2017Unpublished venueRequires access

Effect of insulin on apoptosis in hippocampal neurons of sevoflurane-anesthetized mice

Xueyong Sun, Shenghui Ge, Lihua Jiang

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Abstract

Objective To evaluate the effect of insulin on apoptosis in hippocampal neurons of sevoflurane-anesthetized mice. Methods Forty-five pathogen-free healthy male BALB/c mice, aged 5-6 weeks, weighing 18-22 g, were divided into 3 groups(n=15 each)using a random number table: control group(group C), sevoflurane group(group Sev)and insulin plus sevoflurane group(group IS). Insulin 2 U/20 μl was instilled via the nasal cavity for 7 consecutive days in group IS, and 0.9% normal saline 20 μl was given instead in group C. After the end of insulin treatment, 2.5% sevoflurane was inhaled for 1 h in Sev and IS groups, and Morris water maze test was performed to assess the cognitive function 1 day later.The mice were then sacrificed and hippocampal tissues were obtained for determination of neuronal apoptosis(by TUNEL)and expression of Bcl-2 and Bax(by Western blot). Apoptosis index(AI)was calculated. Results Compared with group C, the escape latency was significantly prolonged at day 4 after operation, the percentage of time spent on the target quadrant was decreased at day 5 after operation, AI was increased, the expression of Bax was up-regulated, and the expression of Bcl-2 was down-regulated in group Sev(P<0.05). Compared with group Sev, the escape latency was significantly shortened at day 4 after operation, the percentage of time spent on the target quadrant was increased at day 5 after operation, AI was decreased, the expression of Bax was down-regulated, and the expression of Bcl-2 was up-regulated in group IS(P<0.05). Conclusion Insulin improves the cognitive function of sevoflurane-anesthetized mice through inhibiting apoptosis in hippocampal neurons. Key words: Insulin; Anesthetics, inhalation; Neuron

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Objective To evaluate the effect of insulin on apoptosis in hippocampal neurons of sevoflurane-anesthetized mice. Methods Forty-five pathogen-free healthy male BALB/c mice, aged 5-6 weeks, weighing 18-22 g, were divided into 3 groups(n=15 each)using a random number table: control group(group C), sevoflurane group(group Sev)and insulin plus sevoflurane group(group IS). Insulin 2 U/20 μl was instilled via the nasal cavity for 7 consecutive days in group IS, and 0.9% normal saline 20 μl was given instead in group C. After the end of insulin treatment, 2.5% sevoflurane was inhaled for 1 h in Sev and IS groups, and Morris water maze test was performed to assess the cognitive function 1 day later.The mice were then sacrificed and hippocampal tissues were obtained for determination of neuronal apoptosis(by TUNEL)and expression of Bcl-2 and Bax(by Western blot). Apoptosis index(AI)was calculated. Results Compared with group C, the escape latency was significantly prolonged at day 4 after operation, the percentage of time spent on the target quadrant was decreased at day 5 after operation, AI was increased, the expression of Bax was up-regulated, and the expression of Bcl-2 was down-regulated in group Sev(P<0.05). Compared with group Sev, the escape latency was significantly shortened at day 4 after operation, the percentage of time spent on the target quadrant was increased at day 5 after operation, AI was decreased, the expression of Bax was down-regulated, and the expression of Bcl-2 was up-regulated in group IS(P<0.05). Conclusion Insulin improves the cognitive function of sevoflurane-anesthetized mice through inhibiting apoptosis in hippocampal neurons. Key words: Insulin; Anesthetics, inhalation; Neuron

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Available abstract

Objective To evaluate the effect of insulin on apoptosis in hippocampal neurons of sevoflurane-anesthetized mice. Methods Forty-five pathogen-free healthy male BALB/c mice, aged 5-6 weeks, weighing 18-22 g, were divided into 3 groups(n=15 each)using a random number table: control group(group C), sevoflurane group(group Sev)and insulin plus sevoflurane group(group IS). Insulin 2 U/20 μl was instilled via the nasal cavity for 7 consecutive days in group IS, and 0.9% normal saline 20 μl was given instead in group C. After the end of insulin treatment, 2.5% sevoflurane was inhaled for 1 h in Sev and IS groups, and Morris water maze test was performed to assess the cognitive function 1 day later.The mice were then sacrificed and hippocampal tissues were obtained for determination of neuronal apoptosis(by TUNEL)and expression of Bcl-2 and Bax(by Western blot). Apoptosis index(AI)was calculated. Results Compared with group C, the escape latency was significantly prolonged at day 4 after operation, the percentage of time spent on the target quadrant was decreased at day 5 after operation, AI was increased, the expression of Bax was up-regulated, and the expression of Bcl-2 was down-regulated in group Sev(P<0.05). Compared with group Sev, the escape latency was significantly shortened at day 4 after operation, the percentage of time spent on the target quadrant was increased at day 5 after operation, AI was decreased, the expression of Bax was down-regulated, and the expression of Bcl-2 was up-regulated in group IS(P<0.05). Conclusion Insulin improves the cognitive function of sevoflurane-anesthetized mice through inhibiting apoptosis in hippocampal neurons. Key words: Insulin; Anesthetics, inhalation; Neuron

Key concepts: Sevoflurane, Hippocampal formation, TUNEL assay, Apoptosis, Morris water navigation task, Saline, Insulin, Anesthesia

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