骨化三醇对佐剂性关节炎模型大鼠血清中TNF-a、IL-4和IL-10的影响

目的:研究骨化三醇对佐剂性关节炎大鼠模型血清中TNF-a、IL-4和IL- 10表达水平的影响,探讨骨化三醇对佐剂性关节炎的治疗作用及相关机制.方法:雌性大鼠45只,随机分为正常对照组,佐剂性关节炎模型组,骨化三醇治疗组,每组15只,2周后,处死全部大鼠,断头取血,检测血清中TNF-a、IL-4和IL- 10表达水平....     

复方碳酸钙片联合骨化三醇对女性绝经后骨质疏松症的疗效观察

目的:观察复方碳酸钙片联合骨化三醇对绝经后骨质疏松症妇女骨密度(BMD)及骨转换指标的影响.方法:采用前瞻性随机对照研究方法,选取年龄55 ～75岁、绝经期＞1年,≥2项骨质疏松性骨折高危因素的女性志愿者116名,随机分为2组.干预组56例,每日给予复方碳酸钙片1片及骨化三醇0.25 μg;对照组60例,维持原有生活方式并定期复查.分别于干预前后测量腰椎及髋部BMD、骨转换指标骨碱性磷酸酶(BALP)及抗酒石酸酸性磷酸酶5b(TRACP5b).结果:干预12个月后,干预组腰椎、股骨颈、大转子及髋部BMD均有明显增加(P＜0.01或0.05);而对照组腰椎、股骨颈及大转子BMD、无明显变化(P＞0.05),髋部BMD增加0.91％(P＜0.05).干预组腰椎及大转子BMD增加优于对照组(P＜0.01),股骨颈及髋部BMD增加无明显差异(P＞0.05).干预组BALP及TRACP5b分别下降23.25％和36.06％(P＜0.01);对照组BALP及TRACP5b无明显变化(P＞0.05).组间比较,干预组抑制骨转换优于对照组(P＜0.01).结论:绝经后女性补充复方碳酸钙片和骨化三醇可抑制骨转换,降低骨转换率,增加腰椎及髋部BMD.     

骨化三醇治疗甲亢性骨质疏松症的临床疗效观察

目的:探讨骨化三醇治疗甲亢性骨质疏松症的临床疗效.方法:以2014年7月~2016年4月笔者参与治疗的72例甲亢性骨质疏松症患者为例,按照双盲法分为两组.对照组(n=36)给予甲状腺药物联合阿仑磷酸钠片治疗,观察组(n=36)在对照组基础上联合使用骨化三醇治疗.治疗结束后,对比两组的疗效.结果:观察组临床总有效率显著优于对照组,两组治疗后症状评分较治疗前均有显著改善,观察组优于对照组,差异有统计学意义(P<0.05).结论:骨化三醇治疗甲亢性骨质疏松症的疗效较好,能帮助患者快速改善临床症状,有助于预后.     

骨化三醇联合钙剂治疗糖尿病伴骨质疏松症患者的效果观察

目的 探讨骨化三醇联合钙剂治疗糖尿病伴骨质疏松症患者的效果.方法 选取2018年10月至2019年10月四川大学华西医院收治的糖尿病伴骨质疏松症患者92例,按照随机数字表法分为对照组与观察组,各46例.对照组在常规干预基础上口服碳酸钙D3片治疗;观察组在对照组基础上口服骨化三醇治疗,2组均治疗8周.比较2组治疗前及治疗...     

骨化三醇在治疗甲亢性骨质疏松症中的临床研究

目的:探讨骨化三醇治疗甲亢性骨质疏松症的临床疗效.方法:选取2016年1月～2017年1月我院收治的甲亢性骨质疏松症患者88例,按照随机数字表法,分为对照组(n=44)和观察组(n=44).对照组采用甲状腺药物联合阿仑膦酸钠片进行治疗,观察组在对照组基础上加用骨化三醇,比较两组治疗效果.结果:经过药物治疗,观察组总有效率为93.18％,高于对照组的81.82％,差异具有统计学意义(P<0.05);观察组症状评分优于对照组,差异具有统计学意义(P<0.05).结论:骨化三醇治疗甲亢性骨质疏松症的临床疗效显著,可使临床症状得以有效改善,值得在临床上推广.     

