目的:探讨子痫前期(PE)患者血清和胎盘中的肿瘤坏死因子-α(TNF-α)、基质金属蛋白酶-1(MMP-1)、基质金属蛋白酶-7(MMP-7)的表达水平。方法:选取2021年11月—2023年8月扬州大学临床医学院妇产科收治的86例PE患者,分为早发型PE(n=33)和...目的:探讨子痫前期(PE)患者血清和胎盘中的肿瘤坏死因子-α(TNF-α)、基质金属蛋白酶-1(MMP-1)、基质金属蛋白酶-7(MMP-7)的表达水平。方法:选取2021年11月—2023年8月扬州大学临床医学院妇产科收治的86例PE患者,分为早发型PE(n=33)和晚发型PE(n=53),另外选取健康孕妇(n=45)作为对照。检测所有纳入患者血清及胎盘组织中的TNF-α、MMP-1和MMP-7水平。结果:早发型PE患者(34.71±1.35周vs 40.43±0.70周)及晚发型PE患者(38.43±0.60周vs 40.43±0.70周)的孕周明显小于对照组(均P<0.05);早发型PE患者血清中TNF-α(507.92±28.99 ng/L vs 478.50±41.15 ng/L)、MMP-1(1156.67±158.07μg/L vs 1037.59±163.10μg/L)和MMP-7(211.00±18.64μg/L vs 196.32±19.87μg/L)的表达较晚发型PE患者显著增加(均P<0.05),晚发型PE患者血清中TNF-α(478.50±41.15 ng/L vs 446.90±41.52 ng/L)、MMP-1(1037.59±163.10μg/L vs 840.78±174.43μg/L)和MMP-7(196.32±19.87μg/L vs 166.01±15.09μg/L)的表达较对照组显著增加(均P<0.05);免疫组化结果显示,早发型PE患者胎盘组织中TNF-α、MMP-1和MMP-7表达水平较晚发型PE及对照组明显升高(均P<0.05)。结论:早发型PE患者及晚发型PE患者的TNF-α、MMP-1和MMP-7表达明显增加,这可能在PE的发生发展中起到重要作用。展开更多
目的 探讨血清α-突触核蛋白(α-synuclein,α-syn)、沉默调节蛋白1(Sirtuin-1,SIRT1)水平与进展性脑梗死患者神经功能、梗死体积及预后的相关性。方法 回顾性分析100例急性脑梗死病例资料。根据脑梗死病情变化情况,分为进展组(n=45)和...目的 探讨血清α-突触核蛋白(α-synuclein,α-syn)、沉默调节蛋白1(Sirtuin-1,SIRT1)水平与进展性脑梗死患者神经功能、梗死体积及预后的相关性。方法 回顾性分析100例急性脑梗死病例资料。根据脑梗死病情变化情况,分为进展组(n=45)和非进展组(n=55)。依据入院时美国国立卫生研究院卒中量表(national institute of health stroke scale,NIHSS)评分、梗死体积及预后,对进展组病例进一步亚分组。比较不同神经功能缺损程度、梗死体积和预后结局,进展组病例血清α-syn、SIRT1水平差异及相关性,采用受试者工作特征(receiver operating characteristic,ROC)曲线分析α-syn、SIRT1对进展性脑梗死的诊断及预后预测价值。结果 进展组血清α-syn水平高于非进展组,SIRT1低于非进展组(均P<0.05)。SIRT1与α-syn联合预测进展性脑梗死的ROC曲线下面积(area under curve,AUC)为0.911(0.849~0.973),敏感度和特异度分别为84.38%和82.33%。随着神经功能缺损程度加重,进展性脑梗死患者血清α-syn水平呈现逐渐升高趋势,而SIRT1不断降低(P<0.05)。随着梗死体积增加,进展性脑梗死患者血清α-syn水平不断升高,而SIRT1表现为降低趋势(P<0.05)。与预后良好组比较,预后不良组血清SIRT1水平较低,α-syn水平偏高(P<0.05)。血清α-syn水平与进展性脑梗死患者神经功能缺损程度、梗死体积及预后不良均呈正相关(r=0.713、0.821、0.739,P<0.05)。血清SIRT1水平与进展性脑梗死患者神经功能缺损程度、梗死体积及预后不良均呈负相关(r=-0.694、-0.773,-0.633,P<0.05)。SIRT1与α-syn联合检测预测进展性脑梗死患者预后不良AUC为0.887(0.812~0.963),敏感度87.64%、特异度77.63%。结论 联合检测α-syn与SIRT1水平对预测脑梗死进展情况及预后不良具有较高价值,可为临床提供指导。展开更多
Angiotensin II (Ang II) is the main mediator of the Renin-Angiotensin-System acting on AT<sub>1</sub> and other AT receptors. It is regarded as a pleiotropic agent that induces many actions, including func...Angiotensin II (Ang II) is the main mediator of the Renin-Angiotensin-System acting on AT<sub>1</sub> and other AT receptors. It is regarded as a pleiotropic agent that induces many actions, including functioning