Limits...
Effect of propofol on brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus of aged rats with chronic cerebral ischemia.

Chen G, Fu Q, Cao J, Mi W - Neural Regen Res (2012)

Bottom Line: We intraperitoneally injected 10 and 50 mg/kg of propofol for 7 consecutive days to treat a rat model of chronic cerebral ischemia.A low-dose of propofol promoted the expression of brain-derived neurotrophic factor, tyrosine kinase receptor B, phosphorylated cAMP response element binding protein, and cAMP in the hippocampus of aged rats with chronic cerebral ischemia, but a high-dose of propofol inhibited their expression.Results indicated that the protective effect of propofol against cerebral ischemia in aged rats is related to changes in the expression of brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus, and that the cAMP-cAMP responsive element binding protein pathway is involved in the regulatory effect of propofol on brain-derived neurotrophic factor expression.

View Article: PubMed Central - PubMed

Affiliation: Anesthesia and Operation Center, PLA General Hospital, Beijing 100853, China.

ABSTRACT
We intraperitoneally injected 10 and 50 mg/kg of propofol for 7 consecutive days to treat a rat model of chronic cerebral ischemia. A low-dose of propofol promoted the expression of brain-derived neurotrophic factor, tyrosine kinase receptor B, phosphorylated cAMP response element binding protein, and cAMP in the hippocampus of aged rats with chronic cerebral ischemia, but a high-dose of propofol inhibited their expression. Results indicated that the protective effect of propofol against cerebral ischemia in aged rats is related to changes in the expression of brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus, and that the cAMP-cAMP responsive element binding protein pathway is involved in the regulatory effect of propofol on brain-derived neurotrophic factor expression.

No MeSH data available.


Related in: MedlinePlus

Brain-derived neurotrophic factor expression in the hippocampus of aged rats (western blot analysis).Data were expressed as the mean ± SD of five rats in each group. Intergroup differences were compared using one-way analysis of variance. aP < 0.05, bP < 0.01, vs. sham-surgery group; cP < 0.05, vs. model group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4308767&req=5

Figure 1: Brain-derived neurotrophic factor expression in the hippocampus of aged rats (western blot analysis).Data were expressed as the mean ± SD of five rats in each group. Intergroup differences were compared using one-way analysis of variance. aP < 0.05, bP < 0.01, vs. sham-surgery group; cP < 0.05, vs. model group.

Mentions: A total of 20 aged Sprague-Dawley rats were randomly assigned to sham-surgery, model, and low- and high-dose propofol groups (n = 4 for each). The rat model of chronic cerebral ischemia was established in the model, low- and high-dose propofol groups; the sham-surgery group was free of occlusion of the common carotid artery. Following model establishment, the sham-surgery and model groups were intraperitoneally injected with 2.5 mL normal saline, while the low- and high-dose propofol groups were intraperitoneally injected with 10 and 50 mg/kg propofol, respectively. All 20 rats were included in the final analysis.


Effect of propofol on brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus of aged rats with chronic cerebral ischemia.

Chen G, Fu Q, Cao J, Mi W - Neural Regen Res (2012)

Brain-derived neurotrophic factor expression in the hippocampus of aged rats (western blot analysis).Data were expressed as the mean ± SD of five rats in each group. Intergroup differences were compared using one-way analysis of variance. aP < 0.05, bP < 0.01, vs. sham-surgery group; cP < 0.05, vs. model group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4308767&req=5

Figure 1: Brain-derived neurotrophic factor expression in the hippocampus of aged rats (western blot analysis).Data were expressed as the mean ± SD of five rats in each group. Intergroup differences were compared using one-way analysis of variance. aP < 0.05, bP < 0.01, vs. sham-surgery group; cP < 0.05, vs. model group.
Mentions: A total of 20 aged Sprague-Dawley rats were randomly assigned to sham-surgery, model, and low- and high-dose propofol groups (n = 4 for each). The rat model of chronic cerebral ischemia was established in the model, low- and high-dose propofol groups; the sham-surgery group was free of occlusion of the common carotid artery. Following model establishment, the sham-surgery and model groups were intraperitoneally injected with 2.5 mL normal saline, while the low- and high-dose propofol groups were intraperitoneally injected with 10 and 50 mg/kg propofol, respectively. All 20 rats were included in the final analysis.

Bottom Line: We intraperitoneally injected 10 and 50 mg/kg of propofol for 7 consecutive days to treat a rat model of chronic cerebral ischemia.A low-dose of propofol promoted the expression of brain-derived neurotrophic factor, tyrosine kinase receptor B, phosphorylated cAMP response element binding protein, and cAMP in the hippocampus of aged rats with chronic cerebral ischemia, but a high-dose of propofol inhibited their expression.Results indicated that the protective effect of propofol against cerebral ischemia in aged rats is related to changes in the expression of brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus, and that the cAMP-cAMP responsive element binding protein pathway is involved in the regulatory effect of propofol on brain-derived neurotrophic factor expression.

View Article: PubMed Central - PubMed

Affiliation: Anesthesia and Operation Center, PLA General Hospital, Beijing 100853, China.

ABSTRACT
We intraperitoneally injected 10 and 50 mg/kg of propofol for 7 consecutive days to treat a rat model of chronic cerebral ischemia. A low-dose of propofol promoted the expression of brain-derived neurotrophic factor, tyrosine kinase receptor B, phosphorylated cAMP response element binding protein, and cAMP in the hippocampus of aged rats with chronic cerebral ischemia, but a high-dose of propofol inhibited their expression. Results indicated that the protective effect of propofol against cerebral ischemia in aged rats is related to changes in the expression of brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus, and that the cAMP-cAMP responsive element binding protein pathway is involved in the regulatory effect of propofol on brain-derived neurotrophic factor expression.

No MeSH data available.


Related in: MedlinePlus