双酚A对雄激素调节学习记忆的影响
发布时间：2019-06-29 12:35
【摘要】：双酚A (Bisphenol A, BPA)是一种广泛使用于塑料制品的环境内分泌干扰物。BPA能经由食品以及饮料进入到人体,也可以从垃圾渗析到周围的生态环境中而对健康产生危害。大量研究发现BPA能够影响激素的合成和代谢,受体的表达以及基因的活性,然而以往的研究多集中在其雌激素活性上。本实验室前期研究发现无论是围生期、青春期还是成年期BPA暴露均性别依赖性地损伤雄性小鼠的空间学习记忆以及被动回避记忆能力。与雌激素对雌性动物的重要作用一样,雄激素对雄性的认知功能以及突触形成具有重要的调节作用。近来研究发现BPA能拮抗雄激素受体(AR)介导的转录活性。所以,本实验旨在探究BPA暴露性别特异性地损伤雄性小鼠学习记忆行为是否与其干扰雄激素对雄鼠学习记忆的调节作用有关。突触可塑性与空间学习记忆行为密切相关。性激素能通过影响海马和前额叶皮层中枢神经系统的突触重塑而影响认知行为。有研究发现睾丸摘除导致雄性小鼠海马突触密度降低,在补充丙酸睾酮(TP)或二氢睾酮(DHT)后,突触密度显著增加。突触界面是一个对化学物质非常敏感的结构,突触间隙、突触活性带长度、突触后致密物(postsynaptic density, PSD)和突触界面曲率等可因外界刺激而发生改变。PSD上分布着大量的脚手架蛋白以及一些与突触传递相关的调节蛋白,其中很多是与后膜上受体通道相关联,这些蛋白表达水平的改变以及彼此间的相互作用都能影响突触的活性和突触可塑性,同时也导致PSD厚度的变化。本研究通过建立成年去势雄鼠模型,将性腺完整、去势、去势后补充雄激素的雄鼠分别暴露于BPA,研究长期BPA暴露对成年雄鼠学习记忆行为的影响,进一步电镜观测雄鼠海马CA1区神经元的突触密度以及突触界面结构的改变；最后通过Western blot检测海马突触蛋白Synapsin Ⅰ和PSD-95,兴奋性氨基酸NMDA受体以及信号通路蛋白ERK1/2、p38及其磷酸化表达的改变,探讨BPA暴露影响雄鼠空间学习记忆行为和突触可塑性的可能机制。研究方法：清洁级8周龄的ICR雄性小鼠,购买于浙江医学科学院实验动物中心。饲养的环境为自然光照和黑暗12h交替,饲养室的温度控制在23±2℃，，50%-60%的湿度控制,水以及食物均能自由取食。适应环境一周后,水合氯醛(400mg/kg)腹腔注射麻醉,然后进行睾丸摘除术建立去势模型。术后恢复2周之后,每天进行颈背部皮下注射染毒：丙酸睾酮(TP,0.5 mg/kg/day), BPA(0.4,4 mg/kg/day), TP+BPA(0.4或4 mg/kg/day),金龙鱼食用油(50μL/day),为期45天。给药结束3天后,每组取14只进行行为检测,6只制作海马超薄切片进行海马突触形态测定,4只用于测定相关蛋白,8只用于测定脑和血清雄激素水平。实验所有的数据以平均值士标准误显示,用SPSS 17.0统计软件进行统计分析。水迷宫4天训练结果采用重复三因素方差分析,水迷宫第5天结果、突触形态测定结果采用双因素方差分析,雄激素水平以及Western blot的蛋白结果采用单因素方差分析。研究结果：1.与假手术对照组相比,性腺摘除显著降低血清和脑内雄激素水平(p0.001；p0.001),当补充TP后,血清和脑雄激素水平上升(p0.001；p0.001)。BPA(0.4,4mg/kg/day)暴露不影响性腺摘除鼠血清和脑中雄激素水平,但是显著降低假手术组小鼠血清(p0.05；p0.01)和脑(p0.05；p0.01)雄激素的水平和TP补充小鼠血清(p0.05)和脑(p0.05；p0.01)雄激素水平。2.水迷宫4天的训练结果表明：与假手术对照组相比,性腺摘除显著延长第4天小鼠找到平台的潜伏期(p0.05),TP补充后,找到平台的潜伏期缩短(p0.05),表明雄激素缺失明显损伤空间学习能力。BPA暴露没有延长去势小鼠找到平台的潜伏期(p0.05),但显著延长假手术组(4 mg/kg/day, p0.01)和TP补充组(0.4 mg/kg/day, p0.05)小鼠找到平台的潜伏期。水迷宫第5天的结果表明,BPA暴露降低假手术组小鼠(0.4 mg/kg/day, p0.05)和TP补充组小鼠(p0.001；p0.01)在目标象限停留的时间百分比,但不影响睾丸摘除小鼠目标象限停留的时间百分比。这些结果表明BPA损伤成年小鼠空间记忆能力,能抑制雄激素对性腺摘除诱导的空间记忆损伤的恢复作用。3.突触密度结果显示,性腺摘除显著降低成年雄鼠海马CA1区突触密度(p0.001),TP补充后突触密度显著提高(p0.001)。BPA (0.4,4mg/kg/day)暴露降低假手术组海马CA1区突触密度(p0.001,p0.001),但对性腺摘除组没有影响。BPA (0.4,4 mg/kg/day)暴露抑制TP诱导的突触密度增多(p0.01,p0.001)。与假手术对照组相比,性腺摘除显著缩短活性带长度(p0.01),减小PSD厚度(p0.001),增大突触间隙宽度(p0.001),但TP补充后这种变化被BPA逆转(p0.05,p0.05,p0.001)。BPA暴露对假手术组突触结构的影响与TP补充组相似。这些结果表明BPA暴露能抑制雄激素的诱导的海马突触的形成和结构修饰。4.进一步的Western blot分析显示,BPA尤其在4 mg/kg/day的剂量,显著下调假手术组小鼠海马synapsin Ⅰ (p0.05), PSD-95 (p0.01), NR2B (p0.05)的表达。性腺摘除微弱下调synapsin I,但显著下调PSD-95 (p0.05), NR2B(p0.01)的表达,在补充TP之后这些蛋白表达上调(p0.05,p0.05)。BPA暴露抑制TP诱导对synapsinⅠ (p0.01), PSD-95 (p0.05), NR2B (p0.05)的上调作用。进一步分析发现,性腺摘除和BPA暴露对p38和ERK1/2的表达没有影响,但是4 mg/kg/day的BPA暴露显著下调ERK1/2的磷酸化(p-ERK1/2)水平(p0.05)并上调p-p38的磷酸化(p-p38)(p0.001)。BPA暴露抑制TP诱导的p-ERK1/2上调(p0.01)和p-p38下调(p0.01)。这些结果表明BPA暴露抑制雄激素诱导的突触蛋白和NR2B的表达,抑制MAPK/ERKs并促进MAPK/p38信号通路的活性。结论：长期暴露于BPA性别特异性地损伤雄性动物的学习记忆功能可能与BPA的抗雄激素作用有关。该作用可能一方面通过降低脑内雄激素水平,并干扰雄激素对ERKs和p38信号通路的活性而下调突触蛋白和NMDA受体水平,负性改变海马神经元的突触可塑性,最终损伤学习记忆功能。