骨化三醇治疗甲亢性骨质疏松症56例临床分析

目的分析骨化三醇治疗甲亢性骨质疏松症疗效,症状体征、实验室指标变化特点,总结治疗经验。方法选择辽宁省辽阳市中心医院2014年2月至2015年7月,以骨化三醇治疗甲亢性骨质疏松症56例,进行安全性指标、疗效指标监测。结果多数患者典型症状都获得不同程度减轻,但仍较明显症状为甲状腺肿、心悸、烦躁易怒、手指震颤、突眼,腰背疼痛、腰膝酸软完全消失占37.5%;显效率12.5%、有效率58.93%、无效率28.57%;后治疗前心率、FT_3、FT_4低于治疗,TSH、腰椎、左侧髋关节节、左侧前壁骨密度高于治疗前,差异具有统计学意义(P<0.05)。治疗前后TGAb、TPNAb差异无统计学意义(P>0.05);发生不良反应28.57%。结论骨化三醇治疗甲亢性骨质疏松症有助于改善OP相关症状,但整体疗效仍有待提高,治疗后甲亢相关症状仍较明显,需积极治疗甲亢。     

骨化三醇加阿伦膦酸钠治疗骨质疏松症的疗效观察

目的探讨使用骨化三醇加阿伦膦酸钠治疗骨质疏松的临床效果。方法选取2012年6月~2013年6月收治的骨质疏松症患者72例,按随机数字表法分为试验组和对照组,对应随机数字为奇数者作为对照组,偶数者作为试验组,每组患者36例。两组患者均口服钙尔奇D常规治疗,对照组服用阿伦膦酸钠进行治疗,试验组在对照组的基础上加服骨化三醇进行治疗,比较两组治疗前后骨痛症状以及骨密度(BMD),并对疗效进行评价。结果试验组总有效率为94.44%(34/36),对照组总有效率为75.00%(27/36),差异有统计学意义(χ2=5.26,P<0.05)。两组患者的股骨颈和腰椎的骨密度均得到了明显的提高(P<0.05),但试验组的骨密度比对照组提高更为显著(P<0.05)。结论骨三醇加阿伦膦酸钙治疗骨质疏松症的临床疗效要优于单纯使用阿伦膦酸钠的疗效。     

阿法骨化醇与活力钙治疗绝经后骨质疏松症各128例的比较

目的 :观察阿法骨化醇治疗绝经后骨质疏松症的疗效。方法 :绝经后骨质疏松症病人 2 5 6例 ,分成 2组 ,阿法骨化醇组 12 8例 ,年龄 ( 5 7±s7)a ,口服阿法骨化醇片剂 0 .5 μg·d- 1;活力钙组 12 8例 ,年龄 ( 5 6± 7)a ,给予活力钙片 2 0 0mg ,po ,qid ,疗程均为 6mo。观察病人用药后疼痛改善情况 ,计算有效率 ,并测定阿法骨化醇组用药前后骨矿含量和骨代谢生化指标。结果 :阿法骨化醇组总有效率为96.1%,活力钙组总有效率为 69.2 %(P <0 .0 1)。用药 6mo后 ,阿法骨化醇组病人血骨钙素、骨碱性磷酸酶、Ⅰ型前胶原羧基肽均上升 ,尿吡啶酚下降 ,与治疗前相比有非常显著意义 (P <0 .0 1)。骨密度无明显改变。结论 :阿法骨化醇治疗绝经后骨质疏松症具有改善症状、降低骨转换率、纠正骨量丢失的作用。     

骨质疏松症的首选药物——骨化三醇

骨质疏松是以骨量减少、骨的微观结构退化为特征的，致使骨的脆性增加以及易于发生骨折的一种全身性骨骼疾病。表现为腰酸背疼、腿抽筋、驼背、变矮，严重的容易骨折且不易愈合。     

