雌激素对可兴奋性细胞K_(ATP)通道的调节及意义
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摘要
研究背景及目的
流行病学研究发现性别不同会导致脑中风、心血管疾病的发生率及预后存在显著的差异。差异产生可能与雌激素的水平相关,如女性绝经前与同龄男性相比,其高血压、心肌缺血、脑中风等发病率较低,绝经后由于女性体内的雌激素水平迅速降低,心脑疾病的发生率急剧上升。雌激素受体除了在生殖系统中表达丰富以外,还广泛表达于多种组织,如血管、心脏、神经系统等。目前研究发现雌激素与雌激素受体结合可以通过多种相关途径介导心、脑及血管的保护作用。
ATP敏感性钾离子通道(ATP-sensitive K+channels, KATP通道)是一种内向整流式钾通道,其开放主要受细胞内ATP水平的调控,将各种兴奋性组织中细胞的电活动与细胞代谢状态相耦联。KATP通道广泛分布于心肌细胞、胰岛β细胞、骨骼肌细胞、血管与非血管平滑肌细胞和神经细胞等多种可兴奋性细胞中。它具有减轻组织缺血再灌注损伤、维持血管的舒张功能、调节胰岛素的分泌等作用。
雌激素和KATP通道对可兴奋性组织有着相似的生理效应。由此我们推测雌激素可能通过调节可兴奋性细胞(心肌细胞、血管平滑肌细胞和神经细胞)中KATP通道来发挥其保护作用。为此本研究拟通过首先建立卵巢去势雌激素干预模型,并在此基础上分别通过以下实验探讨雌激素对可兴奋性细胞KATP通道的调节及意义：(1)评估雌激素对心肌KATP通道表达的影响。(2)检测雌激素对血管平滑肌KATP通道的表达及活性的调节,观察其对血管功能的影响。(3)检测雌激素对脑皮层神经元KATP通道的表达及活性的调节,并评价其在脑缺血再灌注损伤中的作用。
研究方法及结果
1.大鼠卵巢去势雌激素再干预模型的建立及鉴定
方法雌性SD大鼠30只,体重100±10g,随机分为假手术组(Sham)、卵巢切除组(Ovx)、卵巢切除后补充雌激素组(Estr)。通过阴道脱落细胞涂片观察其发情周期的变化,并检测子宫指数、子宫切片HE染色及血清中雌激素浓度的变化。
结果与Sham组相比较,卵巢去势后(Ovx组)大鼠子宫指数、雌激素浓度显著降低(P<0.05)；与Ovx组相比,卵巢去势后又补充雌激素(Estr组)大鼠子宫指数、雌激素浓度明显增加(P<0.05)。
2.雌激素对大鼠心肌ATP敏感性钾离子通道表达的影响
方法雌性SD大鼠18只,体重100±10g,随机分为假手术组(Sham)、卵巢切除组(Ovx)、卵巢切除后补充雌激素组(Estr)。取大鼠心室肌组织采取实时荧光定量PCR及Western-blot方法分别检测大鼠心肌中KATP通道的Kir6.2及SUR2A亚单位mRNA及蛋白的表达变化。
结果与Sham组相比,Ovx组大鼠心肌中的Kir6.2及SUR2A亚单位mRNA及蛋白表达减少(P<0.05),而Estr组无明显差异。与Sham组相比,Estr组则表达增加(P<0.05)。
3.雌激素通过KATP通道影响大鼠肠系膜动脉的反应性
方法雌性SD大鼠48只,体重100±10g,随机分为假手术组(Sham)、卵巢切除组(Ovx)、卵巢切除后补充雌激素组(Estr)。取大鼠肠系膜动脉,采取实时荧光定量PCR检测KATP通道的Kir6.1及SUR2B亚单位mRNA的表达,及观察各组大鼠对去甲肾上腺素(NE)升压效应的反应性。
结果与Sham组相比,Ovx组大鼠肠系膜动脉中的Kir6.1及SUR2B亚单位mRNA表达减少(P<0.05),而Estr组则表达增加(P<0.05)。与Sham组相比,Ovx组大鼠的血管反应性明显增加(P<0.05),Estr组无明显差异。给予KATP通道阻滞剂格列本脲后,Sham组和Estr组的动脉反应性增加(P＜0.05), Ovx组无明显变化(P>0.05),此时三组间比较无明显差异(P>0.05)。
4.雌激素通过KATP通道减轻大鼠脑缺血再灌注损伤
方法实验1实验分为假手术组(Sham)、卵巢切除组(Ovx)、卵巢切除后补充雌激素组(Estr)。取大鼠大脑皮层组织,采取实时荧光定量PCR及Western-blot方法分别检测KATP通道mRNA及蛋白的表达变化。
实验2假手术组(Sham)、卵巢切除组(Ovx)大鼠侧脑室注射DMSO,卵巢切除后补充雌激素组(Estr)则分别侧脑室注射DMSO和格列本脲(Estr+G),观察各组大鼠局灶脑缺血后脑梗死体积和神经功能评分及KATP阻滞剂对其影响。
结果与Sham组相比,Ovx组大鼠大脑皮层中KATP通道mRNA及蛋白表达减少(P<0.05),而Estr组无明显差异。与Ovx组相比,Estr组则表达增加(P<0.05)。与Ovx组大鼠相比,Sham组及Estr组大鼠的局灶脑缺血后脑梗死体积和神经功能评分均减小(P<0.05)。而格列本脲则增加了Estr组大鼠的脑梗死体积及神经功能评分(P<0.05)。
研究结论
1.本实验成功建立了卵巢去势后雌激素干预模型,该模型可以模拟雌激素的生理作用。
2.雌激素可以增加大鼠心肌ATP敏感性钾离子通道的表达。
3.雌激素可能通过调节肠系膜动脉平滑肌细胞KATP通道的表达及活性来降低动脉对去甲肾上腺素升压效应的反应性。
4.雌激素可以调节大脑皮层KATP通道的表达及活性,并且可能与雌激素的神经保护作用有关。
研究总结及展望
本研究建立了卵巢去势后雌激素干预模型,该模型可以模拟雌激素的生理作用。后续研究通过此模型发现,雌激素可以上调可兴奋性细胞如心肌组织、肠系膜动脉平滑肌细胞及大脑皮层组织中的KATP通道的表达。在进一步对其生理功能的研究发现,雌激素对这些可兴奋性组织KATP通道的调节可能与雌激素的血管反应性、神经保护作用等有关。本研究提示了雌激素的生理作用可能通过调节KATP通道来实现这一作用机制。为减少雌激素替代治疗的不良反应,及开发新的治疗药物及方案提供一些线索。为我们下一步研究雌激素调节KATP通道的信号传导途径奠定了基础。
Back ground and objective
