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1.
目的:观察心衰患者血清IRISIN水平变化规律,研究Irisin对心衰诊疗的临床价值。方法:连续收集西京医院心内科住院的心衰患者132例,根据NYHA心功能分级将患者分为三组,其中心功能Ⅱ级48例,Ⅲ级44例,Ⅳ级40例,同时选取心功能正常(左室射血分数LVEF50%)的30例健康体检者为对照组。采用酶联免疫吸附试验(ELISA)检测患者血清中Irisin水平,根据Irisin水平分为低Irisin组和高Irisin组,比较两组间心衰的发生率,分析Irisin水平与心衰的关系。结果:①心衰组Irisin水平显著低于心功能正常组(6790±3628 ng/mL vs 12691±2272 ng/mL,P0.01),且从Ⅱ级到Ⅳ级,逐渐降低;②心衰组LVEF值显著低于心功能正常组(45.7±8 vs 59.7±4.3,P0.01),且从Ⅱ级到Ⅳ级,逐渐降低;③心衰组N末端B型利钠肽原(ProBNP)水平显著高于心功能正常组(2938±2795 pg/mL vs 184±151 pg/mL,P0.01),且从Ⅱ级到Ⅳ级,逐渐升高;④低Irisin组心衰发生率明显高于高Irisin组(92.6%vs47.5%,P0.01);⑤单因素相关分析显示:血清Irisin水平与左室射血分数呈正相关(r=0.694,P0.05),与proBNP呈负相关(r=-0.45,P0.05);结论:心衰患者血清Irisin水平降低,而且随着心功能的恶化显著降低,心衰患者血清Irisin水平与心衰程度有一定的相关性。  相似文献   
2.
摘要 目的:探讨鸢尾素对心肌梗死后大鼠心房颤动和心房间质纤维化的影响。方法:通过结扎左前降支冠状动脉(LADCA)建立急性心肌梗死(MI)大鼠模型,大鼠每天腹腔注射100 μg/kg的鸢尾素1次,共治疗4周。通过超声心动图检查左室舒张末期直径(LVEDD)、左室收缩末期直径(LVESD)、左室射血分数(LVEF)、左室缩短分数(LVFS)。应用苏木精-伊红(HE)染色和Masson三色染色评估大鼠心肌形态和纤维化情况。蛋白质印迹分析检测TGF-β1、Smad2、p-Smad2、Smad3、p-Smad3、MMP9、TIMP-1、collagenⅠ、collagenⅢ、NLRP3、Caspase 1和IL-1β的表达。结果:与模型组相比,鸢尾素组大鼠的LVEF和LVFS升高,而LVEDD和LVESD降低(P<0.05);房颤诱发率和房颤持续时间显著降低(P<0.05);心肌形态明显改善,纤维化面积显著降低(P<0.05);TGFβ1、p-Smad2/3、collagenⅠ、collagenⅢ和MMP9的蛋白表达水平显著降低,TIMP1的蛋白表达水平显著升高(P<0.05);NLRP3炎性体、cleaved-caspase-1和IL-1β的表达水平显著降低(P<0.05)。结论:鸢尾素可显著改善心肌梗死动物模型的心脏功能,抑制心肌纤维化和房颤形成,具有较高的临床应用前景。  相似文献   
3.
The main objective of the study has been to show whether carnosine has positive effects on liver and lung tissues of rats exposed to a range of formaldehyde concentrations, and to explore how irisin expression and antioxidant capacity are altered in these tissues by carnosine supplementation. Sprague-Dawley type male rats were divided into 8 groups with 6 animals in each: (I) Control; no chemical supplementation); (II) sham (100 mg/kg/day carnosine); (III) low dose formaldehyde (LDFA) for 5 days/week; (IV) LDFA for 5 days/week and carnosine); (V) moderate dose formaldehyde (MDFA) for 5 days/week); (VI) MDFA for 5 days/week and carnosine; (VII) high dose formaldehyde (HDFA) for 5 days/week; (VIII) and HDFA for 5 days/week and carnosine. Sham and control groups were exposed to normal air. Irisin levels of the serum, liver and lung tissue supernatants were analyzed by ELISA, while the REL method was used to determine total oxidant/antioxidant capacity. Irisin production by the tissues was detected immunohistochemically. Increasing doses of FA decreased serum/tissue irisin and total antioxidant levels relative to the controls, as also to increases in TUNEL expressions, total oxidant level, oxidant and apoptosis index. Irisin expression was detected in hepatocyte and sinusoidal cells of the liver and parenchymal cells of the lung. In conclusion, while FA exposure reduces irisin and total oxidant in the serum, liver and lung tissues in a dose-dependent manner and increases the total antioxidant capacity, carnosine supplementation reduces the oxidative stress and restores the histopathological and biochemical signs.  相似文献   
4.