手足口病患儿血清肿瘤坏死因子-α、白介素6和白介素10水平的变化

目的观察手足口病(HFMD)患儿血清肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、白介素-10(IL-10)的变化。方法采用酶联免疫吸附实验(ELISA)抗体夹心法测定15例HFMD患儿(急性期、恢复期)及同期10例健康体检儿童血清TNF-α、IL-6和IL-10的含量,用SPSS软件对所得数值进行统计学分析。结果 HFMD患儿急性期TNF-α、IL-6和IL-10含量均显著高于健康对照组(P<0.05)。恢复期IL-6含量与对照组比较差异无统计学意义(P>0.05),而TNF-α和IL-10水平仍高于健康对照组(P<0.05)。结论 HFMD患儿急性期炎症细胞因子(TNF-α、IL-6、IL-10)水平均显著升高,而抑制性细胞因子IL-10水平和TNF-α水平升高持续到恢复期。     

阿托伐他汀对急性冠脉综合征患者白细胞介素6和肿瘤坏死因子的影响

目的 探讨阿托伐他汀对急性冠脉综合征（ACS）患者血清白细胞介素6（IL-6）及肿瘤坏死因子α（TNF-α）水平变化的影响。方法将ACS患者48例随机分为阿托伐他汀组25例和常规治疗组23例,分别于治疗前及治疗4周后采用放射免疫分析方法行血清IL-6及TNF—α检测。结果ACS患者治疗前血清IL-6、TNF-α水平均明显高于对照组（均P〈0．01）。阿托伐他汀组治疗后血清IL-6（0．67±0．05）μg/L、TNF-μ（65．1±13．2）μg／L水平均明显低于治疗前,但仍高于对照组（均P〈0．05）。常规治疗组患者治疗后血清IL-6（0．74±0．08）μg／L、TNF—±（73．6±12．0）μg／L降低不明显（P〉0．05）。结论IL-6、TNF-α水平升高与ACS发病密切相关,阿托伐他汀可降低ACS患者血IL-6、TNF—α水平,具有减轻病变部位炎性反应和保护内皮细胞的作用。     

吡格列酮对合并代谢综合征的非酒精性脂肪性肝病患者血清TNF-α、IL-6的影响及意义

目的:研究吡格列酮对合并代谢综合征(MS)的非酒精性脂肪性肝病(NAFLD)患者血清肿瘤坏死因子α(TNF-α)和白细胞介素6(IL-6)水平的影响及其意义。方法:连续收集2012年1月-2013年6月在长江航运总医院治疗的合并MS的NAFLD患者。患者分别接受非药物治疗(中等程度热量限制和中等量有氧运动)或吡格列酮(30 mg·d^-1)联合非药物治疗6个月。比较治疗后2组病例的TNF-α、IL-6、NAFLD/MS相关指标和疗效的差异,并分析TNF-α、IL-6与胰岛素抵抗指数(HOMA-IR)、疗效之间的关系。结果:共收集合并MS的HAFLD患者64例,每组各32例。非药物组治疗后6个月仅体重指数和空腹胰岛素显著性降低(P<0.05),吡格列酮联合非药物组治疗后TNF-α、IL-6水平及NAFLD/MS指标均显著改善(P<0.05)。联合治疗组的总有效率显著优于非药物组(81.3% vs 21.9%)。患者治疗前后血清TNF-α和IL-6水平差值与HOMA-IR差值显著性正相关(分别为r=0.676,P<0.001;r=0.498,P<0.001);HOMA-IR差值与疗效级别亦呈显著性正相关(r=0.608,P<0.001)。结论:吡格列酮可有效降低合并MS的NAFLD患者血清TNF-α、IL-6水平。TNF-α、IL-6可能通过影响胰岛素敏感性参与病变治疗过程。     

Rehmannia glutinosa inhibits tumour necrosis factor-alpha and interleukin-1 secretion from mouse astrocytes.

We investigated whether an aqueous extract of Rehmannia glutinosa steamed root (RGAE) inhibits secretion of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) from primary cultures of mouse astrocytes. RGAE dose-dependently inhibited the TNF-alpha secretion by astrocytes stimulated with substance P (SP) and lipopolysaccharide (LPS). IL-1 has been shown to elevate TNF-alpha secretion from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. We therefore investigated whether IL-1 mediated inhibition of TNF-alpha secretion from astrocytes by RGAE. Treatment of RGAE to astrocytes stimulated with both LPS+SP decreased IL-1 secretion. Moreover, incubation of astrocytes with IL-1 antibody abolished the synergistic cooperative effect of LPS+SP. These results suggest that RGAE may inhibits TNF-alpha secretion by inhibiting IL-1 secretion and that RGAE has an anti-inflammatory activity in the central nervous system curing some pathological disease states. 1999 Academic Press@p$hr Copyright 1999 Academic Press.     