Epidemiological studies have shown that sex differences in stroke, cardiovascular disease. The incidences of stroke, hypertension and myocardial ischemia in premenopausal women are lower than in men of the same age. However, when estrogen levers fall due to follicular depletion in postmenopausal women, incidences of stroke and cardiovascular disease increase sharply. Estrogen receptor (ERa and ERβ) are not only localized in the reproductive system, also widely expressed in a variety of tissues:blood vessels, heart, nervous system, and so on. Estradiol is thought to exert the majority of its biological actions, the protective effect of the heart, brain and blood, via interaction with two primary estogen receptors.
ATP-sensitive potassium channel (KATP channel) is an inward rectifier potassium channel, which couples the intermediary metabolism to excitability, and mainly modulated by intracellular ATP levels. KATP channels are widely expressed in a variety of excitable cells including myocardium, pancreatic beta cells, skeletal muscle cells, vascular and non-vascular smooth muscle cells and neurons. Previous studies have shown that KATP channels were involved in protection against ischemia-reperfusion injury, maintaining the dilation of blood vessels and regulating insulin secretion.
It has been shown that there are similar physiological effects between KATP channel and estrogen. Therefore, we hypothesize that the effect of estogen in excitable cells is associated with KATP channel. To test this hypotheses, firstly, we established and evaluated a rat model of ovariectomized and estrogen administration. Then we performed the follow studies:(1) Assessed the effects of estrogen on the expression of KATP channel in myocardial of rats.(2) Observed the expression of ATP-sensitive potassium channel mRNA in mesenteric artery smooth muscle of rats with estrogen administration, and to evaluate the role of KATP channel in the effects of estrogen on mesenteric artery reactivity in rats.(3)Observed the effects of estrogen on the expression and activity of KATP channel in cerebral cortex, and evaluated the role of this regulation in cerebral ischemia-reperfusion injury in rats.
Methods and Results
1. Establish and evaluate the rat model of ovariectomized and estrogen administration.
Methods:Thirty female Sprague-Dawley rats, weighing100±10g, were randomly divided into three groups:group sham operation (group Sham), group ovariectomy (group Ovx), and group ovariectomy with estrogen administration (group Estr). Vaginal smears were performed to observe the changes of estrous cycle. Then the uterine index, uterine slice HE staining and serum concentration of estrogen were evaluated after estrogen administration.