[Abstract]:Bisphenol A (BPA) is a widely used environmental endocrine disruptor for plastic products. BPA can enter the human body via food and beverage, and can also be harmful to health by dialysis to the surrounding ecological environment. A large number of studies have found that BPA can affect the synthesis and metabolism of hormones, the expression of receptors, and the activity of genes, however, the previous studies have been focused on their estrogenic activity. The pre-laboratory study found that both perinatal, adolescent and adult-year BPA exposure had sex-dependent impairment of the spatial learning and memory of male mice and passive avoidance of memory. As with the important role of estrogen on female animals, androgens play an important role in the cognitive function of the male and the formation of synapses. Recent studies have found that BPA can antagonize androgen receptor (AR)-mediated transcriptional activity. Therefore, the purpose of this experiment is to explore whether the exposure of BPA to sex-specific damage to male mice is related to the effect of interfering with androgen on learning and memory of male rats. The synaptic plasticity is closely related to the spatial learning and memory behavior. Sex hormones can affect cognitive behavior by affecting the synaptic remodeling of the central nervous system in the hippocampus and the prefrontal cortex. It was found that testicular removal resulted in a decrease in synaptic density in the hippocampus of male mice, and a significant increase in synaptic density following the supplementation of testosterone (TP) or dihydrotestosterone (DHT). The synaptic interface is a very sensitive structure to chemical substances, synaptic cleft, synaptic active band length, postsynaptic density (PSD) and synaptic interface curvature can change due to external stimuli. A large number of scaffolding proteins and some regulatory proteins associated with synaptic transmission are distributed on the PSD, many of which are associated with the receptor channel on the back membrane, the changes in the level of expression of these proteins, and the interaction with each other, can affect the activity and synaptic plasticity of the synapse, And also results in a change in the PSD thickness. The effects of long-term BPA exposure on learning and memory behavior of adult male rats were studied by establishing an adult castrated male mouse model, exposing the male mice with complete, castrated and castrated androgen to BPA, respectively, and studying the effects of long-term BPA exposure on learning and memory behavior of adult male rats. The changes of the synaptic density and the synaptic interface structure of the neurons in the hippocampal CA1 region of the male rats were observed by electron microscopy, and the changes of the expression of the synapsin I and PSD-95, the excitatory amino acid NMDA receptor and the signaling pathway protein ERK1/2, p38 and the phosphorylation of the signal pathway proteins were detected by Western blot. To study the possible mechanism of BPA exposure to the learning and memory