目的检测慢性脑低灌注性血管性认知损害(CCH-VCI)患者血清p75神经营养素受体细胞外段(p75NTR-ECD)水平,并探讨其与肿瘤坏死因子α(TNF-α)、白细胞介素(IL)-1β、IL-6的关系。方法选择海军军医大学(第二军医大学)长海医院2018年8月至12...目的检测慢性脑低灌注性血管性认知损害(CCH-VCI)患者血清p75神经营养素受体细胞外段(p75NTR-ECD)水平,并探讨其与肿瘤坏死因子α(TNF-α)、白细胞介素(IL)-1β、IL-6的关系。方法选择海军军医大学(第二军医大学)长海医院2018年8月至12月收治的34例CCH-VCI患者,以及同期相同年龄段的36名中老年健康人和34例缺血性脑卒中患者作为研究对象。采用酶联免疫吸附试验测定3组研究对象的血清p75NTR-ECD、TNF-α、IL-1β、IL-6水平并进行组间比较。采用Spearman相关分析研究CCH-VCI患者血清p75NTR-ECD水平与TNF-α、IL-1β、IL-6水平的相关性。结果CCH-VCI组血清p75NTR-ECD水平高于健康对照组和缺血性脑卒中组[(544.36(440.88,628.50)pg/mL vs 276.49(262.59,313.87)pg/mL、366.87(337.09,450.43)pg/mL],差异均有统计学意义(U=87.500、335.500,P均<0.05)。CCH-VCI组患者血清TNF-α、IL-1β、IL-6水平分别为196.02(141.20,280.35)pg/mL、68.23(60.79,91.94)pg/mL、51.04(40.24,65.26)pg/mL,缺血性脑卒中组分别为218.67(143.76,281.28)pg/mL、76.87(59.10,99.91)pg/mL、64.45(43.13,86.76)pg/mL,均分别高于健康对照组[分别为73.71(56.94,79.81)pg/mL、42.98(34.52,51.34)pg/mL、14.97(11.76,21.19)pg/mL],差异均有统计学意义(U=31.000、4.000,106.000、132.000,48.000、13.000;P均<0.05)。CCH-VCI患者血清p75NTR-ECD水平与TNF-α水平存在相关性(r=0.391,P=0.022),但与IL-1β和IL-6水平均无明显相关性(r=0.032、0.164,P=0.855、0.355)。结论慢性脑低灌注损伤后p75NTR可能与TNF-α等炎性因子有关,并共同参与了CCH-VCI的发病。展开更多
Background Preeclampsia is a serious disorder of pregnancy characterized by h ypertension, proteinuria, edema, and coagulation and vascular abnormalities. At the cellular level, abnormalities include increased calcium...Background Preeclampsia is a serious disorder of pregnancy characterized by h ypertension, proteinuria, edema, and coagulation and vascular abnormalities. At the cellular level, abnormalities include increased calcium concentration in pla telets, lymphocytes, and erythrocytes. Recent studies have shown that antibodies directed against angiotensin II type I (AT1) receptors are also highly associat ed with preeclampsia. Methods and Results We tested the hypothesis that AT1 rec eptor agonistic antibodies(AT1 AAs) could activate AT1 receptors, leading to a n increased intracellular concentration of free calcium and to downstream activa tion of Ca2+signaling pathways. Sera of 30 pregnant patients, 16 diagnosed with severe preeclampsia and 14 normotensive, were examined for the presence of IgG capable of stimulating intracellular Ca2+mobilization. IgG from all preeclampti c patients activated AT1 receptors and increased intracellular free calcium. In contrast, none of the normotensive individuals had IgG capable of activating AT1 receptors. The specific mobilization of intracellular Ca2+by AT1 AAs was bloc ked by losartan, an AT1 receptor antagonist, and by a 7 amino acid peptide tha t corresponds to a portion of the second extracellular loop of the AT1 receptor. In addition, we have shown that AT1 AA stimulated mobilization of intracellul ar Ca2+results in the activation of the transcription factor, nuclear factor of activated T cells. Conclusions These results suggest that maternal antibodies capable of activating AT1 receptors are likely to account for increased intracel lular free Ca2+concentrations and changes in gene expression associated with pr eeclampsia.展开更多
