穴位敷贴配合辨证施护治疗气阴两虚型糖尿病的疗效观察

目的:观察穴位敷贴配合辨证施护治疗气阴两虚型糖尿病的疗效。方法:将65例气阴两虚型糖尿病患者随机分为治疗组33例,对照组32例。对照组使用糖尿病常规治疗,治疗组在糖尿病常规治疗的基础上加穴位敷贴配合辨证施护,15d为1个疗程。结果:治疗组在降低气阴两虚型糖尿病的血糖水平,改善临床症状方面明显优于对照组。结论:穴位敷贴配合辨证施护可改善气阴两虚型糖尿病的临床症状,降低血糖水平,具有较好的疗效。     

养心康和保心康治疗充血性心力衰竭的临床研究

目的 :观察中药复方制剂养心康和保心康治疗充血性心力衰竭的疗效。方法 :92例患者按中医辨证分为气阴虚型 ( 60型 )和气阳虚型 ( 3 2例 )。两型分别随机分为治疗组和对照组 ,一般治疗相同。气阴虚型治疗组 ( 4 0例 )加服养心康 ,气阳虚型治疗组 ( 2 2例 )加服保心康 ,两型对照组均加服安慰剂 ,均连服药 2周。结果 :两型治疗组证候疗效总有效率 91.9% ,对照组为2 9 .3 % ,有显著差异 (P <0 .0 1) ;心功能疗效总有效率 ,气阴虚型为 80 % ,气阳虚型为 95 .4 %。结论 :养心康和保心康对充血性心力衰竭有良好的疗效。     

景天生脉饮治疗气阴两虚型慢性心功能不全临床疗效观察

目的 观察景天生脉饮治疗气阴两虚型慢性心功能不全患者临床疗效。方法 将60例气阴两虚型慢性心功能不全患者随机分为治疗组和对照组各30例,治疗组和对照组均予以一般治疗和西药地高辛强心治疗。治疗组加用景天生脉饮中药汤药口服。对比两组临床疗效和中医证候积分。结果 治疗组临床疗效及中医证候积分均显著优于对照组,差异有统计学意义(PO.05)。结论 景天生脉饮对气阴两虚型慢性心功能不全患者的症状治疗效果较佳,可以明显改善患者的生活质量,为临床从中医角度治疗慢性心功能不全提供新方向。     

降糖十二味对气阴两虚型2型糖尿病患者胰岛素抵抗的影响

目的:观察降糖十二味对气阴两虚型2型糖尿病患者胰岛素抵抗的影响。方法:将70例气阴两虚型2型糖尿病患者按就诊顺序随机分为两组。对照组予盐酸二甲双胍治疗,治疗组在对照组基础上加服降糖十二味。1个月后观察临床疗效、空腹血糖和胰岛素抵抗指数等。结果:治疗组显效25例,有效9例,无效1例,总有效率97.1%;对照组显效15例,有效11例,无效9例,总有效率74.3%,两组比较有显著意义(P<0.05)。治疗后治疗组胰岛素敏感指数较对照组改善明显,两者比较有统计学意义(P<0.05)。结论:降糖十二味对气阴两虚型2型糖尿病疗效确切,且能有效降低胰岛素的抵抗。     

黄芪桂枝五物汤治疗气血两虚型类风湿关节炎的效果

目的探讨黄芪桂枝五物汤治疗类风湿关节炎气血两虚型的疗效。方法将40例我科收治的气血两虚型类风湿关节炎患者按照随机数字表法分为观察组及对照组。对照组患者接受再造生血胶囊治疗,观察组患者接受黄芪桂枝五物汤加味治疗。比较两组患者治疗前后关节肿胀数、关节压痛数、晨僵时间、类风湿关节炎患者病情评价(DAS28评分)、中医症候积分、类风湿因子(RF)、红细胞沉降率(ESR)及C反应蛋白(CRP)水平,比较两组患者治疗后的疗效。结果治疗3个疗程后,观察组患者关节肿胀数、关节压痛数、晨僵时间、DAS28评分及中医证候积分均低于对照组患者(P 0.05);观察组患者的RF、ESR及CRP水平均低于对照组患者(P 0.05);观察组患者总有效率(95.0%)高于对照组患者(70.0%),两组疗效资料差异有统计学意义(P 0.05)。结论黄芪桂枝五物汤治疗类风湿关节炎气血两虚型的疗效显著,能够减轻患者的疾病症状,降低RF、ESR及CRP水平。     

