The effect of sevoflurane anesthesia on cognitive function and the expression of Insulin-like Growth Factor-1 in CA1 region of hippocampus in old rats

Abstract

To investigate the effects of sevoflurane on cognitive function in old Sprague-Dawley (SD) rats and the expression of insulin-like growth factor-1 (IGF-1) in CA1 region of hippocampus. Forty Sprague-Dawley rats of 12 months old were randomly divided into five groups: the normal control group; 1.5% sevoflurane I group (be tested after received 1.5% sevoflurane for 1 day); 1.5% sevoflurane II group (be tested after received 1.5% sevoflurane for 7 day); 3.0% sevoflurane I group (be tested after received 3.0% sevoflurane for 1 day) and 3.0% sevoflurane II group (be tested after received 3.0% sevoflurane for 7 day). All SD rats were received 1.5 or 3.0% sevoflurane in a special glass anesthesia box for 2 h respectively, except for the normal control group. Y-maze was used to test the ability of learning and memory after being received sevoflurane for 1 or 7 days at the same moment portion. The altered expression level of IGF-1 in the hippocampus was tested to compare its transcripts by RT-PCR analysis. The results showed that 3% sevoflurane induced the decline of cognitive function and significantly deceased the IGF-1 expression at mRNA levels at 1 day in the 3.0% sevoflurane I group when compared with the normal control group. However, there were no significant difference among the other groups when compared with normal control group. Therefore, administration of sevoflurane might temporally affect the ability of cognitive function of rats through suppressing the IGF-1 expression at mRNA levels in hippocampus.

Decreased PSD95 expression in medial prefrontal cortex (mPFC) was associated with cognitive impairment induced by sevoflurane anesthesia

“…Cognitive function is one of the most basic and important high-level neurological functions in the brain, and it is a basic indicator of the development of human intelligence. Supporting our result, many previous studies also reported the effect of sevoflurane, as well as other anesthetics, on cognitive function (Chen et al, 2001;Millar et al, 2006;Peng et al, 2011;Gong et al, 2012). Interestingly, Peng et al (2011) found that exposure to 1.5% sevoflurane, for as long as 3 d (2 h/d), did not cause significantly different cognitive performance, while exposure to 3% sevoflurane for 2 h was enough to induce cognitive impairment.…”

The change of circulating insulin like growth factor binding protein 7 levels may correlate with postoperative cognitive dysfunction

“…Exogenous IGF-1 can protect neurons from diverse forms of injury in vivo and in vitro [25,26]. Sevoflurane decreased expression of the IGF-1 and impaired cognition [27], which suggested that IGF-1 expression may be involved in the mechanical-stress-and sevofluraneinduced cognitive impairment. IGF-1 can be produced in the brain [28] but it is mainly produced in the liver, and can enter the brain via the blood-brain barrier.…”

Sevoflurane exposure in postnatal rats induced long-term cognitive impairment through upregulating caspase-3/cleaved-poly (ADP-ribose) polymerase pathway

“…More specifically, rats in the developmental stages (P7) did not present cognitive impairment and nerve inflammation due to exposure to 3% sevoflurane for 2 h at one time, while those inhaling 3% sevoflurane for 2 h per day for 3 consecutive days exhibited marked impairment of cognition. Furthermore, Peng et al (33) revealed that low concentration of sevoflurane (1.5%) may not cause significant cognitive impairment even with exposure for as long as 3 days (2 h per day), while high concentration of sevoflurane (3%) for only 2 h was sufficient to induce severe cognitive impairment. Therefore, the present study, along with other similar studies, suggested that minimizing the use dosage and concentration of anesthetics, particularly sevoflurane, in clinical practice may greatly reduce the neurological damage.…”