ATP suppression of interleukin-12 and tumour necrosis factor-alpha release from macrophages

Immune cell activation releases ATP into the extracellular space. ATP-sensitive P2 purinergic receptors are expressed on immune cells and activation of these receptors alters immune cell function. Furthermore, ATP is metabolized by ectonucleotidases to adenosine, which has also been shown to alter cytokine production. In the present study, we investigated how extracellular ATP affects interleukin (IL)-12 and tumour necrosis factor (TNF)-alpha production in bacterial lipopolysaccharide (LPS)-treated murine peritoneal macrophages and we also examined whether extracellular ATP alters the production of the T helper 1 cytokine interferon (IFN)-gamma. Pretreatment of the peritoneal macrophages with ATP or various ATP analogues decreased both IL-12 and TNF-alpha production induced by LPS (10 microgram ml(-1)). The effect of ATP was partially reversed by cotreatment with adenosine deaminase (0.1 - 1 u ml(-1)), suggesting that the suppressive effect of ATP on cytokine production is, in part, due to its degradation products. Immunoneutralization with an anti-IL-10 antibody demonstrated that although ATP increases IL-10 production, the inhibition of IL-12 and TNF-alpha production is independent of the increased IL-10. The effect of ATP was pretranslational, as it suppressed steady state levels of mRNAs for IL-12 (both p35 and p40). In spleen cells stimulated with either LPS (10 microgram ml(-1)) or anti-CD3 (2 microgram ml(-1)) antibody, ATP suppressed, in a concentration-dependent manner, the production of IFN-gamma. These results suggest that extracellular ATP has multiple anti-inflammatory effects and that release of ATP into the extracellular space may play a role in blunting the overactive immune response in autoimmune diseases.     

The role of nitric oxide in cardiac depression induced by interleukin-1 beta and tumour necrosis factor-alpha.

1. Myocardial dysfunction during septic shock is associated with enhanced production of cytokines such as interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha). These cytokines depress cardiac mechanical function by a mechanism which is not well defined. 2. Bacterial endotoxin or cytokines cause the expression of Ca(2+)-independent nitric oxide (NO) synthase in cardiac myocytes, vascular endothelial cells and endocardial endothelial cells, causing enhanced production of NO. As NO has negative inotropic actions on cardiac muscle, we tested the sum effects of IL-1 beta plus TNF-alpha in the intact heart to determine whether enhanced expression of NO synthase activity in the cells that comprise the heart is involved in cardiac depression associated with cytokine stimulation. 3. Rat isolated working hearts perfused with IL-1 beta plus TNF-alpha showed a markedly greater depression in contractile function, measured as cardiac work, after 2 h of perfusion compared with time-matched control hearts. The depressant action of IL-1 beta plus TNF-alpha was first apparent after 1 h of perfusion; no early (15 min) cardiac depressant actions were seen. 4. The competitive inhibitor of Ca(2+)-dependent and Ca(2+)-independent NO synthases, NG-nitro-L-arginine methyl ester (L-NAME, 3 microM) when given concurrently with IL-1 beta plus TNF-alpha prevented the loss in contractile function such that these hearts after 2 h of perfusion had similar function to time-matched controls. L-NAME did not acutely reverse the loss of contractile function in hearts exposed for 2 h to IL-1 beta plus TNF-alpha.(ABSTRACT TRUNCATED AT 250 WORDS)     

Negative inotropic effects of tumour necrosis factor-alpha and interleukin-1beta are ameliorated by alfentanil in rat ventricular myocytes