益气养阴收敛固涩方治疗气阴两虚型糖尿病肾病30例临床观察

目的:探讨益气养阴收敛固涩方治疗气阴两虚型糖尿病肾病的临床疗效。方法:将60例气阴两虚型糖尿病肾病患者随机分成观察组和对照组各30例,对照组采用门冬胰岛素30降糖及厄贝沙坦分散片降低尿蛋白;观察组在对照组基础上予益气养阴收敛固涩方治疗12周。观察两组患者治疗前后尿微量白蛋白、24 h尿蛋白定量及中医症状评分指标。结果:治疗12周后观察组患者尿微量白蛋白、24 h尿蛋白定量及中医症状评分均较治疗前有所下降,且与治疗前及对照组相比较均具有统计学差异。结论:益气养阴收敛固涩方联合ARB类能够有效改善糖尿病肾病气阴两虚型患者的临床症状,控制早期糖尿病肾病的进展。     

中医食疗对气阴两虚型糖尿病患者生活质量的影响

目的观察中医食疗对气阴两虚型糖尿病患者生活质量的影响。方法按随机数字表将72例糖尿病患者分为观察组和对照组各36例,观察组脱落3例、对照组脱落1例。对照组给予社区常规饮食指导,观察组在常规饮食指导上辅以气阴两虚型食疗指导。两组患者在干预前后分别进行生活质量的评价。结果干预3个月后,观察组患者生活质量高于对照组患者,差异有统计学意义(P0.05),尤其是疾病维度和满意度维度方面。结论气阴两虚型糖尿病患者在现代营养学饮食指导的基础上加入中医食疗思路,更能有效提高患者生活质量。     

消渴安糖方对2型糖尿病气阴两虚证胃肠激素水平的影响

目的：研究消渴安糖方对2型糖尿病气阴两虚证患者空腹血清胃动素(MTL)、胰高血糖素(PG)、P物质(SP)异常的影响，同时观察该方对2型糖尿病植物神经病变气阴两虚证的疗效。方法：将90例2型糖尿病气阴两虚证患者随机分为两组治疗(分别为观察组和对照组)，每组45例；另设30例健康人作为对照。观察组及对照组均给予常规糖尿病治疗，观察组另加用消渴安糖方每日1剂，两组均治疗1个月。采用放射免疫法检测治疗前后空腹血清MTL、SP、PG；邻甲苯胺法测定空腹及餐后2h血糖(BS)；同时观察两组胃肠功能紊乱症状评分变化。健康人组仅测1次血清MTL、SP、PG。结果：2型糖尿病气阴两虚证患者MTL、PG值高于健康人组，SP则低于健康人组，均有非常显著性差异(P均＜0．01)。治疗前后结果比较显示，观察组MTL、PG、SP的异常以及胃肠功能紊乱症状有明显的改善(P均＜0．01)，观察组治疗后MTL、PG、SP和阳改善组，均优于对照组(P均＜0．05)。结论：消渴安糖方对2型糖尿病气阴两虚证MTL、SP和PG异常有较好的改善作用，表明2型糖尿病气阴两虚证与MTL、SP和PG异常有关；该方对2型糖尿病植物神经病变证属气阴两虚证者有较好的治疗作用，并有一定的辅助降血糖作用。     

中药熏蒸对类风湿关节炎疼痛影响的观察及护理

目的 观察中药熏蒸对减轻类风湿关节炎疼痛的增效作用及护理方法.方法 类风湿关节炎风寒湿痹型患者40例,随机分为观察组和对照组各20例,对照组采用MTX及非甾体抗炎药治疗.观察组在上述药治的基础上辅以中药熏蒸.并于治疗一周后进行两组患者组间关节疼痛程度和疗效比较.结果 观察组关节疼痛评分低于对照组.且观察组总有效率为55%,对照组总有效率为35%.差异有显著意义(P＞0.05).结论 中药熏蒸对减轻类风湿关节炎疼痛有增效作用.     