Irisin converts white adipose tissue (WAT) into brown adipose tissue (BAT), as regulated by energy expenditure. The relationship between irisin concentrations after exercise in rats compared humans after exercise remains controversial. We therefore: (1) measured irisin expression in cardiac and skeletal muscle, liver, kidney, peripheral nerve sheath and skin tissues, as also serum irisin level in 10 week-old rats without exercise, and (2) measured tissue supernatant irisin levels in cardiac and skeletal muscle, and in response to exercise in young and old rats to establishing which tissues produced most irisin. Young (12 months) and old rats (24 months) with or without 10 min exercise (water floating) and healthy 10 week-old Sprague-Dawley rats without exercise were used. Irisin was absent from sections of skeletal muscle of unexercised rats, the only part being stained being the perimysium. In contrast, cardiac muscle tissue, peripheral myelin sheath, liver, kidneys, and skin dermis and hypodermis were strongly immunoreactivity. No irisin was seen in skeletal muscle of unexercised young and old rats, but a slight amount was detected after exercise. Strong immunoreactivity occurred in cardiac muscle of young and old rats with or without exercise, notably in pericardial connective tissue. Serum irisin increased after exercise, being higher in younger than older rats. Irisin in tissue supernatants (cardiac and skeletal muscle) was high with or without exercise. High supernatant irisin could come from connective tissues around skeletal muscle, especially nerve sheaths located within it. Skeletal muscle is probably not a main irisin source.  相似文献   
5.
常规适量运动与合理营养是健康的基石,是健康生活方式与防病治病的核心内容。本文从运动和营养的健康效应机制、线粒体营养素作用与机制等简要综述了相关研究进展。  相似文献   
6.
摘要 目的:分析血浆鸢尾素、生长分化因子-8在老年肌肉减少症患者中的表达及其诊断价值。方法:选择2020年4月至2022年4月在我院接受体检的620例老年体检者作为研究对象,其中238例肌肉减少症者作为观察组,382例非肌肉减少症者作为对照组。检测两组血浆鸢尾素、生长分化因子-8表达水平,观察血浆鸢尾素、生长分化因子-8在不同严重程度的老年肌肉减少症患者中差异性,使用Pearson相关性分析血浆鸢尾素、生长分化因子-8与全身骨骼肌质量、四肢骨骼肌质量、相对骨骼肌指数、握力和步速的关系,通过ROC下面积(AUC)评价血浆鸢尾素、生长分化因子-8对老年肌肉减少症的诊断效能。结果:观察组血浆鸢尾素表达水平低于对照组,生长分化因子-8表达水平高于对照组(P<0.05);肌肉减少症前期、肌肉减少症期、重度肌肉减少症期的患者血浆鸢尾素表达水平依次降低,生长分化因子-8表达水平依次升高(P<0.05);经Pearson相关性分析,老年肌肉减少症患者全身骨骼肌质量、四肢骨骼肌质量、相对骨骼肌指数、握力和步速均与子鸢尾素呈正相关(P<0.05),与生长分化因子-8呈负相关(P<0.05);经ROC曲线分析,血浆鸢尾素、生长分化因子-8诊断老年肌肉减少症的敏感度为78.49 %,特异度为90.67 %,AUC为0.914。结论:老年肌肉减少症患者血浆鸢尾素表达明显下调、生长分化因子-8表达明显上调,两者与病情严重程度密切相关,联合诊断此病的效能较好,值得临床予以重视应用。  相似文献   
7.
