Effect of lithium chloride pretreatment on isoflurane-induced cognitive dysfunction and inflammatory response in hippocampus in aged rats / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of lithium chloride (LiCl) pretreatment on isoflurane-induced cognitive dysfunction and inflammatory response in hippocampus in aged rats.Methods Eighty 20-month-old male Sprague-Dawley rats,weighing 350-400 g,were randomly assigned into 4 groups (n =20 each)control group (group C),1.4％ isoflurane group (group I),100 mg/kg LiCI + 1.4％ isoflurane group (group L+ I),and 100 mg/kg LiC1 group (group L).Group I was exposed to 1.4％ isoflurane in 30％ O2-70％ N2 for 6 h,while group C was exposed to 30％ O2-70％ N2 only.LiCl 100 mg/kg was injected intraperitoneally once a day for 3 consecutive days and isoflurane anesthesia was performed on 4th day in group L + I.LiCl 100 mg/kg was injected intraperitoneally once a day for 3 consecutive days and then the rats inhaled 30％ O2-70％ N2 for 6 h on 4th day in group L.Blood samples were taken immediately after the end of anesthesia for blood gas analysis.Hippocampi were isolated 24 h after the end of anesthesia for determination of the expression of glycogen synthase kinase-3β (GSK-3β) and acetyl-NF-κB (Lys310) (by Western blot) and TNF-α,IL-1β and IL-6 mRNA (by RT-PCR).The levels of TNF-α,IL-1β and IL-6 were determined by ELISA and the contents of TNF-α,IL-1β and IL-6 were calculated.The cognitive function was assessed on 2nd day after the end of anesthesia.Results Compared with group C,the expression of GSK-3β and acetyl-NF-κB (Lys310) was significantly up-regulated,the expression of TNF-α,IL-1β and IL-6 mRNA and contents of TNF-α,IL-1β and IL-6 were increased,the escape latency was prolonged,and the time of staying at the original platform quadrant was shortened in group I (P ＜ 0.05).Compared with group I,the expression of GSK-3β and acetyl-NF-κB (Lys310) was significantly down-regulated,the expression of TNF-α,IL-1β and IL-6 mRNA and contents of TNF-α,IL-1β and IL-6 were decreased,the escape latency was shortened,and the time of staying at the original platform quadrant was prolonged in group L + I (P ＜ 0.05).Conclusion LiC1 pretreatment can improve isoflurane-induced cognitive dysfunction and inhibition of inflammatory response in hippocampus is involved in the mechanism in aged rats.