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Objective To evaluate the effect of sevoflurane anesthesia on the expression of phosphorylated cAMP response element-binding protein (p-CREB) in the hippocampal neurons of developing rats.Methods Thirty-two healthy male Sprague-Dawley rats, aged 7 days, weighing 10-15 g, were equally and randomly divided into either control group (group C) or sevoflurane anesthesia group (group Sev) using a random number table.Group C inhaled 30％ oxygen for 6 h.Group Sev inhaled 3％ sevoflurane for 6 h.Eight rats in each group were sacrificed immediately after the end of oxygen or sevoflurane inhalation, and the hippocampus was removed for determination of the expression of p-CREB.The rats at ages 2 months underwent Morris water maze test.The rats were then sacrificed, and the hippocampus was removed for determination of the expression of p-CREB by Western blot.Results Compared with group C, the escape latency and swimming distance were significantly prolonged, the frequency of crossing the original platform was decreased, the percentage of the time of staying at the quadrant Ⅱ was decreased, and the expression of p-CREB in hippocampal neurons was down-regulated in group Sev.Conclusion The mechanism of sevoflurane anesthesia-induced neurotoxicity is related to inhibition of p-CREB expression in hippocampal neurons of developing rats.
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Objective To evaluate the changes in the expression of CC-chemokine ligand 3 (CCL3) and CC-chemokine receptor 5 (CCR5) in the spinal cord during hyperalgesia induced by remifentanil in rats with incisional pain.Methods Thirty-two male Sprague-Dawley rats,aged 2-3 months,weighing 240-260 g,were randomly divided into 4 groups (n=8 each) using a random number table:control group (group C),incisional pain group (group Ⅰ),remifentanil group (group R) and remifentanil+incisional pain group (group R+I).A 1-cm longitudinal incision was made in the plantar surface of the left hindpaw in anesthetized rats.While the model of incisional pain was established,remifentanil was infused for 60 min at 1 μg · kg-1 · min-1.At 24 h before infusion of remifentanil (baseline) and 2,6,24 and 48 h after the end of infusion,the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured.The rats were sacrificed after the last measurement of pain threshold,the lumbar segment (L4-6) of the spinal cord was removed for determination of CL3 and CCR5 mRNA expression (by real-time PCR) and CL3 and CCR5 expression (by Western blot).Results Compared with group C,the MWT was significantly decreased,the TWL was shortened,and the expression of CCL3 and CCR5 mRNA and protein was up-regulated in I,R and R+ I groups.Compared with I and R groups,the MWT was significantly dccreascd,the TWL was shortened,and the expression of CCL3 and CCR5 mRNA and protein was up-regulated in group R+I.Conclusion The mechanism by which remifentanil induces hyperalgesia is related to up-regulated expression of CCL3 and CCR5 in the spinal cord of rats with incisional pain.
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Objective To evaluate the changes in the expression of protein interacting with Cα kinase 1 (PICK1) in the spinal cord and dorsal root ganglion (DRG) neurons during remifentanil-induced hyperalgesia in rats with incisional pain.Methods Thirty-two male Sprague-Dawley rats, weighing 240-260 g, aged 42-49 days, were randomly divided into 4 groups (n =8 each) using a random number table: control group (group C) , incisional pain group (group Ⅰ) , remifentanil group (group R), and remifentanil + incisional pain group (group R + Ⅰ).In R and R+Ⅰ groups, remifentanil was infused intravenously for 60 min at the rate of 1.2 p,g · kg-1 · min-1.In C and Ⅰ groups, normal saline was infused intravenously for 60 min at the rate of 0.12 ml · kg-1 · min-1.In Ⅰ and R+Ⅰ groups, the model of incisional pain was established, and remifentanil and normal saline were infused intravenously, respectively, at the same time.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured before normal saline or remifentanil infusion, and at 2, 6, 24, and 48 h after the end of normal saline or remifentanil infusion (T1-4).The rats were sacrificed after the last measurement of pain threshold.The lumbar segment (L4-6) of the spinal cord and left DRGs were removed for determination of the expression of PICKl mRNA (by quantitative real-time reverse transcriptase-polymerase chain reaction) and PICK1 protein (by Western blot).Results Compared with group C, the MWT was significantly decreased, the TWL was shortened, and the expression of PICK1 protein and mRNA was up-regulated in R and R+Ⅰ groups, and the MWT was significantly decreased, the TWL was shortened (P＜0.05) , and no significant change was found in the expression of PICK1 protein and mRNA in group Ⅰ (P＞0.05).Compared with group Ⅰ, the MWT was significantly decreased, the TWL was shortened, and the expression of PICK1 protein and mRNA was up-regulated in group R+Ⅰ (P＜0.05).Compared with group R, the MWT was significantly decreased, the TWL was shortened (P＜0.05) , and no significant change was found in the expression of PICK1 protein and mRNA in group R+ Ⅰ (P＞0.05).Conclusion The mechanism by which remifentanil induces hyperalgesia may be related to up-regulation of PICK1 expression in the spinal cord and DRG neurons of rats with incisional pain.
ABSTRACT
Objective To evaluate the effects of hydrogen on apoptosis in hippocampal neurons caused by sevoflurane anesthesia in neonatal rats.Methods Forty-eight healthy male Sprague-Dawley rats,aged 7 days,weighing 12-20 g,were randomly divided into 3 groups (n=16 each) using a random number table:control group (group C);sevoflurane anesthesia group (group S);hydrogen group (group H).In C and S groups,the rats inhaled 30％ oxygen and 3％ sevoflurane for 6 h,respectively.In group H,3％ sevoflurane and 2％ hydrogen were inhaled for 6 h.Eight rats in each group were randomly selected and sacrificed at 7 days after birth (after the end of oxygen,sevoflurane or hydrogen inhalation),and the hippocampus was removed for determination of the expression of activated caspase-3 and myelin basic protein by Western blot.At 28 days after birth,8 rats were selected,and Y-maze and Morris water maze tests were performed to evaluate the cognitive function.The total number of entries into each arm,the number of spontaneous alternation,escape latency and time of staying at the platform quadrant were recorded.Results Compared with group C,the percentage of spontaneous alternation was significantly decreased,the escape latency was prolonged,and the time of staying at the platform quadrant was shortened,and the expression of activated caspase-3 was significantly up-regulated,and the expression of myelin basic protein was down-regulated in group S.Compared with group S,the percentage of spontaneous alternation was significantly increased,the escape latency was shorten,and the time of staying at the platform quadrant was prolonged,and the expression of activated caspase-3 was significantly downregulated,and the expression of myelin basic protein was up-regulated in group H.There was no significant difference in the number of entries into each arm in Y-maze test between the three groups.Conclusion Hydrogen can inhibit apoptosis in hippocampal neurons caused by sevoflurane anesthesia in neonatal rats.