Results:After ovariectomy, the uterus/body ratio and serum estradiol levels in female rats were lower than those in the Sham group (P<0.05). With17b-estradiol treatment, the uterine index and serum estradiol levels in Estr group were higher than those in the Ovx group (P<0.05).
2. Regualting of KATP channel gene expression by estrogen in ratcardiaomyocytes
Methods:Eighteen female Sprague-Dawley rats, weighing100+10g, were randomly divided into three groups:group sham operation (group Sham), group ovariectomy (group Ovx), and group ovariectomy with estrogen administration (group Estr). The expression of KATP subunits mRNA and protein of cardiac myocytes were detected by quantitive real time PCR and western blot.
Results:Compared with group Sham, the expression of Kir6.2and SUR2A mRNA and protein were significantly decreased in group Ovx (P＜0.05). But compared with group Ovx, they were increased in group Estr (P<0.05).
3. Estrogen afftects rats'mesenteric artery reactivity through ATP-sensitive potassium channel
Methods:Forty-eight female Sprague-Dawley rats, weighing100±10g, were randomly divided into three groups:group sham operation (group Sham), group ovariectomy (group Ovx), and group ovariectomy with estrogen administration (group Estr). The expression of KATP subunits mRNA of mesenteric artery smooth muscle was detected by quantitive real time PCR. Artery reactivity in rats was observed by norepinephrine induced pressor response.
Results:Compared with group Sham, the expression of Kir6.1and SUR2B mRNA was significantly decreased in group Ovx (P<0.05), but increased in group Estr (P<0.05).Compared with group Sham and group Estr, the pressor response induced by norepinephrine of rats were enhanced in group Ovx (P＜0.05). But there was no significantly difference between group Sham and group Estr. After administration glibenclamide, a KATP channel blocker, the pressor response induced by norepinephrine were enhanced in group Sham and group Estr, but no changed in group Ovx. Meanwhile, there were no differences in three groups.
4. Neuroprotective effects of17b-estradiol associate with KATP in rat brain
Methods:In experiment1:Randomly divided three groups of rats:ovariectomized rats (Ovx), sham operation (Sham), ovariectomized rats receiving17β-estradiol (Estr). The KATP mRNA and proteins in cortex of three group rats were measured respectively.
In experiment2:Randomly assigned four groups of rats:ovariectomized female rats (Ovx), sham operation(Sham), ovariectomized female rats receiving17β-estradiol (Estr) and ovariectomized rats receiving both17β-estradiol and the stereotaxic injection of glibenclamide (Estr+G). The rats in Ovx, Sham and Estr groups were received the stereotaxic injection of vehicle (dimethyl sulfoxide).30minutes after drug administration, the rats received middle cerebral artery occlusion for60minutes. Twenty-four hours after reperfusion, the neurobehavioral scores and infract volume were evaluated.
Results:The Kir6.2and SUR1mRNA and protein levels of brain cortex in female ovarectomied rats were decreased compared to rats with sham operation. However, the expressions of Kir6.2and SUR1in brain cortex of ovarectomied rats were recovered with supplement17β-estradiol. The protective effects of17β-estradiol were abolished by glibenclamide, a KATP channels blocker.
Conclusions
1. A rat model of ovariectomized and estrogen administration was successfully established, and it is able to mimic the physiological effects of estrogen.
2. Estrogen can up-regulate KATP channel subunits gene expressions in rat cardiomyocytes.
3. Estrogen can up-regulate the gene expression of KATP channel subunits, and that regualtion may be involved in estrogen-reduced the pressor response of norepinephrine.
4. Estrogen significantly upregulates the gene expression of KATP channel subunits and channel activity in the brain cortices of ovariectomized rats. This regulation is associated with the neuroprotective effects of estradiol.
Summary
This study has successfully established an ovariectomized and estrogen intervention rat model.The studies fellowing have shown that estrogen can up-regulate the expression of KATP channel in excitable cells such as cardiomyocytes, mesenteric artery smooth muscle cells and cerebral cortex. The results of physiological function revealed that, the regulation of KATP channel by estrogen in excitable cells may be related to vascular reactivity and neuroprotection. These studies suggest another potential mechanism of estrogen physiological effects, and provide some hints for reducing the adverse effects of estrogen replacement therapy and development of novel treatment.
