Apelin受体APJ是加拿大学者O＇Dowd等于1993年发现的一种孤儿G蛋白偶联受体（orphan GPCRs,o GPCRs）,因其与血管紧张素Ⅱ1型受体（angiotensinl I typel receptor,ATI）有30%~50%的同源性,故取名为血管紧张素Ⅱ1型受体相关蛋白（putati...Apelin受体APJ是加拿大学者O＇Dowd等于1993年发现的一种孤儿G蛋白偶联受体（orphan GPCRs,o GPCRs）,因其与血管紧张素Ⅱ1型受体（angiotensinl I typel receptor,ATI）有30%~50%的同源性,故取名为血管紧张素Ⅱ1型受体相关蛋白（putative receptor protein related to the angiotensin II typel receptor,APJ）（[1]）。为探寻APJ内源性配体,日本学者Tatemoto于1998年用反向药理学方法,展开更多
目的:探讨Apelin-血管紧张素Ⅱ1型受体相关受体蛋白J(angiotension II protein J,APJ)系统在低氧性肺动脉高压大鼠肺组织中的变化情况。方法:20只雄性SD大鼠随机分为两组,其中10只为低氧2周组,另10只为对照组。通过放射免疫分析法、免...目的:探讨Apelin-血管紧张素Ⅱ1型受体相关受体蛋白J(angiotension II protein J,APJ)系统在低氧性肺动脉高压大鼠肺组织中的变化情况。方法:20只雄性SD大鼠随机分为两组,其中10只为低氧2周组,另10只为对照组。通过放射免疫分析法、免疫组织化学法及RT-PCR法检测两组大鼠肺组织中Apelin-APJ系统的变化情况。结果:低氧2周组大鼠肺动脉平均压(mean pulmonary artery pressure,m PAP)与右心室游离壁质量/左心室加室间隔质量[RV/(LV+S)]均高于对照组(P<0.05),APJ mRNA水平低于对照组(P<0.01);但两组大鼠的颈动脉压(carotid artery pressure,m CAP)和Apelin-36水平比较,差异无统计学意义(P>0.05)。结论:Apelin-APJ系统的变化在低氧性肺动脉高压发生发展过程中可能起到重要的作用。展开更多
Objective： To investigate whether ginsenoside-Rbl （Gs-Rb1） inhibits the apoptosis of hypoxia cardiomyocytes by up-regulating apelin-APJ system and whether the system is affected by hypoxia-induced factor 1α （Hif-...Objective： To investigate whether ginsenoside-Rbl （Gs-Rb1） inhibits the apoptosis of hypoxia cardiomyocytes by up-regulating apelin-APJ system and whether the system is affected by hypoxia-induced factor 1α （Hif-1α）. Methods： Neonatal rat cardiomyocytes were randomly divided into 6 groups： a control group, a simple COCl2 group, a simple Gs-Rbl group, a CoCl2 and Gs-Rbl hypoxia group, a CoCl2 and 3-（5＇-hydroxymethyl-2＇-furyl）-1-benzylindazole （YC-1） group, a CoCl2 and YC-1 group and a Gs-Rbl group, in which YC-1 inhibits the synthesis and accelerates the degradation of Hif-la. The concentration of COCI2, Gs-Rbl and YC-1 was 500 μmol/L, 200 μ mol/L and 5 μmol/L, respectively; the apoptosis ratio was analyzed with a flow cytometer; and apelin, APJ and Hif-1 c= were assayed with immunocytochemistry, Western blot assays and reverse transcription polymerase chain reaction （RT-PCR）. Results： （1） The anti-apoptosis effect of Gs-Rbl on hypoxia cardiomyocytes was significantly inhibited by YC-1; （2） Hypoxia significantly up-graded the expression of mRNA and protein of apelin; this effect was further reinforced by Gs-Rbl and significantly inhibited by YC-1; （3） Gs-Rb1 further strengthened the expression of APJ mRNA and APJ proteins once hypoxia occurred, which was significantly inhibited by YC-1; （4） Gs-Rb1 significantly increased the expression of Hif-1α, which was completely abolished by YC-1; （5） There was a negative relationship between AR and apelin （or APJ, including mRNA and protein）, a positive correlation between apelin （or APJ） protein and Hif-1a protein, in hypoxia cardiomyocytes. Conclusion： The apelin-APJ system plays an important role in the anti-apoptosis effect of Gs- Rb1 on hypoxia neonatal cardiomyocytes, which was partly adjusted by Hif-1α.展开更多