behavior and synaptic plasticity of male rats. The method of the study was to clean the ICR male mice at 8 weeks of age and to purchase the experimental animal center of Zhejiang Academy of Medical Sciences. The environment of the feeding is natural light and dark 12h, and the temperature of the feeding room is controlled at 23-2 & deg; C and 50-60% of the humidity control, and the water and the food can be freely fed. After a week of acclimation, a castrated model was established by intraperitoneal injection of chloral (400 mg/ kg). After 2 weeks of post-operation, the neck and back were injected subcutaneously each day: Testosterone Propionate (TP, 0.5 mg/ kg/ day), BPA (0.4,4 mg/ kg/ day), TP + BPA (0.4 or 4 mg/ kg/ day), and Golden Dragon Fish Oil (50.mu. L/ day) for a period of 45 days. Three days after the end of the administration,14 animals were tested for behavioral tests,6 of which were used for hippocampal synapse morphometry,4 for the determination of related proteins and 8 for the determination of brain and serum androgen levels. All the data of the experiment were misdisplayed by means of the mean value, and the statistical analysis was made with the SPSS 17.0 statistical software. The results of 3-factor analysis of variance and the fifth day of the water maze were used in the water maze. The results of the five-day analysis of the water maze and the results of the morphological measurement of the water maze were the two-factor analysis of variance, the level of androgens and the results of Western blot. Study results:1. Compared with the sham-operated control group, gonad removal significantly decreased the levels of androgen in serum and brain (p0.001; p0.001), and the levels of serum and brain androgen increased after supplementation of TP (p0.001; p0.001). The exposure of BPA (0.4,4 mg/ kg/ day) did not affect the levels of androgen in the serum and brain of the gonads, but significantly reduced the levels of androgen in the sham-operated group (p0.05; p0.01) and the brain (p0.05; p0.01), and the androgen levels in the brain (p0.05) and the brain (p0.05; p0.01). The results of the 4-day training of the water maze showed that, compared with the sham-operated control group, the latency of the platform was significantly prolonged on the 4th day after the gonad removal (p0.05), and the latency of the platform was shortened after the addition of TP (p0.05), indicating that the androgen deficiency obviously damaged the learning ability of the space. The exposure of BPA did not prolong the incubation period of the castrated mice (p0.05), but significantly prolonged the latency of the platform in the sham operation group (4 mg/ kg/ day, p0.01) and the TP supplementation group (0.4 mg/ kg/ day, p0.05). The results of the fifth day of the water maze showed that BPA exposure reduced the percentage of time that the sham-operated mice (0.4 mg/ kg/ day, p0.05) and TP-supplemented mice (p0.001; p0.01) remained in the target