This study investigated the regulation of thermogenic capacity in classical brown adipose tissue (BAT) and subcutaneous inguinal (SC Ing) white adipose tissue (WAT) and how it affects whole-body energy expenditure in sedentary and endurance-trained rats fed ad libitum either low fat or high fat (HF) diets. Analysis of tissue mass, PGC-1α and UCP-1 content, the presence of multilocular adipocytes, and palmitate oxidation revealed that a HF diet increased the thermogenic capacity of the interscapular and aortic brown adipose tissues, whereas exercise markedly suppressed it. Conversely, exercise induced browning of the SC Ing WAT. This effect was attenuated by a HF diet. Endurance training neither affected skeletal muscle FNDC5 content nor circulating irisin, but it increased FNDC5 content in SC Ing WAT. This suggests that locally produced FNDC5 rather than circulating irisin mediated the exercise-induced browning effect on this fat tissue. Importantly, despite reducing the thermogenic capacity of classical BAT, exercise increased whole-body energy expenditure during the dark cycle. Therefore, browning of subcutaneous WAT likely exerted a compensatory effect and raised whole-body energy expenditure in endurance-trained rats. Based on these novel findings, we propose that exercise-induced browning of the subcutaneous WAT provides an alternative mechanism that reduces thermogenic capacity in core areas and increases it in peripheral body regions. This could allow the organism to adjust its metabolic rate to accommodate diet-induced thermogenesis while simultaneously coping with the stress of chronically increased heat production through exercise.  相似文献   
8.
Irisin, an exercise-induced myokine, induces conversion of white into brown adipocytes, promoting mitochondrial biogenesis and energy expenditure. Irisin has a vascular protective effect on endothelial function in animals, including humans. Defects in irisin signaling pathways result in endothelial dysfunction in obesity and diabetes. However, the mechanisms underlying the effects of irisin on endothelial function have not been elucidated. Transient receptor potential vanilloid subtype 4 (TRPV4) channels are one of the most important Ca2+-permeable cation channels in vascular endothelial cells. In this study, we hypothesized that irisin may induce endothelium-dependent vasodilation by activating Ca2+ influx into endothelial cells via TRPV4 channels. In primary cultured rat mesenteric artery endothelial cells, irisin caused an increase in [Ca2+]i due to extracellular Ca2+ influx rather than release from Ca2+ stores. Moreover, irisin-induced increases in [Ca2+]i were completely abolished by a TRPV4 inhibitor. In addition, irisin induced endothelium-dependent vasodilation of rat mesenteric arteries. However, irisin had no effect on endothelium-independent vasodilation. Furthermore, irisin-induced vasodilation was fully abolished in the presence of a TRPV4 inhibitor, indicating the involvement of TRPV4 channels in endothelium-dependent vasodilation. This study provides the first evidence that irisin-induced endothelium-dependent vasodilation is related to the stimulation of extracellular Ca2+ influx via TRPV4 channels in rat mesenteric arteries.  相似文献   
9.
Beige adipose cells are a distinct and inducible type of thermogenic fat cell that express the mitochondrial uncoupling protein-1 and thus represent a powerful target for treating obesity. Mice lacking the TGF-β effector protein SMAD3 are protected against diet-induced obesity because of browning of their white adipose tissue (WAT), leading to increased whole body energy expenditure. However, the role SMAD3 plays in WAT browning is not clearly understood. Irisin is an exercise-induced skeletal muscle hormone that induces WAT browning similar to that observed in SMAD3-deficient mice. Together, these observations suggested that SMAD3 may negatively regulate irisin production and/or secretion from skeletal muscle. To address this question, we used wild-type and SMAD3 knock-out (Smad3−/−) mice subjected to an exercise regime and C2C12 myotubes treated with TGF-β, a TGF-β receptor 1 pharmacological inhibitor, adenovirus expressing constitutively active SMAD3, or siRNA against SMAD3. We find that in Smad3−/− mice, exercise increases serum irisin and skeletal muscle FNDC5 (irisin precursor) and its upstream activator peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) to a greater extent than in wild-type mice. In C2C12 myotubes, TGF-β suppresses FNDC5 and PGC-1α mRNA and protein levels via SMAD3 and promotes SMAD3 binding to the FNDC5 and PGC-1α promoters. These data establish that SMAD3 suppresses FNDC5 and PGC-1α in skeletal muscle cells. These findings shed light on the poorly understood regulation of irisin/FNDC5 by demonstrating a novel association between irisin and SMAD3 signaling in skeletal muscle.  相似文献   
10.
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