as a growth factor, and as a contractile hormone, among others. The aim of this work was to examine the impact of Ang II on the expression and function of α<sub>1</sub>-adrenergic receptors (α<sub>1</sub>-ARs) in cultured rat aorta, and aorta-derived smooth muscle cells. Isolated Wistar rat aorta was incubated for 24 h in DMEM at 37˚C, then subjected to isometric tension and to the action of added norepinephrine, in concentration-response curves. Ang II was added (1 × 10<sup>−5</sup> M), and in some experiments, 5-Methylurapidil (α<sub>1A</sub>-AR antagonist), AH11110A (α<sub>1B</sub>-AR antagonist), or BMY-7378 (α<sub>1D</sub>-AR antagonist), were used to identify the α<sub>1</sub>-AR involved in the response. Desensitization of the contractile response to norepinephrine was observed due to incubation time, and by the Ang II action. α<sub>1D</sub>-AR was protected from desensitization by BMY-7378;while RS-100329 and prazosin partially mitigated desensitization. In another set of experiments, isolated aorta-derived smooth muscle cells were exposed to Ang II and α<sub>1</sub>-ARs proteins were evaluated. α<sub>1D</sub>-AR increased at 30 and 60 min post Ang II exposure, the α<sub>1A</sub>-AR diminished from 1 to 4 h, while α<sub>1B</sub>-AR remained unchanged over 24 h of Ang II exposure. Ang II induced an increase of α<sub>1D</sub>-AR at short times, and BMY-7378 protected α<sub>1D</sub>-AR from desensitization.展开更多
文摘目的:探讨子痫前期(PE)患者血清和胎盘中的肿瘤坏死因子-α(TNF-α)、基质金属蛋白酶-1(MMP-1)、基质金属蛋白酶-7(MMP-7)的表达水平。方法:选取2021年11月—2023年8月扬州大学临床医学院妇产科收治的86例PE患者,分为早发型PE(n=33)和晚发型PE(n=53),另外选取健康孕妇(n=45)作为对照。检测所有纳入患者血清及胎盘组织中的TNF-α、MMP-1和MMP-7水平。结果:早发型PE患者(34.71±1.35周vs 40.43±0.70周)及晚发型PE患者(38.43±0.60周vs 40.43±0.70周)的孕周明显小于对照组(均P<0.05);早发型PE患者血清中TNF-α(507.92±28.99 ng/L vs 478.50±41.15 ng/L)、MMP-1(1156.67±158.07μg/L vs 1037.59±163.10μg/L)和MMP-7(211.00±18.64μg/L vs 196.32±19.87μg/L)的表达较晚发型PE患者显著增加(均P<0.05),晚发型PE患者血清中TNF-α(478.50±41.15 ng/L vs 446.90±41.52 ng/L)、MMP-1(1037.59±163.10μg/L vs 840.78±174.43μg/L)和MMP-7(196.32±19.87μg/L vs 166.01±15.09μg/L)的表达较对照组显著增加(均P<0.05);免疫组化结果显示,早发型PE患者胎盘组织中TNF-α、MMP-1和MMP-7表达水平较晚发型PE及对照组明显升高(均P<0.05)。结论:早发型PE患者及晚发型PE患者的TNF-α、MMP-1和MMP-7表达明显增加,这可能在PE的发生发展中起到重要作用。