quadrant, but did not affect the percentage of time that the testicle removed the target quadrant of the mouse. These results show that the ability of BPA to damage the space memory of adult mice can inhibit the recovery of the spatial memory damage induced by androgen on the gonad removal. The results of synaptic density showed that the synaptic density (p0.001) in the CA1 region of the hippocampus of the adult male rats was significantly reduced, and the postsynaptic density was significantly increased after the addition of TP (p0.001). BPA (0.4,4 mg/ kg/ day) exposure reduced the synaptic density in the hippocampal CA1 region of the sham-operated group (p0.001, p0.001), but had no effect on the gonad removal group. The exposure of BPA (0.4,4 mg/ kg/ day) inhibited the increase in synaptic density induced by TP (p0.01, p0.001). Compared with the sham operation control group, gonad removal significantly shortened the length of the active band (p0.01), decreased the PSD thickness (p0.001), increased the synaptic cleft width (p0.001), but the change was reversed by the BPA after the addition of TP (p0.05, p0.05, p0.001). The effect of BPA exposure on the synaptic structure of the sham-operated group was similar to that of the TP-supplemented group. These results suggest that BPA exposure can inhibit the formation and structural modification of androgen-induced hippocampal synapses. Further Western blot analysis showed that the expression of p0.05, PSD-95 (p0.01), NR2B (p0.05) in the hippocampus of the sham-operated mice was significantly reduced, especially at the dose of 4 mg/ kg/ day. In addition, the expression of PSD-95 (p0.05) and NR2B (p0.01) was significantly reduced, and the expression of these proteins was up-regulated after the supplementation of TP (p0.05, p0.05). The exposure of BPA inhibited the up-regulation of synapsin I (p0.01), PSD-95 (p0.05), NR2B (p0.05). Further analysis found that the exposure of gonad and BPA did not affect the expression of p38 and ERK1/2, but the exposure of 4 mg/ kg/ day to BPA significantly reduced the phosphorylation of ERK1/2 (p-ERK1/2) (p0.05) and increased the phosphorylation of p-p38 (p-p38) (p0.001). BPA exposure inhibited TP-induced p-ERK1/2 up-regulation (p0.01) and p-p38 down-regulation (p0.01). These results suggest that the exposure of BPA inhibits the expression of the androgen-induced mutant and NR2B, inhibits the MAPK/ ERKs and promotes the activity of the MAPK/ p38 signaling pathway. Conclusion: Long-term exposure to BPA sex-specific damage to the learning and memory function of male animals may be related to the anti-androgenic effect of BPA. This effect may reduce the level of the synaptoprotein and the NMDA receptor by reducing the level of androgen in the brain and interfering with the activity of the androgen on the ERKs and p38 signaling pathways, negatively altering the synaptic plasticity of the hippocampal neurons, and eventually damaging the learning and memory function.
