2018Zhonghua mazuixue zazhiRequires access

Effect of prostaglandin E1 on propofol-induced neuroapoptosis in hippocampus of newborn rats

Bin Li, Wenbo Li, Xianhui Yang, Tieli Dong

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Abstract

Objective To evaluate the effect of prostaglandin E1(PGE1)on propofol-induced neuroapoptosis in hippocampus of newborn rats. Methods Thirty-six clean-grade healthy newborn Sprague-Dawley rats, aged 7 days, weighing 11-16 g, were divided into 3 groups(n=12 each)using a random number table method: control group(group C), propofol group(group P)and group PGE1.Propofol 75 mg/kg was intraperitoneally injected once every other day for 7 consecutive days in P and PGE1 groups.PGE1 10 μg/kg was injected via the tail vein at 30 min before each injection of propofol in group PGE1.Normal saline 3 ml/kg was intraperitoneally injected once every other day for 7 consecutive days in group C. The rats were sacrificed at 60 min after emergence from the last injection.The hippocampi were harvested for determination of neuroapoptosis(by TUNEL), expression of caspase-3, Bcl-2 and Bax(by Western blot), and contents of interleukin-1beta(IL-1β), IL-6 and tumor necrosis factor-alpha(TNF-α)(by enzyme-linked immunosorbent assay). Results Compared with group C, the contents of hippocampal IL-1β, IL-6 and TNF-α were significantly increased, apoptosis index was increased, the expression of caspase-3 and Bax was up-regulated, and the expression of Bcl-2 was down-regulated in P and PGE1 groups(P<0.05). Compared with group P, the contents of hippocampal IL-1β, IL-6 and TNF-α were significantly decreased, apoptosis index was decreased, the expression of caspase-3 and Bax was down-regulated, and the expression of Bcl-2 was up-regulated in group PGE1(P<0.05). Conclusion PGE1 can reduce propofol-induced neuroapoptosis in hippocampus of newborn rats, and the mechanism may be related to inhibiting inflammatory responses of the hippocampus. Key words: Alprostadil; Propofol; Infant, newborn; Hippocampus; Neurons; Apoptosis

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Objective To evaluate the effect of prostaglandin E1(PGE1)on propofol-induced neuroapoptosis in hippocampus of newborn rats. Methods Thirty-six clean-grade healthy newborn Sprague-Dawley rats, aged 7 days, weighing 11-16 g, were divided into 3 groups(n=12 each)using a random number table method: control group(group C), propofol group(group P)and group PGE1.Propofol 75 mg/kg was intraperitoneally injected once every other day for 7 consecutive days in P and PGE1 groups.PGE1 10 μg/kg was injected via the tail vein at 30 min before each injection of propofol in group PGE1.Normal saline 3 ml/kg was intraperitoneally injected once every other day for 7 consecutive days in group C. The rats were sacrificed at 60 min after emergence from the last injection.The hippocampi were harvested for determination of neuroapoptosis(by TUNEL), expression of caspase-3, Bcl-2 and Bax(by Western blot), and contents of interleukin-1beta(IL-1β), IL-6 and tumor necrosis factor-alpha(TNF-α)(by enzyme-linked immunosorbent assay). Results Compared with group C, the contents of hippocampal IL-1β, IL-6 and TNF-α were significantly increased, apoptosis index was increased, the expression of caspase-3 and Bax was up-regulated, and the expression of Bcl-2 was down-regulated in P and PGE1 groups(P<0.05). Compared with group P, the contents of hippocampal IL-1β, IL-6 and TNF-α were significantly decreased, apoptosis index was decreased, the expression of caspase-3 and Bax was down-regulated, and the expression of Bcl-2 was up-regulated in group PGE1(P<0.05). Conclusion PGE1 can reduce propofol-induced neuroapoptosis in hippocampus of newborn rats, and the mechanism may be related to inhibiting inflammatory responses of the hippocampus. Key words: Alprostadil; Propofol; Infant, newborn; Hippocampus; Neurons; Apoptosis

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Available abstract

Objective To evaluate the effect of prostaglandin E1(PGE1)on propofol-induced neuroapoptosis in hippocampus of newborn rats. Methods Thirty-six clean-grade healthy newborn Sprague-Dawley rats, aged 7 days, weighing 11-16 g, were divided into 3 groups(n=12 each)using a random number table method: control group(group C), propofol group(group P)and group PGE1.Propofol 75 mg/kg was intraperitoneally injected once every other day for 7 consecutive days in P and PGE1 groups.PGE1 10 μg/kg was injected via the tail vein at 30 min before each injection of propofol in group PGE1.Normal saline 3 ml/kg was intraperitoneally injected once every other day for 7 consecutive days in group C. The rats were sacrificed at 60 min after emergence from the last injection.The hippocampi were harvested for determination of neuroapoptosis(by TUNEL), expression of caspase-3, Bcl-2 and Bax(by Western blot), and contents of interleukin-1beta(IL-1β), IL-6 and tumor necrosis factor-alpha(TNF-α)(by enzyme-linked immunosorbent assay). Results Compared with group C, the contents of hippocampal IL-1β, IL-6 and TNF-α were significantly increased, apoptosis index was increased, the expression of caspase-3 and Bax was up-regulated, and the expression of Bcl-2 was down-regulated in P and PGE1 groups(P<0.05). Compared with group P, the contents of hippocampal IL-1β, IL-6 and TNF-α were significantly decreased, apoptosis index was decreased, the expression of caspase-3 and Bax was down-regulated, and the expression of Bcl-2 was up-regulated in group PGE1(P<0.05). Conclusion PGE1 can reduce propofol-induced neuroapoptosis in hippocampus of newborn rats, and the mechanism may be related to inhibiting inflammatory responses of the hippocampus. Key words: Alprostadil; Propofol; Infant, newborn; Hippocampus; Neurons; Apoptosis

Key concepts: Hippocampal formation, Propofol, Saline, Apoptosis, TUNEL assay, Hippocampus, Endocrinology, Internal medicine

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