2017Zhonghua mazuixue zazhiRequires access

Effect of 17β estradiol pretreatment on inflammatory responses during propofol-induced apoptosis in hippocampal nerve cells of developing rats

Jianli Li, Xiaoqian Wu, Yudong Zhang, Junfang Rong

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Abstract

Objective To evaluate the effect of 17β estradiol pretreatment on inflammatory responses during propofol-induced apoptosis in hippocampal nerve cells of developing rats. Methods Thirty-nine pathogen-free healthy male Sprague-Dawley rats, aged 7 days, weighing 11-18 g, were divided into 3 groups (n=13 each) using a random number table: fat emulsion group (group F), propofol group (group P) and propofol plus 17β estradiol group (group P+ E). Propofol 75 mg/kg was intraperitoneally injected once every 24 h for 7 consecutive days in group P, and the equal volume of fat emulsion was given instead in group F. In group P+ E, 17β estradiol 600 μg/kg was subcutaneously injected, and 30 min later propofol 75 mg/kg was intraperitoneally injected once every 24 h for 7 consecutive days.The rats were sacrificed at 24 h after the last injection, the brains were removed and hippocampi were isolated for determination of activated caspase-3 expression (using Western blot) and interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) contents (by enzyme-linked immunosorbent assay). Results The levels of activated caspase-3, IL-1β and TNF-α in hippocampi were significantly higher in group P than in group F (P<0.05). The levels of activated caspase-3, IL-1β and TNF-α in hippocampi were significantly lower in group P+ E than in group P (P<0.05). Conclusion The mechanism by which 17β estradiol pretreatment inhibits propofol-induced apoptosis in hippocampal nerve cells is related to inhibition of inflammatory responses of developing rats. Key words: Propofol; Estradiol; Apoptosis; Hippocampus; Inflammation

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Objective To evaluate the effect of 17β estradiol pretreatment on inflammatory responses during propofol-induced apoptosis in hippocampal nerve cells of developing rats. Methods Thirty-nine pathogen-free healthy male Sprague-Dawley rats, aged 7 days, weighing 11-18 g, were divided into 3 groups (n=13 each) using a random number table: fat emulsion group (group F), propofol group (group P) and propofol plus 17β estradiol group (group P+ E). Propofol 75 mg/kg was intraperitoneally injected once every 24 h for 7 consecutive days in group P, and the equal volume of fat emulsion was given instead in group F. In group P+ E, 17β estradiol 600 μg/kg was subcutaneously injected, and 30 min later propofol 75 mg/kg was intraperitoneally injected once every 24 h for 7 consecutive days.The rats were sacrificed at 24 h after the last injection, the brains were removed and hippocampi were isolated for determination of activated caspase-3 expression (using Western blot) and interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) contents (by enzyme-linked immunosorbent assay). Results The levels of activated caspase-3, IL-1β and TNF-α in hippocampi were significantly higher in group P than in group F (P<0.05). The levels of activated caspase-3, IL-1β and TNF-α in hippocampi were significantly lower in group P+ E than in group P (P<0.05). Conclusion The mechanism by which 17β estradiol pretreatment inhibits propofol-induced apoptosis in hippocampal nerve cells is related to inhibition of inflammatory responses of developing rats. Key words: Propofol; Estradiol; Apoptosis; Hippocampus; Inflammation

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Available abstract

Objective To evaluate the effect of 17β estradiol pretreatment on inflammatory responses during propofol-induced apoptosis in hippocampal nerve cells of developing rats. Methods Thirty-nine pathogen-free healthy male Sprague-Dawley rats, aged 7 days, weighing 11-18 g, were divided into 3 groups (n=13 each) using a random number table: fat emulsion group (group F), propofol group (group P) and propofol plus 17β estradiol group (group P+ E). Propofol 75 mg/kg was intraperitoneally injected once every 24 h for 7 consecutive days in group P, and the equal volume of fat emulsion was given instead in group F. In group P+ E, 17β estradiol 600 μg/kg was subcutaneously injected, and 30 min later propofol 75 mg/kg was intraperitoneally injected once every 24 h for 7 consecutive days.The rats were sacrificed at 24 h after the last injection, the brains were removed and hippocampi were isolated for determination of activated caspase-3 expression (using Western blot) and interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) contents (by enzyme-linked immunosorbent assay). Results The levels of activated caspase-3, IL-1β and TNF-α in hippocampi were significantly higher in group P than in group F (P<0.05). The levels of activated caspase-3, IL-1β and TNF-α in hippocampi were significantly lower in group P+ E than in group P (P<0.05). Conclusion The mechanism by which 17β estradiol pretreatment inhibits propofol-induced apoptosis in hippocampal nerve cells is related to inhibition of inflammatory responses of developing rats. Key words: Propofol; Estradiol; Apoptosis; Hippocampus; Inflammation

Key concepts: Propofol, Hippocampal formation, Apoptosis, Endocrinology, Internal medicine, Tumor necrosis factor alpha, Western blot, Necrosis

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