流行病学研究发现性别不同会导致脑中风、心血管疾病的发生率及预后存在显著的差异。差异产生可能与雌激素的水平相关,如女性绝经前与同龄男性相比,其高血压、心肌缺血、脑中风等发病率较低,绝经后由于女性体内的雌激素水平迅速降低,心脑疾病的发生率急剧上升。雌激素受体除了在生殖系统中表达丰富以外,还广泛表达于多种组织,如血管、心脏、神经系统等。目前研究发现雌激素与雌激素受体结合可以通过多种相关途径介导心、脑及血管的保护作用。
ATP敏感性钾离子通道(ATP-sensitive K+channels, KATP通道)是一种内向整流式钾通道,其开放主要受细胞内ATP水平的调控,将各种兴奋性组织中细胞的电活动与细胞代谢状态相耦联。KATP通道广泛分布于心肌细胞、胰岛β细胞、骨骼肌细胞、血管与非血管平滑肌细胞和神经细胞等多种可兴奋性细胞中。它具有减轻组织缺血再灌注损伤、维持血管的舒张功能、调节胰岛素的分泌等作用。
雌激素和KATP通道对可兴奋性组织有着相似的生理效应。由此我们推测雌激素可能通过调节可兴奋性细胞(心肌细胞、血管平滑肌细胞和神经细胞)中KATP通道来发挥其保护作用。为此本研究拟通过首先建立卵巢去势雌激素干预模型,并在此基础上分别通过以下实验探讨雌激素对可兴奋性细胞KATP通道的调节及意义：(1)评估雌激素对心肌KATP通道表达的影响。(2)检测雌激素对血管平滑肌KATP通道的表达及活性的调节,观察其对血管功能的影响。(3)检测雌激素对脑皮层神经元KATP通道的表达及活性的调节,并评价其在脑缺血再灌注损伤中的作用。
研究方法及结果
1.大鼠卵巢去势雌激素再干预模型的建立及鉴定
方法雌性SD大鼠30只,体重100±10g,随机分为假手术组(Sham)、卵巢切除组(Ovx)、卵巢切除后补充雌激素组(Estr)。通过阴道脱落细胞涂片观察其发情周期的变化,并检测子宫指数、子宫切片HE染色及血清中雌激素浓度的变化。
结果与Sham组相比较,卵巢去势后(Ovx组)大鼠子宫指数、雌激素浓度显著降低(P<0.05)；与Ovx组相比,卵巢去势后又补充雌激素(Estr组)大鼠子宫指数、雌激素浓度明显增加(P<0.05)。
2.雌激素对大鼠心肌ATP敏感性钾离子通道表达的影响
方法雌性SD大鼠18只,体重100±10g,随机分为假手术组(Sham)、卵巢切除组(Ovx)、卵巢切除后补充雌激素组(Estr)。取大鼠心室肌组织采取实时荧光定量PCR及Western-blot方法分别检测大鼠心肌中KATP通道的Kir6.2及SUR2A亚单位mRNA及蛋白的表达变化。
结果与Sham组相比,Ovx组大鼠心肌中的Kir6.2及SUR2A亚单位mRNA及蛋白表达减少(P<0.05),而Estr组无明显差异。与Sham组相比,Estr组则表达增加(P<0.05)。
3.雌激素通过KATP通道影响大鼠肠系膜动脉的反应性
方法雌性SD大鼠48只,体重100±10g,随机分为假手术组(Sham)、卵巢切除组(Ovx)、卵巢切除后补充雌激素组(Estr)。取大鼠肠系膜动脉,采取实时荧光定量PCR检测KATP通道的Kir6.1及SUR2B亚单位mRNA的表达,及观察各组大鼠对去甲肾上腺素(NE)升压效应的反应性。
结果与Sham组相比,Ovx组大鼠肠系膜动脉中的Kir6.1及SUR2B亚单位mRNA表达减少(P<0.05),而Estr组则表达增加(P<0.05)。与Sham组相比,Ovx组大鼠的血管反应性明显增加(P<0.05),Estr组无明显差异。给予KATP通道阻滞剂格列本脲后,Sham组和Estr组的动脉反应性增加(P＜0.05), Ovx组无明显变化(P>0.05),此时三组间比较无明显差异(P>0.05)。
4.雌激素通过KATP通道减轻大鼠脑缺血再灌注损伤
方法实验1实验分为假手术组(Sham)、卵巢切除组(Ovx)、卵巢切除后补充雌激素组(Estr)。取大鼠大脑皮层组织,采取实时荧光定量PCR及Western-blot方法分别检测KATP通道mRNA及蛋白的表达变化。
实验2假手术组(Sham)、卵巢切除组(Ovx)大鼠侧脑室注射DMSO,卵巢切除后补充雌激素组(Estr)则分别侧脑室注射DMSO和格列本脲(Estr+G),观察各组大鼠局灶脑缺血后脑梗死体积和神经功能评分及KATP阻滞剂对其影响。
结果与Sham组相比,Ovx组大鼠大脑皮层中KATP通道mRNA及蛋白表达减少(P<0.05),而Estr组无明显差异。与Ovx组相比,Estr组则表达增加(P<0.05)。与Ovx组大鼠相比,Sham组及Estr组大鼠的局灶脑缺血后脑梗死体积和神经功能评分均减小(P<0.05)。而格列本脲则增加了Estr组大鼠的脑梗死体积及神经功能评分(P<0.05)。
研究结论
1.本实验成功建立了卵巢去势后雌激素干预模型,该模型可以模拟雌激素的生理作用。
2.雌激素可以增加大鼠心肌ATP敏感性钾离子通道的表达。
3.雌激素可能通过调节肠系膜动脉平滑肌细胞KATP通道的表达及活性来降低动脉对去甲肾上腺素升压效应的反应性。
4.雌激素可以调节大脑皮层KATP通道的表达及活性,并且可能与雌激素的神经保护作用有关。
研究总结及展望
本研究建立了卵巢去势后雌激素干预模型,该模型可以模拟雌激素的生理作用。后续研究通过此模型发现,雌激素可以上调可兴奋性细胞如心肌组织、肠系膜动脉平滑肌细胞及大脑皮层组织中的KATP通道的表达。在进一步对其生理功能的研究发现,雌激素对这些可兴奋性组织KATP通道的调节可能与雌激素的血管反应性、神经保护作用等有关。本研究提示了雌激素的生理作用可能通过调节KATP通道来实现这一作用机制。为减少雌激素替代治疗的不良反应,及开发新的治疗药物及方案提供一些线索。为我们下一步研究雌激素调节KATP通道的信号传导途径奠定了基础。
Back ground and objective
