-gal) to generate an animal model of aging and the involvement and causative m...Mitochondrial DNA(mtDNA) common deletion(CD) plays a significant role in aging and age-related diseases.In this study,we used D-galactose(D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated.Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups:D-gal group(n=10) and control group(n=10).The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay.Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus.Western blot was used to detect the protein levels of NADPH oxidase(NOX) and uncoupling protein 2(UCP2).We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats.In comparison with the control group,the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged,and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats.This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats.These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.展开更多
文摘Objective: To investigate the colocalization of Somatostatin (SOM ) and NADPH--diaphorase (NADPHd ) of the neurons in raphe nuclei innervating pharyngeal muscles in the rats. Methods: After PRV was injected into the pharyngeal muscles. PRV and SOM immunofluorescence double labeling procedure was completed at first,then proceeded NADPH -d histochemistry. Results: PRV and SOM double--labled cells were present mainly in the nucleus raphe magnus. but some PRV and SOM double labled neurons were found in the other raphe nuclei as well, such as nucleus raphe pallidus. nucleus raphe obsurus, median raphe nucleus and dorsal raphe nucleus.NADPH -d positive neurons were also observed in the raphe nuclei. PRV. SOM and NADPH-d triple labeling neurons were found in the nucleus raphe magnus. Conclusion: It is suggested that the colocalization of SOM and NADPH--d of the neurons in the raphe nuclei innervating pharyngeal muscles may play an important role in the coordination of the pharyngeal motility.
基金supported by grants from the Natural Science Foundation of Hubei province (No. 2010CDB08005)the National Natural Science Foundation of China (No. 30730094 and81000409)Special Funds for State Key Development Program for Basic Research of China (973 Program) (No.2011CB504504)
文摘Mitochondrial DNA(mtDNA) common deletion(CD) plays a significant role in aging and age-related diseases.In this study,we used D-galactose(D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated.Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups:D-gal group(n=10) and control group(n=10).The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay.Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus.Western blot was used to detect the protein levels of NADPH oxidase(NOX) and uncoupling protein 2(UCP2).We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats.In comparison with the control group,the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged,and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats.This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats.These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.