目的探究血管紧张素受体AT1相关受体蛋白(putative receptor protein related to AT1,APJ)同源二聚体对人脐静脉内皮细胞(HUVECs)行为,即增殖、迁移和成管的作用。方法将HUVECs随机分为对照组(PBS)、APJ单体组[爱帕琳肽13(Apelin-13)+T...目的探究血管紧张素受体AT1相关受体蛋白(putative receptor protein related to AT1,APJ)同源二聚体对人脐静脉内皮细胞(HUVECs)行为,即增殖、迁移和成管的作用。方法将HUVECs随机分为对照组(PBS)、APJ单体组[爱帕琳肽13(Apelin-13)+TM1]和APJ同源二聚体组(Apelin-13+PBS),分别用Western blot和基质辅助激光解吸飞行时间质谱仪(MALDI-TOF MS)检测APJ和APJ同源二聚体在HUVECs中的表达;实时细胞分析仪(RTCA)检测Apelin-13引起50%最大效应的浓度(EC_(50));CCK-8法测定HUVECs的细胞活力;划痕实验检测HUVECs的迁移能力;人工基底膜(matrigel)检测HUVECs的成管。结果Western blot和MALDI-TOF MS实验结果显示,APJ和APJ同源二聚体均表达于HUVECs中。Apelin-13的EC_(50)为2.26×10^(-8)mol·L^(-1),且引起最大效应的浓度为1.0×10^(-6)mol·L^(-1)。CCK-8实验、迁移实验和成管实验结果显示,各组细胞随着时间的延长逐渐向划痕裸区迁移,镜下也观察到各组细胞均出现成管,数据统计发现Apelin-13+PBS和Apelin-13+TM1组的HUVECs增殖、迁移和成管能力均较PBS组明显增加,且Apelin-13+PBS组的增殖、迁移和成管能力明显好于Apelin-13+TM1组(P<0.05)。结论APJ同源二聚体对HUVECs的增殖、迁移和成管均具有促进作用,且效果优于APJ单体。展开更多
文摘Apelin受体APJ是加拿大学者O＇Dowd等于1993年发现的一种孤儿G蛋白偶联受体（orphan GPCRs,o GPCRs）,因其与血管紧张素Ⅱ1型受体（angiotensinl I typel receptor,ATI）有30%~50%的同源性,故取名为血管紧张素Ⅱ1型受体相关蛋白（putative receptor protein related to the angiotensin II typel receptor,APJ）（[1]）。为探寻APJ内源性配体,日本学者Tatemoto于1998年用反向药理学方法,
基金Supported by Liaoning Province Science and Technique Foundation of China(No.201102107)
文摘Objective： To investigate whether ginsenoside-Rbl （Gs-Rb1） inhibits the apoptosis of hypoxia cardiomyocytes by up-regulating apelin-APJ system and whether the system is affected by hypoxia-induced factor 1α （Hif-1α）. Methods： Neonatal rat cardiomyocytes were randomly divided into 6 groups： a control group, a simple COCl2 group, a simple Gs-Rbl group, a CoCl2 and Gs-Rbl hypoxia group, a CoCl2 and 3-（5＇-hydroxymethyl-2＇-furyl）-1-benzylindazole （YC-1） group, a CoCl2 and YC-1 group and a Gs-Rbl group, in which YC-1 inhibits the synthesis and accelerates the degradation of Hif-la. The concentration of COCI2, Gs-Rbl and YC-1 was 500 μmol/L, 200 μ mol/L and 5 μmol/L, respectively; the apoptosis ratio was analyzed with a flow cytometer; and apelin, APJ and Hif-1 c= were assayed with immunocytochemistry, Western blot assays and reverse transcription polymerase chain reaction （RT-PCR）. Results： （1） The anti-apoptosis effect of Gs-Rbl on hypoxia cardiomyocytes was significantly inhibited by YC-1; （2） Hypoxia significantly up-graded the expression of mRNA and protein of apelin; this effect was further reinforced by Gs-Rbl and significantly inhibited by YC-1; （3） Gs-Rb1 further strengthened the expression of APJ mRNA and APJ proteins once hypoxia occurred, which was significantly inhibited by YC-1; （4） Gs-Rb1 significantly increased the expression of Hif-1α, which was completely abolished by YC-1; （5） There was a negative relationship between AR and apelin （or APJ, including mRNA and protein）, a positive correlation between apelin （or APJ） protein and Hif-1a protein, in hypoxia cardiomyocytes. Conclusion： The apelin-APJ system plays an important role in the anti-apoptosis effect of Gs- Rb1 on hypoxia neonatal cardiomyocytes, which was partly adjusted by Hif-1α.
文摘目的探究血管紧张素受体AT1相关受体蛋白(putative receptor protein related to AT1,APJ)同源二聚体对人脐静脉内皮细胞(HUVECs)行为,即增殖、迁移和成管的作用。方法将HUVECs随机分为对照组(PBS)、APJ单体组[爱帕琳肽13(Apelin-13)+TM1]和APJ同源二聚体组(Apelin-13+PBS),分别用Western blot和基质辅助激光解吸飞行时间质谱仪(MALDI-TOF MS)检测APJ和APJ同源二聚体在HUVECs中的表达;实时细胞分析仪(RTCA)检测Apelin-13引起50%最大效应的浓度(EC_(50));CCK-8法测定HUVECs的细胞活力;划痕实验检测HUVECs的迁移能力;人工基底膜(matrigel)检测HUVECs的成管。结果Western blot和MALDI-TOF MS实验结果显示,APJ和APJ同源二聚体均表达于HUVECs中。Apelin-13的EC_(50)为2.26×10^(-8)mol·L^(-1),且引起最大效应的浓度为1.0×10^(-6)mol·L^(-1)。CCK-8实验、迁移实验和成管实验结果显示,各组细胞随着时间的延长逐渐向划痕裸区迁移,镜下也观察到各组细胞均出现成管,数据统计发现Apelin-13+PBS和Apelin-13+TM1组的HUVECs增殖、迁移和成管能力均较PBS组明显增加,且Apelin-13+PBS组的增殖、迁移和成管能力明显好于Apelin-13+TM1组(P<0.05)。结论APJ同源二聚体对HUVECs的增殖、迁移和成管均具有促进作用,且效果优于APJ单体。
