运动对胰岛素抵抗大鼠脂肪组织氧化应激及炎症的影响

目的 观察运动对胰岛素抵抗(Insulin Resistance IR)大鼠脂肪组织SOD活性,MDA及TNF-α含量的影响,探讨运动对IR改善的机制.方法 22只雄性SD大鼠随机分为空白对照组6只(CG)、胰岛素抵抗组(IRG)和胰岛素抵抗运动组(EIRG)各8只,采用高脂饲料诱导IR动物模型,EIRG大鼠进行为期10周游泳训练,测定各组大鼠脂肪组织中SOD活性,MDA及TNF-α含量.结果 采用高脂饲料诱导IR模型成功,运动干预后与CG比较,IRG大鼠脂肪组织MDA和TNF-α水平显著升高(P<0.05);与IRG比较,EIRG脂肪组织SOD活性显著提高(P<0.05),MDA和TNF-α水平显著降低(P<0.05);IR指数与MDA,IR指数与TNF-α,MDA与TNF-α均成正相关(r:0.430,P:0.01;r:0.475,P:0.025;r:0.432.P:0.045).结论 运动对大鼠IR的改善机制可能是通过运动上调脂肪组织抗氧化酶活性,进而降低炎性脂肪因子表达实现的.     

Exercise and inflammation in coronary artery disease: A systematic review and meta-analysis of randomised trials

ABSTRACT

Current evidence suggests that chronic inflammation contributes to the development of coronary artery disease (CAD). Interestingly, exercise may constitute a method of reducing inflammation in this patient population. As such, this systematic review and meta-analysis examined the evidence generated by randomised studies that investigated the effect of exercise on inflammatory biomarkers in CAD. Literature was sought from various sources. Outcomes were pooled in a random-effects model to calculate standardised mean differences (SMD) with 95% confidence intervals (CI). Twenty-five studies were reviewed; post-intervention C-reactive protein (SMD: ?0.55 (95% CI: ?0.93, ?0.16), P = 0.005), fibrinogen (SMD: ?0.52 (95% CI: ?0.74, ?0.29, P = <0.00001)), and von Willebrand factor (SMD: ?1.57 (95% CI: ?2.23, ?0.92), P = <0.00001) values were significantly lower in exercise groups compared to controls. In addition, qualitative analyses identified evidence that supports a beneficial effect of exercise on these acute-phase reactants. However, the impact of exercise on anti–inflammatory cytokines, adhesion molecules, and chemokines is equivocal, which may be attributed to a paucity of research. Nevertheless, the findings of this review suggest that exercise induces an anti–inflammatory effect in CAD patients. Although, the quality of evidence needs to be improved by further randomised studies with high methodological qualities and large sample sizes.     

GSK3在抑郁症发病机制中的研究进展

尽管锂制剂在临床上使用了几十年,但其确切机制并不清楚。人们通过研究认识到锂可能是通过抑制糖原合成酶激酶3（glycogen synthase kinase 3,GSK3）而发挥抗抑郁作用的。锂可以调控GSK3下游的许多分子,许多抗抑郁类药物可以调控GSK3的信号。使用药理方法或基因沉默方法抑制GSK3均具有稳定情绪、抵抗抑郁的作用,这些研究表明GSK3可能是抗抑郁的潜在靶点。近些年来对GSK3在神经生物学中的作用机制的研究进一步证实了锂可能是通过作用于GSK3来达到治疗目的的。如GSK3可以调节生物体应激反应、炎症反应、神经发生、5-羟色胺（5-hydroxytryptamin,5-HT）传递过程,并参与生物周期节律的调控。因此,特异的GSK3抑制剂能否在临床上发挥抗抑郁作用有待进一步研究。该文对GSK3在应激反应、炎症反应、神经发生、5-HT传递过程以及生物周期节律这五个方面对抑郁发病机制的研究进行了综述。     