参芪地黄汤加减治疗气阴两虚兼血瘀型糖尿病的临床效果评价

目的:探讨运用参芪地黄汤加减治疗气阴两虚兼血瘀型糖尿病患者的治疗效果。方法:选择本院2014年2月到2017年2月收治的36例气阴两虚兼血瘀型糖尿病患者,随机分为对照组和治疗组,对照组行西医治疗,治疗组则在对照组的基础上进行参芪地黄汤加减治疗,观察两组临床疗效。结果:与对照组相比,治疗组的总有效率较高,中医证候积分也明显偏低,由此可见,治疗组的临床效果相对较好(P <0.05)。结论:对气阴两虚兼血瘀型糖尿病患者行中医参芪地黄汤加减治疗临床效果较好,降低患者血糖,并有效减少了中医证候积分改善患者临床症状。     

Interleukin 1 receptor dependence of serum transferred arthritis can be circumvented by toll-like receptor 4 signaling

Inflammatory arthritis is associated with the release of a network of key cytokines. In T cell receptor transgenic K/BxN mice interleukin (IL)-1 plays a key role in joint swelling and destruction, as suggested by the ability of anti-IL-1receptor (IL-1R) antibody treatment to delay the onset and slow the progression of this disease. This mechanism is dependent on the signaling pathway intermediary myeloid differentiation factor 88 (MyD88), such that neither IL-1R nor MyD88-deficient mice developed visually detectable synovitis after transfer of arthritogenic sera. The Toll-like receptors (TLRs) share the same signaling pathway through MyD88 as the IL-1R. The administration of a TLR-4 ligand, lipopolysaccharide, concomitant with arthritogenic serum in IL-1 receptor-deficient mice resulted in acute paw swelling, but not in MyD88-deficient mice. Also, serum transferred arthritis was not sustained in TLR-4 mutant mice compared with controls. These results suggest that innate immune functions via TLR-4 might perpetuate inflammatory mechanisms and bypass the need for IL-1 in chronic joint inflammation.     

青藤碱对佐剂性关节炎大鼠滑膜细胞核因子κB信号转导的影响及其机制

背景青藤碱是从中药青风藤中提取的生物碱单体,在治疗类风湿关节炎(rheumatoid arthritis,RA)方面,具有较明确的疗效,但其治疗机制尚不清楚.目的观察不同剂量的青藤碱体外作用对佐剂性关节炎(adjuvant arthritis,AA)大鼠滑膜细胞核因子-κB(NF-κB)活性及肿瘤坏死因子(TNF-αmRNA、白细胞介素1β(IL-1β)mRNA、白细胞介素10(IL-10)mRNA的影响,以阐明该药治疗RA的可能机制.设计以细胞为研究对象,分组对照的重复测量设计.单位一所军医大学医院的中医科和烧伤研究所.材料实验于2002-03/2002-10在全军烧伤研究所实验室完成.实验动物为健康清洁级雄性Wistar大鼠25只.以AA大鼠为模型,收集滑膜细胞,依次作如下分组正常对照组,AA组,AA+青藤碱30 mg/L组,AA+青藤碱60 mg/L组,AA+青藤碱120 mg/L组.电泳迁移率改变分析法测NF-κB的活性,反转录PCR检测TNF-α mRNA,IL-1β mRNA,IL-10 mRNA的表达.主要观察指标不同剂量的青藤碱体外作用对后佐剂性关节炎大鼠滑膜细胞NF-κB活性,TNF-1β mRNA,IL-1β mRNA及IL-10 mRNA的对比结果.结果与正常对照组相比,AA后滑膜细胞内NF-κB活性与TNF-α mR-NA,IL-1β mRNA,IL-10 mRNA的表达均显著升高,分别为17±6,0.570±0.047,0.730±0.093,0.683±0.081(t=2.71～4.07,P<0.05).经青藤碱作用后,NF-κB活性的变化趋势与TNF-α mRNA,IL-1 mRNA的相关性较好(r=0.810,P<0.001;r=0.562,P<0.05),与IL-10 mRNA无统计学上的相关性,青藤碱在一定的浓度范围(30～120 mg/L)内呈浓度依赖性抑制NF-κB活性与TNF-α mR-NA,IL-1β mRNA的表达,而对IL-10 mRNA的抑制效应与浓度无关.结论青藤碱可能通过抑制NF-κB活性而降低滑膜细胞内TNF-α mR-NA及IL-1β mRNA的表达.     