文摘目的 探讨血清α-突触核蛋白(α-synuclein,α-syn)、沉默调节蛋白1(Sirtuin-1,SIRT1)水平与进展性脑梗死患者神经功能、梗死体积及预后的相关性。方法 回顾性分析100例急性脑梗死病例资料。根据脑梗死病情变化情况,分为进展组(n=45)和非进展组(n=55)。依据入院时美国国立卫生研究院卒中量表(national institute of health stroke scale,NIHSS)评分、梗死体积及预后,对进展组病例进一步亚分组。比较不同神经功能缺损程度、梗死体积和预后结局,进展组病例血清α-syn、SIRT1水平差异及相关性,采用受试者工作特征(receiver operating characteristic,ROC)曲线分析α-syn、SIRT1对进展性脑梗死的诊断及预后预测价值。结果 进展组血清α-syn水平高于非进展组,SIRT1低于非进展组(均P<0.05)。SIRT1与α-syn联合预测进展性脑梗死的ROC曲线下面积(area under curve,AUC)为0.911(0.849~0.973),敏感度和特异度分别为84.38%和82.33%。随着神经功能缺损程度加重,进展性脑梗死患者血清α-syn水平呈现逐渐升高趋势,而SIRT1不断降低(P<0.05)。随着梗死体积增加,进展性脑梗死患者血清α-syn水平不断升高,而SIRT1表现为降低趋势(P<0.05)。与预后良好组比较,预后不良组血清SIRT1水平较低,α-syn水平偏高(P<0.05)。血清α-syn水平与进展性脑梗死患者神经功能缺损程度、梗死体积及预后不良均呈正相关(r=0.713、0.821、0.739,P<0.05)。血清SIRT1水平与进展性脑梗死患者神经功能缺损程度、梗死体积及预后不良均呈负相关(r=-0.694、-0.773,-0.633,P<0.05)。SIRT1与α-syn联合检测预测进展性脑梗死患者预后不良AUC为0.887(0.812~0.963),敏感度87.64%、特异度77.63%。结论 联合检测α-syn与SIRT1水平对预测脑梗死进展情况及预后不良具有较高价值,可为临床提供指导。
文摘Angiotensin II (Ang II) is the main mediator of the Renin-Angiotensin-System acting on AT<sub>1</sub> and other AT receptors. It is regarded as a pleiotropic agent that induces many actions, including functioning as a growth factor, and as a contractile hormone, among others. The aim of this work was to examine the impact of Ang II on the expression and function of α<sub>1</sub>-adrenergic receptors (α<sub>1</sub>-ARs) in cultured rat aorta, and aorta-derived smooth muscle cells. Isolated Wistar rat aorta was incubated for 24 h in DMEM at 37˚C, then subjected to isometric tension and to the action of added norepinephrine, in concentration-response curves. Ang II was added (1 × 10<sup>−5</sup> M), and in some experiments, 5-Methylurapidil (α<sub>1A</sub>-AR antagonist), AH11110A (α<sub>1B</sub>-AR antagonist), or BMY-7378 (α<sub>1D</sub>-AR antagonist), were used to identify the α<sub>1</sub>-AR involved in the response. Desensitization of the contractile response to norepinephrine was observed due to incubation time, and by the Ang II action. α<sub>1D</sub>-AR was protected from desensitization by BMY-7378;while RS-100329 and prazosin partially mitigated desensitization. In another set of experiments, isolated aorta-derived smooth muscle cells were exposed to Ang II and α<sub>1</sub>-ARs proteins were evaluated. α<sub>1D</sub>-AR increased at 30 and 60 min post Ang II exposure, the α<sub>1A</sub>-AR diminished from 1 to 4 h, while α<sub>1B</sub>-AR remained unchanged over 24 h of Ang II exposure. Ang II induced an increase of α<sub>1D</sub>-AR at short times, and BMY-7378 protected α<sub>1D</sub>-AR from desensitization.