文摘目的检测慢性脑低灌注性血管性认知损害(CCH-VCI)患者血清p75神经营养素受体细胞外段(p75NTR-ECD)水平,并探讨其与肿瘤坏死因子α(TNF-α)、白细胞介素(IL)-1β、IL-6的关系。方法选择海军军医大学(第二军医大学)长海医院2018年8月至12月收治的34例CCH-VCI患者,以及同期相同年龄段的36名中老年健康人和34例缺血性脑卒中患者作为研究对象。采用酶联免疫吸附试验测定3组研究对象的血清p75NTR-ECD、TNF-α、IL-1β、IL-6水平并进行组间比较。采用Spearman相关分析研究CCH-VCI患者血清p75NTR-ECD水平与TNF-α、IL-1β、IL-6水平的相关性。结果CCH-VCI组血清p75NTR-ECD水平高于健康对照组和缺血性脑卒中组[(544.36(440.88,628.50)pg/mL vs 276.49(262.59,313.87)pg/mL、366.87(337.09,450.43)pg/mL],差异均有统计学意义(U=87.500、335.500,P均<0.05)。CCH-VCI组患者血清TNF-α、IL-1β、IL-6水平分别为196.02(141.20,280.35)pg/mL、68.23(60.79,91.94)pg/mL、51.04(40.24,65.26)pg/mL,缺血性脑卒中组分别为218.67(143.76,281.28)pg/mL、76.87(59.10,99.91)pg/mL、64.45(43.13,86.76)pg/mL,均分别高于健康对照组[分别为73.71(56.94,79.81)pg/mL、42.98(34.52,51.34)pg/mL、14.97(11.76,21.19)pg/mL],差异均有统计学意义(U=31.000、4.000,106.000、132.000,48.000、13.000;P均<0.05)。CCH-VCI患者血清p75NTR-ECD水平与TNF-α水平存在相关性(r=0.391,P=0.022),但与IL-1β和IL-6水平均无明显相关性(r=0.032、0.164,P=0.855、0.355)。结论慢性脑低灌注损伤后p75NTR可能与TNF-α等炎性因子有关,并共同参与了CCH-VCI的发病。
文摘Background Preeclampsia is a serious disorder of pregnancy characterized by h ypertension, proteinuria, edema, and coagulation and vascular abnormalities. At the cellular level, abnormalities include increased calcium concentration in pla telets, lymphocytes, and erythrocytes. Recent studies have shown that antibodies directed against angiotensin II type I (AT1) receptors are also highly associat ed with preeclampsia. Methods and Results We tested the hypothesis that AT1 rec eptor agonistic antibodies(AT1 AAs) could activate AT1 receptors, leading to a n increased intracellular concentration of free calcium and to downstream activa tion of Ca2+signaling pathways. Sera of 30 pregnant patients, 16 diagnosed with severe preeclampsia and 14 normotensive, were examined for the presence of IgG capable of stimulating intracellular Ca2+mobilization. IgG from all preeclampti c patients activated AT1 receptors and increased intracellular free calcium. In contrast, none of the normotensive individuals had IgG capable of activating AT1 receptors. The specific mobilization of intracellular Ca2+by AT1 AAs was bloc ked by losartan, an AT1 receptor antagonist, and by a 7 amino acid peptide tha t corresponds to a portion of the second extracellular loop of the AT1 receptor. In addition, we have shown that AT1 AA stimulated mobilization of intracellul ar Ca2+results in the activation of the transcription factor, nuclear factor of activated T cells. Conclusions These results suggest that maternal antibodies capable of activating AT1 receptors are likely to account for increased intracel lular free Ca2+concentrations and changes in gene expression associated with pr eeclampsia.
