化瘀通痹方对活动期类风湿关节炎疗效及血清内TNF-α、IL-1β、CRP变化的研究

目的分析化瘀通痹方对活动期类风湿关节炎患者的疗效及患者血清肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、C反应蛋白(CRP)的变化情况。方法选取2016年8月-2018年8月收治的活动期类风湿关节炎患者104例,根据治疗方法不同分为对照组(西医常规治疗)和观察组(西医常规治疗基础上联合化瘀通痹方治疗),分析两组患者治疗后的临床疗效。结果观察组总有效率为92.31%(48/52),对照组为76.92%(40/52),观察组患者总有效率高于对照组(P<0.05)。两组治疗前症状、体征情况组间比较,差异不具有统计学意义(P>0.05)。观察组治疗后晨僵持续时间短于对照组,关节压痛和关节肿胀积分低于对照组(P<0.05)。两组治疗前TNF-α、IL-1β、CRP、葡萄糖6磷酸异构酶(GPI)、类风湿因子(RF)、血肿瘤坏死因子样配体1A(TL1A)水平组间比较,差异不具有统计学意义(P>0.05)。观察组治疗后TNF-α、IL-1β、CRP、GPI、RF、TL1A水平低于对照组(P<0.05)。两组治疗前28处关节疾病活动度(DAS28)积分组间比较,差异不具有统计学意义(P>0.05)。观察组治疗后DAS28积分低于对照组(P<0.05)。结论化瘀通痹方治疗活动期类风湿关节炎可改善患者临床症状,降低患者TNF-α、IL-1β、CRP、GPI的表达水平,提高疗效。     

载紫杉醇的大黄酸偶联物纳米胶束的制备及初步评价

目的制备载紫杉醇的D-α-生育酚聚乙二醇1000琥珀酸酯(D-α-tocopheryl polyethylene glycol 1000 succinate,TPGS)修饰的羧甲基壳聚糖-大黄酸偶联物(PTX/TPGS-CR)纳米胶束,并对其进行初步评价。方法采用透析法,以载药量、包封率及粒径为指标,通过单因素考察优化PTX/TPGS-CR纳米胶束的制备工艺并进行验证。以溶血实验及血管刺激性实验初步考察PTX/TPGS-CR纳米胶束的安全性。四甲基偶氮唑盐微量酶反应比色法(MTT)法考察PTX/TPGS-CR纳米胶束对Hela细胞的毒性。通过激光扫描共聚焦显微镜定性和流式细胞仪定量考察Hela细胞对PTX/TPGS-CR纳米胶束的摄取情况。结果制备工艺优化后制得的PTX/TPGS-CR纳米胶束粒径为(197.3±4.4)nm,PDI为(0.131±0.021),电位为(-31.8±0.5)mV,载药量为(48.20±3.03)%,包封率为(87.26±4.91)%。溶血实验结果表明,其溶血率低于1.71%;血管静脉注射无明显刺激性。其对Hela细胞的杀伤作用具有浓度和时间依赖性,能被Hela细胞高效摄取。结论PTX/TPGS-CR纳米胶束载药量和包封率高,安全性好,其体外抗肿瘤活性稍优于Taxol?。     

养阴利咽饮与玉液散吹喉对阴虚肺燥型慢性咽炎患者血清因子的影响

目的:探讨养阴利咽饮与玉液散吹喉对阴虚肺燥型慢性咽炎患者血清炎性因子的影响。方法:将2015年8月至2017年3月山东省淄博市第四人民医院收治的慢性咽炎患者118例作为研究对象,按治疗方法不同分为对照组和观察组,每组59例。对照组用常规西药治疗,观察组用养阴利咽饮与玉液散吹喉治疗,均连续治疗30 d。比较2组临床疗效,观察并比较治疗前后2组患者主要临床症状改善情况,唾液中分泌型免疫球蛋白A(SIgA)、血清炎性因子水平及生命质量变化。结果:治疗后观察组总有效率为91.53%,高于对照组的76.27%(P<0.05)。治疗后2组咽痛、干咳、咽黏膜充血水肿临床症状积分低于治疗前,且观察组低于对照组(P<0.01)。与治疗前比较,治疗后2组患者唾液中SIgA水平均明显升高,血清肿瘤坏死因子-α(TNF-α)及C-反应蛋白(CRP)水平均明显降低,且2组比较差异均有统计学意义(均P<0.01)。治疗后2组患者SF-36各项评分均明显高于治疗前,且观察组高于对照组(P<0.05或P<0.01)。结论:养阴利咽饮与玉液散吹喉联用可降低阴虚肺燥型慢性咽炎患者血清TNF-α、CRP水平,升高唾液中SIgA含量,改善患者临床症状,提高患者生命质量。     

穴位埋线治疗卒中后肩关节半脱位疗效及对血清TNF-α、IL-6的影响

目的观察穴位埋线治疗卒中后肩关节半脱位临床疗效及对血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)因子水平的影响,探讨抑制炎症反应的相关机制。方法将92例卒中后肩关节半脱位患者按1:1:1随机分3组,共剔除2例,最终每组30例。埋康组采用康复训练加穴位埋线;针康组采用康复训练加针刺治疗;康复组采用单纯康复治疗。分别于治疗前后采用Fugl-Meyer(FMA)上肢运动能力、视觉模拟评分(VAS)及血清TNF-α、IL-6炎性因子水平进行评价。结果治疗后3组患者Fugl-Meyer及VAS评分比较差异有统计学意义(P<0.05);血清TNF-α、IL-6炎性因子水平降低(P<0.05);3组中埋康组疗效最优;且3组治疗前后组内比较差异均有统计学意义(P<0.05)。结论穴位埋线能改善卒中肩关节半脱位患者上肢肩痛及运动功能,降低机体炎症性应激反应。     

The relationships among monocyte subsets,miRNAs and inflammatory cytokines in patients with acute myocardial infarction

Background

Acute myocardial infarction (AMI) causes irreversible myocardial damage and release of inflammatory mediators, including cytokines, chemokines and miRNAs. We aimed to investigate changes in the levels of cytokines (IL-6, TNF-α and IL-10), miRNAs profiles (miR-146 and miR-155) and distribution of different monocyte subsets (CD14++CD16-, CD14++CD16+, CD14+CD16++) in the acute and post-healing phases of AMI.