Epidemiological studies have shown that sex differences in stroke, cardiovascular disease. The incidences of stroke, hypertension and myocardial ischemia in premenopausal women are lower than in men of the same age. However, when estrogen levers fall due to follicular depletion in postmenopausal women, incidences of stroke and cardiovascular disease increase sharply. Estrogen receptor (ERa and ERβ) are not only localized in the reproductive system, also widely expressed in a variety of tissues:blood vessels, heart, nervous system, and so on. Estradiol is thought to exert the majority of its biological actions, the protective effect of the heart, brain and blood, via interaction with two primary estogen receptors.
ATP-sensitive potassium channel (KATP channel) is an inward rectifier potassium channel, which couples the intermediary metabolism to excitability, and mainly modulated by intracellular ATP levels. KATP channels are widely expressed in a variety of excitable cells including myocardium, pancreatic beta cells, skeletal muscle cells, vascular and non-vascular smooth muscle cells and neurons. Previous studies have shown that KATP channels were involved in protection against ischemia-reperfusion injury, maintaining the dilation of blood vessels and regulating insulin secretion.
It has been shown that there are similar physiological effects between KATP channel and estrogen. Therefore, we hypothesize that the effect of estogen in excitable cells is associated with KATP channel. To test this hypotheses, firstly, we established and evaluated a rat model of ovariectomized and estrogen administration. Then we performed the follow studies:(1) Assessed the effects of estrogen on the expression of KATP channel in myocardial of rats.(2) Observed the expression of ATP-sensitive potassium channel mRNA in mesenteric artery smooth muscle of rats with estrogen administration, and to evaluate the role of KATP channel in the effects of estrogen on mesenteric artery reactivity in rats.(3)Observed the effects of estrogen on the expression and activity of KATP channel in cerebral cortex, and evaluated the role of this regulation in cerebral ischemia-reperfusion injury in rats.
Methods and Results
1. Establish and evaluate the rat model of ovariectomized and estrogen administration.
Methods:Thirty female Sprague-Dawley rats, weighing100±10g, were randomly divided into three groups:group sham operation (group Sham), group ovariectomy (group Ovx), and group ovariectomy with estrogen administration (group Estr). Vaginal smears were performed to observe the changes of estrous cycle. Then the uterine index, uterine slice HE staining and serum concentration of estrogen were evaluated after estrogen administration.