【学位授予单位】：浙江师范大学
【学位级别】：硕士
【学位授予年份】：2016
【分类号】：R114
本文编号：2507823
[Abstract]:Bisphenol A (BPA) is a widely used environmental endocrine disruptor for plastic products. BPA can enter the human body via food and beverage, and can also be harmful to health by dialysis to the surrounding ecological environment. A large number of studies have found that BPA can affect the synthesis and metabolism of hormones, the expression of receptors, and the activity of genes, however, the previous studies have been focused on their estrogenic activity. The pre-laboratory study found that both perinatal, adolescent and adult-year BPA exposure had sex-dependent impairment of the spatial learning and memory of male mice and passive avoidance of memory. As with the important role of estrogen on female animals, androgens play an important role in the cognitive function of the male and the formation of synapses. Recent studies have found that BPA can antagonize androgen receptor (AR)-mediated transcriptional activity. Therefore, the purpose of this experiment is to explore whether the exposure of BPA to sex-specific damage to male mice is related to the effect of interfering with androgen on learning and memory of male rats. The synaptic plasticity is closely related to the spatial learning and memory behavior. Sex hormones can affect cognitive behavior by affecting the synaptic remodeling of the central nervous system in the hippocampus and the prefrontal cortex. It was found that testicular removal resulted in a decrease in synaptic density in the hippocampus of male mice, and a significant increase in synaptic density following the supplementation of testosterone (TP) or dihydrotestosterone (DHT). The synaptic interface is a very sensitive structure to chemical substances, synaptic cleft, synaptic active band length, postsynaptic density (PSD) and synaptic interface curvature can change due to external stimuli. A large number of scaffolding proteins and some regulatory proteins associated with synaptic transmission are distributed on the PSD, many of which are associated with the receptor channel on the back membrane, the changes in the level of expression of these proteins, and the interaction with each other, can affect the activity and synaptic plasticity of the synapse, And also results in a change in the PSD thickness. The effects of long-term BPA exposure on learning and memory behavior of adult male rats were studied by establishing an adult castrated male mouse model, exposing the male mice with complete, castrated and castrated androgen to BPA, respectively, and studying the effects of long-term BPA exposure on learning and memory behavior of adult male rats. The changes of the synaptic density and the synaptic interface structure of the neurons in the hippocampal CA1 region of the male rats were observed by electron microscopy, and the changes of the expression of the synapsin I and PSD-95, the excitatory amino acid NMDA receptor and the signaling pathway protein ERK1/2, p38 and the phosphorylation of the signal pathway proteins were detected by Western blot. To study the possible mechanism of BPA exposure to the learning and memory behavior and synaptic plasticity of male rats. The method of the study was to clean the ICR male mice at 8 weeks of age and to purchase the experimental animal center of Zhejiang Academy of Medical Sciences. The environment of the feeding is natural light and dark 12h, and the temperature of the feeding room is controlled at 23-2 & deg; C and 50-60% of the humidity control, and the water and the food can be freely fed. After a week of acclimation, a castrated model was established by intraperitoneal injection of chloral (400 mg/ kg). After 2 weeks of post-operation, the neck and back were injected subcutaneously each day: Testosterone Propionate (TP, 0.5 mg/ kg/ day), BPA (0.4,4 mg/ kg/ day), TP + BPA (0.4 or 4 mg/ kg/ day), and Golden Dragon Fish Oil (50.mu. L/ day) for a period of 45 days. Three days after the end of the administration,14 animals were tested for behavioral tests,6 of which were used for hippocampal synapse morphometry,4 for the determination of related proteins and 8 for the determination of brain and serum androgen levels. All the data of the experiment were misdisplayed by means of the mean value, and the statistical analysis was made with the SPSS 17.0 statistical software. The results of 3-factor analysis of variance and the fifth day of the water maze were used in the water maze. The results of the five-day analysis of the water maze and the results of the morphological measurement of the water maze