TLR4-mediated MyD88-dependent signaling pathway is activated by cerebral ischemia–reperfusion in cortex in mice

To study whether the signaling pathway is activated in the inflammatory reaction of cerebral ischemia–reperfusion and its mechanism. The mice were randomly divided into sham group, ischemia–reperfusion group and TLR4-blocked group with different time points of reperfusion 12 h, 24 h, 48 h and 72 h group. We observed the different expression of TLR4 mRNA and MyD88 mRNA, activation of NF-κB and the TNF-α and IL-1β protein levels in each group at different time point after ischemia–reperfusion. Mice cerebral ischemia was induced by occlusion of common carotid arteries (CCA) bilaterally. TLR4 signaling pathway could be inhibited by specific anti-TLR4 binding protein to prevent TLR4 from interacting with its receptors. We determined the result of TLR4 antibodies-blocking and mice cerebral ischemia–reperfusion injuries by Western blot, and evaluated neuronal damage in cortex. We also determined the expression of TLR4 mRNA and MyD88 mRNA by in situ hybridization (ISH), the activation of NF-κB by EMSA, and the expression of TNF-α protein by Western blot. Anti-TLR4 binding TLR4 receptors before reperfusion was effective; There was distinct difference among each group respecting neuronal damage; The expression of TLR4 mRNA and MyD88 mRNA, the activation of NF-κB, and the expression of TNF-α protein showed clear difference as well. LR4-mediated MyD88-dependent signaling pathway activated by ischemia–reperfusion may be involved in the mechanism of ischemia–reperfusion through upregulation of NF-κB and TNF-α.     

情绪弹性疗法结合口腔护理对干燥综合征患者不良情绪及口腔情况的影响

目的:探讨情绪弹性疗法结合护理对干燥综合征(SS)患者不良情绪及口腔情况的影响。方法:将2019年8月1日~2020年8月31日收治的120例SS患者随机分为对照组和观察组各60例,对照组给予常规口腔护理,观察组在常规口腔护理基础上给予情绪弹性疗法;比较两组干预7 d后口腔状况和口腔pH值变化情况、干预前后心理状况[采用中文版心理弹性量表(CD-RISC)、抑郁自评量表(SDS)、焦虑自评量表(SAS)]、疾病疼痛和疾病活跃度[采用干燥综合征患者报告指数(ESSPRI)、干燥综合征疾病活动指数(ESSDAI)]。结果:干预7 d后,观察组灼口症改善率、口腔溃疡治愈率均高于对照组(P<0.05),口腔溃疡治愈时间短于对照组(P<0.01);干预后,两组口腔pH高于干预前(P<0.05),且观察组高于对照组(P<0.01);干预后,观察组CD-RISC评分高于干预前和同期对照组(P<0.05,P<0.01);干预后,两组SDS、SAS评分均低于干预前(P<0.05),且观察组低于对照组(P<0.01);干预后,两组ESSPRI、ESSDAI评分均低于干预前(P<0.05),且观察组低于对照组(P<0.05)。结论:情绪弹性疗法结合口腔护理可明显改善干燥综合征患者的口腔感染状况,缓解患者不良情绪。     