Visceral and somatic hypersensitivity,autonomic cardiovascular dysfunction and low-grade inflammation in a subset of irritable bowel syndrome patients

The pathophysiology of irritable bowel syndrome (IBS) is complex and not fully understood, so the aim of this study was to evaluate whether visceral and somatic hypersensitivity, autonomic cardiovascular dysfunction, and low-grade inflammation of the gut wall are associated with diarrhea-predominant IBS (D-IBS). Sixty-two patients with D-IBS and 20 control subjects participated in the study. Using the ascending method of limits (AML) protocol, we demonstrated that D-IBS patients had significantly lower sensory thresholds compared with healthy controls (P<0.001). Using diverse methods, especially the ischemic sensitivity test, for the first time in China, we confirmed that D-IBS patients have somatic hypersensitivity. They had a significantly higher systolic blood pressure and heart rate after a cold stimulus, indicative of autonomic cardiovascular dysfunction. Compared with the control group, D-IBS patients had a significantly higher level of calprotectin (P<0.001). We also found significant correlations between visceral and somatic hypersensitivity, visceral hypersensitivity and autonomic cardiovascular dysfunction, and somatic hypersensitivity and autonomic cardiovascular dysfunction. Our findings may provide valuable suggestions for the treatment of D-IBS.     

2014年“第61届美国运动医学会年会”专栏：慢性持续性低度炎症与运动、健康和疾病的研究进展

摘要：背景：研究表明慢性低度炎症在多数非传染性疾病的发病中起着关键作用,2014年ACSM年会把炎症在运动、健康和疾病中的作用作为热点专题。目的：探讨运动、营养、衰老、脂肪和骨骼肌与慢性炎症的关联。方法：分析归纳目前本方向年会的热点研究结果及进展。结果与结论：1.衰老及不良生活方式是慢性低度炎症的重要致炎因素;2.急性运动可促进产生炎症因子,规律运动可以减低炎性标志物;3.运动能降低骨骼肌慢性炎症;4.运动能降低脂肪组织的慢性炎症; 5.规律运动是降低年龄相关的慢性炎症反应的一种手段;6.营养补给对急性运动诱导的炎性反应的干预效果有待进一步研究。本年会的研究表明运动的抗炎作用可能是其降低慢性低度炎性疾病发生的重要机制。     

Serum macrophage migration inhibitory factor as a potential biomarker to evaluate therapeutic response in patients with allergic asthma: an exploratory study

Background: Previous studies have shown that macrophage migration inhibitory factor(MIF) is involved in the pathogenesis of asthma. This study aimed to investigate whether serum MIF reflects a therapeutic response in allergic asthma.Methods: We enrolled 30 asthmatic patients with mild-to-moderate exacerbations and 20 healthy controls, analyzing the parameter levels of serum MIF, serum total immunoglobulin E(tIgE), peripheral blood eosinophil percentage(EOS%), and fractional exhaled nitric oxide(FeNO). Lung function indices were used to identify disease severity and therapeutic response.Results: Our study showed that all measured parameters in patients were at higher levels than those of controls. After one week of treatment, most parameter levels decreased significantly except for serum tIgE. Furthermore, we found that serum MIF positively correlated with EOS% as well as FeNO, but negatively correlated with lung function indices. Receiver operator characteristic(ROC) curve analysis indicated that among the parameters, serum MIF exhibited a higher capacity to evaluate therapeutic response. The area under the curve(AUC) of MIF was 0.931, with a sensitivity of 0.967 and a specificity of 0.800.Conclusions: Our results suggested that serum MIF may serve as a potential biomarker for evaluating therapeutic response in allergic asthma with mild-to-moderate exacerbations.     