were the two-factor analysis of variance, the level of androgens and the results of Western blot. Study results:1. Compared with the sham-operated control group, gonad removal significantly decreased the levels of androgen in serum and brain (p0.001; p0.001), and the levels of serum and brain androgen increased after supplementation of TP (p0.001; p0.001). The exposure of BPA (0.4,4 mg/ kg/ day) did not affect the levels of androgen in the serum and brain of the gonads, but significantly reduced the levels of androgen in the sham-operated group (p0.05; p0.01) and the brain (p0.05; p0.01), and the androgen levels in the brain (p0.05) and the brain (p0.05; p0.01). The results of the 4-day training of the water maze showed that, compared with the sham-operated control group, the latency of the platform was significantly prolonged on the 4th day after the gonad removal (p0.05), and the latency of the platform was shortened after the addition of TP (p0.05), indicating that the androgen deficiency obviously damaged the learning ability of the space. The exposure of BPA did not prolong the incubation period of the castrated mice (p0.05), but significantly prolonged the latency of the platform in the sham operation group (4 mg/ kg/ day, p0.01) and the TP supplementation group (0.4 mg/ kg/ day, p0.05). The results of the fifth day of the water maze showed that BPA exposure reduced the percentage of time that the sham-operated mice (0.4 mg/ kg/ day, p0.05) and TP-supplemented mice (p0.001; p0.01) remained in the target quadrant, but did not affect the percentage of time that the testicle removed the target quadrant of the mouse. These results show that the ability of BPA to damage the space memory of adult mice can inhibit the recovery of the spatial memory damage induced by androgen on the gonad removal. The results of synaptic density showed that the synaptic density (p0.001) in the CA1 region of the hippocampus of the adult male rats was significantly reduced, and the postsynaptic density was significantly increased after the addition of TP (p0.001). BPA (0.4,4 mg/ kg/ day) exposure reduced the synaptic density in the hippocampal CA1 region of the sham-operated group (p0.001, p0.001), but had no effect on the gonad removal group. The exposure of BPA (0.4,4 mg/ kg/ day) inhibited the increase in synaptic density induced by TP (p0.01, p0.001). Compared with the sham operation control group, gonad removal significantly shortened the length of the active band (p0.01), decreased the PSD thickness (p0.001), increased the synaptic cleft width (p0.001), but the change was reversed by the BPA after the addition of TP (p0.05, p0.05, p0.001). The effect of BPA exposure on the synaptic structure of the sham-operated group was similar to that of the TP-supplemented group. These results suggest that BPA exposure can inhibit the formation and structural modification of androgen-induced hippocampal synapses. Further Western blot analysis showed that the expression of p0.05, PSD-95 (p0.01), NR2B (p0.05) in the hippocampus of the sham-operated mice was significantly reduced, especially at the dose of 4 mg/ kg/ day. In addition, the expression of PSD-95 (p0.05) and NR2B (p0.01) was significantly reduced, and the expression of these proteins was up-regulated after the supplementation of TP (p0.05, p0.05). The exposure of BPA inhibited the up-regulation of synapsin I (p0.01), PSD-95 (p0.05), NR2B (p0.05). Further analysis found that the exposure of gonad and BPA did not affect the expression of p38 and ERK1/2, but the exposure of 4 mg/ kg/ day to BPA significantly reduced the phosphorylation of ERK1/2 (p-ERK1/2) (p0.05) and increased the phosphorylation of p-p38 (p-p38) (p0.001). BPA exposure inhibited TP-induced p-ERK1/2 up-regulation (p0.01) and p-p38 down-regulation (p0.01). These results suggest that the exposure of BPA inhibits the expression of the androgen-induced mutant and NR2B, inhibits the MAPK/ ERKs and promotes the activity of the MAPK/ p38 signaling pathway. Conclusion: Long-term exposure to BPA sex-specific damage to the learning and memory function of male animals may be related to the anti-androgenic effect of BPA. This effect may reduce the level of the synaptoprotein and the NMDA receptor by reducing the level of androgen in the brain and interfering with the activity of the androgen on the ERKs and p38 signaling pathways, negatively altering the synaptic plasticity of the hippocampal neurons, and eventually damaging the learning and memory function.
【学位授予单位】：浙江师范大学
【学位级别】：硕士
【学位授予年份】：2016
【分类号】：R114
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