金骨莲胶囊治疗大鼠类风湿性关节炎的作用及其机制研究

目的探讨金骨莲胶囊对大鼠类风湿性关节炎的治疗作用及相关机制。方法将60只大鼠随机分为6组,10只作为正常对照组,其余50只通过皮下注射Freund’s完全佐剂建立类风湿性关节炎大鼠模型。造模成功后随机分为五组,对照组不给于任何干预,另外四组分别给予塞来昔布、金骨莲胶囊(低剂量组,每次1粒,3次/d)、金骨莲胶囊(中剂量组,每次2粒,3次/d)以及金骨莲胶囊(高剂量组,每次3粒,3次/d)。观察各组大鼠给药后1 h与给药后7 d足关节肿胀度,给药后7 d血清白介素-17(IL-17)、白介素-23(IL-23)和肿瘤坏死因子-α(TNF-α)含量的变化;HE染色观察局部组织情况变化并应用关节组织病理学评分进行比较。结果给药后1 h与给药后7 d,模型组的足趾肿胀度高于正常对照组(P<0.05);与模型组比较,塞来昔布组、金骨莲胶囊组均可以明显减轻RA大鼠足关节肿胀度,差异有统计学意义(P<0.05),金骨莲胶囊组的作用呈剂量依赖性(P<0.05)。末次给药后7 d,与正常对照组比较,模型组大鼠血清IL-17、IL-35、TNF-α水平以及关节组织病理学评分均明显升高,差异有统计学意义(P<0.05)。与模型组比较,塞来昔布组以及金骨莲胶囊组的IL-17、IL-35、TNF-α以及关节组织病理学评分均明显降低,差异有统计学意义(P<0.05),金骨莲胶囊组的作用呈剂量依赖性(P<0.05)。结论金骨莲胶囊具有较好的治疗类风湿性关节炎作用,并且作用呈剂量依赖性,其作用机制可能与降低炎性因子的释放有关。     

MyD88-dependent IL-1 receptor signaling is essential for gouty inflammation stimulated by monosodium urate crystals

While it is known that monosodium urate (MSU) crystals cause the disease gout, the mechanism by which these crystals stimulate this inflammatory condition has not been clear. Here we find that the Toll/IL-1R (TIR) signal transduction adaptor myeloid differentiation primary response protein 88 (MyD88) is required for acute gouty inflammation. In contrast, other TIR adaptor molecules, TIRAP/Mal, TRIF, and TRAM, are not required for this process. The MyD88-dependent TLR1, -2, -4, -6, -7, -9, and -11 and IL-18 receptor (IL-18R) are not essential for MSU-induced inflammation. Moreover, MSU does not stimulate HEK cells expressing TLR1-11 to activate NF-kappaB. In contrast, mice deficient in the MyD88-dependent IL-1R showed reduced inflammatory responses, similar to those observed in MyD88-deficient mice. Similarly, mice treated with IL-1 neutralizing antibodies also showed reduced MSU-induced inflammation, demonstrating that IL-1 production and IL-1R activation play essential roles in MSU-triggered inflammation. IL-1R deficiency in bone marrow-derived cells did not affect the inflammatory response; however, it was required in non-bone marrow-derived cells. These results indicate that IL-1 is essential for the MSU-induced inflammatory response and that the requirement of MyD88 in this process is primarily through its function as an adaptor molecule in the IL-1R signaling pathway.     

TIR domain--containing adaptors regulate TLR-mediated signaling pathways

Recognition of pathogens by Toll-like receptors (TLRs) triggers innate immune responses via signaling pathways mediated by several Toll/IL-1R (TIR) domain-containing adaptors such as MyD88, TIRAP, and TRIF. MyD88 is a common adaptor that is essential for proinflammatory cytokine production, whereas TRIF mediates the MyD88-independent pathway from TLR3 and TLR4 that is responsible for type I interferon production in response to double-stranded RNA and LPS, respectively. TIRAP specifically participates in the MyD88-dependent pathways shared by TLR2 and TLR4, and TRAM is essential for the TLR4-mediated MyD88-independent pathway. Thus, TIR domain-containing adaptors play an important role in the TLR mediated signaling pathways.     