中药热奄包治疗慢性盆腔炎的护理体会

目的:总结中药热奄包治疗慢性盆腔炎的护理体会。方法:将加有跌打酊蒸热后的中药热奄包对慢性盆腔炎患者进行治疗,每次30分钟,每天一次,一个疗程10次,连续2个疗程后,观察疗效。结果:治疗组总有效率达83.4%,与对照组总有效率比较,P0.05。结论:中药热奄包治疗慢性盆腔炎,疗效确切,简单方便,患者无痛苦。     

他汀类药物的调脂外作用

他汀类药物是一类主要降低血脂的药物,临床已广泛应用于多种心血管疾病的治疗。近期研究发现其除具有调节血脂作用外,还有较为重要的调脂外作用,如抗氧化作用,保护血管内皮细胞,抑制平滑肌细胞的增殖和迁移等,为进一步扩大他汀类药物的临床应用提供了理论和实践依据。     

Mechanisms of beneficial effects of exercise training on non-alcoholic fatty liver disease (NAFLD): Roles of oxidative stress and inflammation

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disorder which is associated with accumulation of fats in the liver. It causes a wide variety of pathological effects such as non-alcoholic steatohepatitis (NASH) and cirrhosis, insulin resistance, obesity, hypertension, dyslipidaemia, diabetes and cardiovascular disease. The molecular mechanisms that cause the initiation and progression of NAFLD are not fully understood. Oxidative stress (OS) induced by reactive oxygen species (ROS) and inflammation are likely a significant mechanism which can lead to hepatic cell death and tissue injury. Mitochondrial abnormalities, down-regulation of several antioxidant enzymes, glutathione (GSH) depletion and decreased activity of GSH-dependent antioxidants, accumulation of leukocytes and hepatic inflammation are the major sources of ROS overproduction in NAFLD. Excessive production of ROS suppresses the capacity of other antioxidant defence systems in NAFLD and causes further oxidative damage. Regular exercise can be considered as an effective strategy for treatment of NAFLD. It improves NAFLD by reducing intrahepatic fat content, increasing β-oxidation of fatty acids, inducing hepato-protective autophagy, overexpressing peroxisome proliferator-activated receptor- γ (PPAR-γ), as well as attenuating hepatocyte apoptosis and increasing insulin sensitivity. Exercise training also suppresses ROS overproduction and OS in NAFLD via up-regulation of several antioxidant enzymes and anti-inflammatory mediators. Therefore, an understanding of these molecules and signalling pathways gives us valuable information about NAFLD progression and a method for developing a suitable clinical treatment. This review aimed to evaluate sources of ROS and OS in NAFLD and the molecular mechanisms involved in the beneficial effects of exercises on NAFLD.     

Effects of sensory-level high-volt pulsed electrical current ondelayed-onset muscle soreness

Abstract

Ten healthy males and ten healthy females aged 21.5 ± 3.2 years (mean ± s) participated in the study, which was designed to evaluate the effectiveness of sensory level-high volt pulsed electrical current (HVPC) on delayed-onset muscle soreness (DOMS). Arm discomfort, elbow extension range of motion and isometric elbow flexion strength were obtained as baseline measurements. Delayed-onset muscle soreness was induced in the participants' dominant or non-dominant arm using two sets of 20 maximal eccentric elbow flexion contractions. After the induction of DOMS, the participants were randomly divided into an experimental condition (HVPC) or a placebo condition. The experimental condition consisted of 20 min of HVPC immediately after the induction of DOMS, and 20 min every 24 h for three consecutive days thereafter. The participants in the placebo condition received an intervention similar in design; however, no electrical current was administered. Baseline measurements were reevaluated at 24, 48, 72 and 96 h after the induction of DOMS. Three weeks later, the participants returned and the protocol was repeated on the contralateral limb, using the opposite intervention (HVPC or placebo). Repeated-measures analysis of variance revealed a significant increase in overall arm discomfort, decrease in elbow extension and decrease in isometric strength for both conditions over time. No significant main effect of treatment, or time-by-treatment interaction, was found for the HVPC condition when compared with the placebo condition for any variable. Sensory-level HVPC, as utilized in our application, was ineffective in reducing the measured variables associated with DOMS.