Glibenclamide ameliorates the expression of neurotrophic factors in sevoflurane anaesthesia-induced oxidative stress and cognitive impairment in hippocampal neurons of old rats
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Fig. 1
Experimental protocol
Fig. 2
Effects of glibenclamide on memory in rats with sevoflurane-induced cognitive impairment as demonstrated by the Y maze test. Values are presented as (A) mean ± SEM (n = 15) of total arm entries and (B) percentage of spontaneous alternations: # – p < 0.05 and ## – p < 0.01 for significant difference versus the control group; * – p < 0.05 for significant difference versus the low-dose sevoflurane group; GBC – glibenclamide; LDS – low-dose sevoflurane
Fig. 3
Effects of glibenclamide treatment on learning and memory in rats with sevoflurane-induced cognitive impairment in the Morris water maze test. Values are presented as mean ± SEM (n = 15) escape latency, time spent in the platform quadrant or the platform crossings. # – p < 0.05 and ## – p < 0.01 for significant difference versus the control group; * – p < 0.05 and ** - p < 0.01 for significant difference versus the low-dose sevoflurane group
Fig. 4
Effects of glibenclamide treatment on interleukin 6 (IL-6) (A) and tumour necrosis factor alpha (TNF-α) (B) levels in the hippocampus of rats with sevoflurane-induced cognitive impairment. Values are presented as mean ± SEM (n = 15) of the concentrations. # –p < 0.05 for significant difference versus the control group; * – p < 0.05 and ** - p < 0.01 for significant difference versus the low-dose sevoflurane group; GBC – glibenclamide; LDS – low-dose sevoflurane
Fig. 5
Effects of glibenclamide treatment on attenuation of phosphoinositide 3-kinase (PI3K)/Akt signalling pathways in sevoflurane-induced cognitive impairment in the hippocampal regions of aged rats. Values are presented as mean ± SEM (n = 15) of the concentrations. # – p < 0.05 for significant difference versus the control group; * – p < 0.05 and ** - p < 0.01 for significant difference versus the low-dose sevoflurane group; GBC – glibenclamide; LDS – low-dose sevoflurane
Fig. 6
Effects of glibenclamide treatment on BDNF expression in sevoflurane-induced cognitive impairment in rats. (A) Serum levels of BDNF and indicated oxidative stress markers in rats with or without effects of sevoflurane inhalation; (B) Expression of BDNF mRNA in sevoflurane-induced cognitive impairment in the hippocampal regions of aged rats. Data represent mean ± SEM (n = 15). # – p < 0.05 and ## – p < 0.01 for significant difference versus the control group; * – p < 0.05 and ** - p < 0.01 for significant difference versus the low-dose sevoflurane group; GBC – glibenclamide; LDS – low-dose sevoflurane
Fig. 7
Brain-derived neurotrophic factor (BDNF) expression in sevoflurane-induced cognitive impairment in rats. (A) Expression of BDNF protein in the control group; (B) BDNF expression in sevoflurane-induced cognitive impairment in the hippocampal regions of aged rats; (C) Expression of BDNF protein after treatment with glibenclamide in sevoflurane-induced cognitive impairment in the hippocampal regions of aged rats; (D) Relative quantification of BDNF expression in the control group, GBC-only group, low-dose sevoflurane group without GBC, and low-dose sevoflurane group with GBC (n = 5). Significant differences versus the low-dose sevoflurane group: ### – p < 0.01 for significant difference versus the control group; ** – p < 0.01 and *** - p < 0.001 for significant difference versus the low-dose sevoflurane group; GBC – glibenclamide; LDS – low-dose sevoflurane