当归四逆汤联合甲氨蝶呤 洛索洛芬钠治疗类风湿关节炎疗效分析

目的探讨当归四逆汤联合甲氨蝶呤、洛索洛芬钠治疗类风湿关节炎患者的临床效果.方法将243例娄风湿关节炎患者按简单随机化分组法分为3组,每组81例,西药组口服甲氨蝶呤、洛索洛芬钠治疗,中药组口服当归四逆汤治疗,联合组予以当归四逆汤联合甲氨蝶呤及洛索洛芬钠治疗,观察1个月.比较3组治疗1个月后总有效率,曼彻斯特大学骨性关节炎指数评分、中医症候积分、实验室指标(血沉、C反应蛋白、娄风湿因子、抗环瓜氨酸肽抗体)、Wnt/β-catenin信号通路(Wnt3α、β-catenin)表达水平及不良反应发生率.结果(1)联合组治疗1个月后总有效率(90.1%)显著高于西药组(75.3%)、中药组(72.8%)(P<0.05),西药组与中药组比较差异无统计学意义(P>0.05);(2)联合组治疗1个月后曼彻斯特大学骨性关节炎指数评分、中医症候积分显著低于西药组、中药组(P<0.01),西药组与中药组比较差异均无统计学意义(P>0.05)(3);联合组治疗1个月后血沉、C反应蛋白、类风湿因子、抗环瓜氨酸肽抗体水平及Wnt3α、β-catenin表达水平均显著低于西药组、中药组(P<0.01),西药组与中药组各项指标比较差异均无统计学意义(P>0.05);(4)联合组、中药组不良反应发生率(2.5%、1.2%)显著低于西药组(13.6%)(P<0.01),中药组、联合组不良反应发生率比较差异无统计学意义(P>0.05).结论当归四逆汤联合甲氨蝶呤及洛索洛芬钠治疗类风湿关节炎患者具有协同增效作用,能有效改善患者疼痛、晨僵等临床症状,缓解炎症反应,控制患者病情,且安全性高.     

中药熏蒸辅助治疗对重度类风湿膝关节炎人工膝关节置换术后患者康复效果的影响

目的:探讨中药熏蒸辅助治疗对重度类风湿膝关节炎人工膝关节置换术后患者康复效果。方法:选取我院骨科2017年1月至2018年2月收治的重度类风湿膝关节炎需行人工膝关节置换术患者83例。按就诊先后顺序分为试验组和对照组,试验组40例,对照组43例。对照组患者常规康复功能锻炼,试验组患者在对照组的基础上给予中药熏蒸辅助治疗,治疗3个月。对比两组患者治疗治疗前和治疗后后血清因子水平,治疗前后生活质量评分量表(SF-36)评分,两组患者骨关节炎指数评分(The Western Ontario and Mcmaster Universities Osteoarthritis Index,WOMAC)、膝关节评分(Hospital for special surgery,HSS)。结果:经治疗治疗前和治疗后后试验组血浆纤维蛋白(FIB)、D-二聚体、IL-1β、白细胞介素8(IL-8)水平均明显降低(P<0.05);试验组SF-36量表评分显著高于对照组(P<0.05);试验组WOMAC评分、HSS评分显著高于对照组(P<0.05)。结论:中药熏蒸辅助治疗能有效提高重度类风湿膝关节炎人工膝关节置换术后患者康复效果。     

Activation of RAW264.7 macrophage by Exopolysaccharide from Aphanothece halaphytica (EPSAH) and the underlying mechanisms

Exopolysaccharide from Aphanothece halophytica (EPSAH), a potent antitumor agent and immunological adjuvant, was investigated for the activation effect on RAW264.7 macrophages and the underlying mechanisms. EPSAH could significantly enhance macrophage phagocytosis and the secretion of nitric oxide, increase the mRNA expression levels of the pro-inflammatory cytokines (IL-1β, IL-6, IL-12, and TNF-α), anti-inflammatory cytokine IL-10, and chemokines (MCP-1 and MIP-1α). When RAW264.7 cells were treated with EPSAH, the mRNA expression of TLR4 and its downstream molecules TRAF6 and MyD88 were upregulated. When TLR4 was blocked using a TLR4-specific neutralizing antibody, nitric oxide secretion from the macrophages was significantly inhibited. EPSAH was further shown to induce phosphorylation of the mitogen-activated protein kinases (MAPKs) ERK, JNK, and p38, and promote cytoplasmic IκB phosphorylation and increase nuclear NF-κB p65 levels remarkably in RAW264.7 cells. These data demonstrate the capacity of EPSAH to induce macrophage activation possibly via TLR4/MyD88 pathway, which leads to the activation of its main signaling downstream molecules MAPKs and NF-κB.