BACKGROUND AND PURPOSE: Serum levels of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) increase during an inflammatory response and have been reported to induce a negative inotropic effect on the myocardium. Alfentanil, an opioid analgesic often used in the critical care of patients with sepsis, has been shown to enhance ventricular contractility. This study characterised the effects of TNF-alpha and IL-1beta on contraction and the Ca(2+) transient and investigated whether depressed ventricular function was ameliorated by alfentanil. EXPERIMENTAL APPROACH: Isolated rat ventricular myocytes were loaded with fura-2 and electrically stimulated at 1 Hz. Contraction and Ca(2+) transients were measured after 60, 120 and 180 min incubations in TNF-alpha (0.05 ng ml(-1)) and IL-1beta (2 ng ml(-1)). The effects of 10 microM alfentanil on contractility and Ca(2+) transients of TNF-alpha and IL-1beta treated cells were determined.Key results:After 180 min of TNF-alpha and IL-1beta treatment, the amplitude of contraction, the Ca(2+) transient and sarcoplasmic reticulum (SR) Ca(2+) content were significantly reduced. Alfentanil significantly increased contraction of TNF-alpha and IL-1beta treated cells via a small increase in the Ca(2+) transient and a larger increase in myofilament Ca(2+) sensitivity, effects that were not blocked by 10 microM naloxone, a broad spectrum opioid receptor antagonist. CONCLUSIONS AND IMPLICATIONS:TNF-alpha and IL-1beta induce a significant negative inotropic effect on ventricular myocytes in a time dependent manner through disruption of SR Ca(2+) handling and the Ca(2+) transient. This negative inotropic effect was ameliorated by alfentanil, but this response may not be mediated via opioid receptors.     

慢性酒精中毒血清肿瘤坏死因子α的检测及其临床意义

~~慢性酒精中毒血清肿瘤坏死因子α的检测及其临床意义$遵义医学院第一附属医院神经内科!563003@徐平 $遵义医学院第一附属医院神经内科!563003@雷显泽 $遵义医学院第一附属医院神经内科!563003@胡泳涛 $重庆医科大学第一附属医院神经内科!400016@邹德智~~~~~~~~     

Association of serum tumour necrosis factor-alpha with serum low-density lipoprotein-cholesterol and blood pressure in apparently healthy Japanese women

1. The pro-inflammatory cytokine tumour necrosis factor (TNF)-alpha is considered to be involved in the development of atherosclerosis by inducing local inflammatory responses in the vascular wall. Because TNF-alpha is also known to affect lipid and glucose metabolism, the association between the circulating concentration of TNF-alpha and atherogenic risk factors was examined in 82 apparently healthy Japanese women (aged 19-69 years; mean age 48.5 years). 2. The mean (+/-SD) serum TNF-alpha concentration was 2.7+/-0.9 pg/mL (range 1.4-5.9 pg/mL). The TNF-alpha concentration showed significant correlations with age (r = 0.28; P = 0.01), body mass index (r = 0.27; P = 0.01), the waist-hip ratio (r = 0.41; P = 0.0002), percentage body fat (r = 0.30; P = 0.006), systolic (r = 0.32; P = 0.004) and diastolic (r = 0.24; P = 0.03) blood pressure, total cholesterol (r = 0.27; P = 0.02) and low-density lipoprotein-cholesterol (LDL-C; r = 0.36; P = 0.001), while the correlations with high-density lipoprotein-cholesterol (r = -0.20; P = 0.08) and insulin resistance estimated by the homeostasis model assessment (HOMA(IR); r = 0.16; P = 0.15) were not statistically significant. 3. When adjusted for age and menopause, TNF-alpha was significantly associated with systolic blood pressure (r = 0.25; P = 0.02) and LDL-C (r = 0.27; P = 0.02). The association between TNF-alpha and LDL-C remained significant when adjustment was made for age, menopause and the waist-hip ratio (r = 0.24; P = 0.03). 4. Our results indicate that TNF-alpha may play a role in modulating blood pressure and LDL-C.     

生殖器疱疹患者血清IL-4、IL-6、TNF-α水平的研究

目的:探讨白介素-4(IL-4)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)在生殖器疱疹发病机理中的作用.方法:采用酶联免疫吸附试验,测定60例生殖器疱疹患者及60例正常人血清IL-4、IL-6、TNF-α含量.结果:生殖器疱疹患者血清IL-6水平低于正常对照组(P<0.05),而IL-4、TNF-α水平高于正常对照组(P<0.05).结论:生殖器疱疹患者体内存在细胞因子表达异常是导致生殖器疱疹反复发作的原因之一.