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
Abstract
Jianli Li, Xiaoqian Wu, Yudong Zhang, Junfang Rong
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
Key concepts: Propofol, Hippocampal formation, Apoptosis, Endocrinology, Internal medicine, Tumor necrosis factor alpha, Western blot, Necrosis