Results:After ovariectomy, the uterus/body ratio and serum estradiol levels in female rats were lower than those in the Sham group (P<0.05). With17b-estradiol treatment, the uterine index and serum estradiol levels in Estr group were higher than those in the Ovx group (P<0.05).
2. Regualting of KATP channel gene expression by estrogen in ratcardiaomyocytes
Methods:Eighteen female Sprague-Dawley rats, weighing100+10g, were randomly divided into three groups:group sham operation (group Sham), group ovariectomy (group Ovx), and group ovariectomy with estrogen administration (group Estr). The expression of KATP subunits mRNA and protein of cardiac myocytes were detected by quantitive real time PCR and western blot.
Results:Compared with group Sham, the expression of Kir6.2and SUR2A mRNA and protein were significantly decreased in group Ovx (P＜0.05). But compared with group Ovx, they were increased in group Estr (P<0.05).
3. Estrogen afftects rats'mesenteric artery reactivity through ATP-sensitive potassium channel
Methods:Forty-eight female Sprague-Dawley rats, weighing100±10g, were randomly divided into three groups:group sham operation (group Sham), group ovariectomy (group Ovx), and group ovariectomy with estrogen administration (group Estr). The expression of KATP subunits mRNA of mesenteric artery smooth muscle was detected by quantitive real time PCR. Artery reactivity in rats was observed by norepinephrine induced pressor response.
Results:Compared with group Sham, the expression of Kir6.1and SUR2B mRNA was significantly decreased in group Ovx (P<0.05), but increased in group Estr (P<0.05).Compared with group Sham and group Estr, the pressor response induced by norepinephrine of rats were enhanced in group Ovx (P＜0.05). But there was no significantly difference between group Sham and group Estr. After administration glibenclamide, a KATP channel blocker, the pressor response induced by norepinephrine were enhanced in group Sham and group Estr, but no changed in group Ovx. Meanwhile, there were no differences in three groups.
4. Neuroprotective effects of17b-estradiol associate with KATP in rat brain
Methods:In experiment1:Randomly divided three groups of rats:ovariectomized rats (Ovx), sham operation (Sham), ovariectomized rats receiving17β-estradiol (Estr). The KATP mRNA and proteins in cortex of three group rats were measured respectively.
In experiment2:Randomly assigned four groups of rats:ovariectomized female rats (Ovx), sham operation(Sham), ovariectomized female rats receiving17β-estradiol (Estr) and ovariectomized rats receiving both17β-estradiol and the stereotaxic injection of glibenclamide (Estr+G). The rats in Ovx, Sham and Estr groups were received the stereotaxic injection of vehicle (dimethyl sulfoxide).30minutes after drug administration, the rats received middle cerebral artery occlusion for60minutes. Twenty-four hours after reperfusion, the neurobehavioral scores and infract volume were evaluated.
Results:The Kir6.2and SUR1mRNA and protein levels of brain cortex in female ovarectomied rats were decreased compared to rats with sham operation. However, the expressions of Kir6.2and SUR1in brain cortex of ovarectomied rats were recovered with supplement17β-estradiol. The protective effects of17β-estradiol were abolished by glibenclamide, a KATP channels blocker.
Conclusions
1. A rat model of ovariectomized and estrogen administration was successfully established, and it is able to mimic the physiological effects of estrogen.
2. Estrogen can up-regulate KATP channel subunits gene expressions in rat cardiomyocytes.
3. Estrogen can up-regulate the gene expression of KATP channel subunits, and that regualtion may be involved in estrogen-reduced the pressor response of norepinephrine.
4. Estrogen significantly upregulates the gene expression of KATP channel subunits and channel activity in the brain cortices of ovariectomized rats. This regulation is associated with the neuroprotective effects of estradiol.
Summary
This study has successfully established an ovariectomized and estrogen intervention rat model.The studies fellowing have shown that estrogen can up-regulate the expression of KATP channel in excitable cells such as cardiomyocytes, mesenteric artery smooth muscle cells and cerebral cortex. The results of physiological function revealed that, the regulation of KATP channel by estrogen in excitable cells may be related to vascular reactivity and neuroprotection. These studies suggest another potential mechanism of estrogen physiological effects, and provide some hints for reducing the adverse effects of estrogen replacement therapy and development of novel treatment.
引文
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