磷脂酰肌醇3-激酶p110α/β在甲状腺乳头状癌组织中的表达及与预后的相关性

目的检测甲状腺乳头状癌病人癌组织中磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase,PI3K)p110α、PI3Kp110β表达水平及其与预后的关系。方法2008年1月~2013年7月我院收治的甲状腺乳头状癌病人60例(甲状腺乳头状癌组),结节性甲状腺肿60例(结节性甲状腺肿组),其他非癌病例正常甲状腺组织60例(正常组)。随访甲状腺乳头状癌组5年生存情况。免疫组化检测各组PI3Kp110α、PI3Kp110β蛋白表达情况,Kaplan-Meier生存曲线分析甲状腺乳头状癌病人PI3Kp110α、PI3Kp110β阳性组和阴性组生存情况,Spearman法分析PI3Kp110α与PI3Kp110β的相关性。结果分别与正常组、结节性甲状腺肿组相比,甲状腺乳头状癌组PI3Kp110α、PI3Kp110β阳性率升高(P<0.05)。甲状腺乳头状癌病人癌组织PI3Kp110α、PI3Kp110β阳性表达与肿瘤大小、淋巴结转移情况、TNM分期明显相关(P<0.05)。单因素分析显示,PI3Kp110α、PI3Kp110β、淋巴结转移、TNM分期均为影响甲状腺乳头状癌预后不良的危险因素;多因素分析显示,PI3Kp110α、PI3Kp110β、淋巴结转移、TNM分期均是影响甲状腺乳头状癌预后不良的独立危险因素。60例病人14例出现复发,无失访病例。PI3Kp110α、PI3Kp110β阳性累计生存率明显低于PI3Kp110α、PI3Kp110β阴性累计生存率(P均<0.05)。Spearman法分析甲状腺乳头状癌病人癌组织中PI3Kp110α与PI3Kp110β呈正相关(P<0.05)。结论甲状腺乳头状癌病人癌组织中PI3Kp110α、PI3Kp110β阳性率升高,是预后不良的独立危险因素,且二者关系密切。     

MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism

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化浊清解愈溃煎对溃疡性结肠炎大鼠p38MAPK、TNF-α、IL-4的影响

目的观察化浊清解愈溃煎对溃疡性结肠炎(UC)大鼠血清及结肠组织p38MAPK、肿瘤坏死因子-α(TNF-α)、白细胞介素-4(IL-4)含量的影响。方法清洁级Wistar雄性大鼠50只按随机数字表法分为两组,空白组8只,其余大鼠均为造模组。采用TNBS/乙醇联合造模法构建UC大鼠模型。造模成功后按照随机数字表法将模型大鼠分为模型组、西药组(予美沙拉嗪肠溶片混悬液0.42 g/kg)及中药高、中、低剂量组。中药高、中、低剂量组予化浊清解愈溃煎中药混悬液,剂量分别为22、11、5.5 g/(kg·d),每日灌胃1次,疗程14 d。采用免疫组化法检测各组大鼠结肠组织内p38MAPK的蛋白表达量。ELISA法检测各组大鼠血清内TNF-α、IL-4含量。结果与空白组比较,模型组一般情况较差,血清中TNF-α含量显著升高(P<0.05),IL-4含量则明显降低(P<0.05),结肠组织中p38MAPK水平明显升高(P<0.05)。与模型组比较,西药组、中药各剂量组大鼠一般生存状况改善明显,血清中TNF-α含量下降,IL-4含量明显升高,尤以中药高剂量组和西药组疗效显著(P<0.05)。结论化浊清解愈溃煎高、中剂量可改善UC大鼠一般生存状况,并通过调节血清中IL-4含量,下调TNF-α表达水平和结肠组织中p38MAPK蛋白表达水平而达到保护结肠黏膜和治疗UC的作用。     

MiR-92b-3p ameliorates inflammation and autophagy by targeting TRAF3 and suppressing MKK3-p38 pathway in caerulein-induced AR42J cells

Acute pancreatitis (AP) is an inflammatory disease with high morbidity and mortality. Dysregulation of microRNAs (miRNAs) was involved in human diseases, including AP. However, the effects of miR-92b-3p on AP process and its mechanism remain not been fully clarified. The expression levels of miR-92b-3p and tumor necrosis factor receptor-associated factor-3 (TRAF3) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of TRAF3, tumor necrosis factor α (TNF-α) TNF-α, interleukin-6 (IL-6), phosphorylated mitogen-activated protein kinase kinase 3 (p-MKK3), MKK3, p38 and phosphorylated p38 (p-p38) were detected by western blot. The concentration of TNF-α and IL-6 in the medium was measured using ELISA kits. The possible binding sites of miR-92b-3p and TRAF3 were predicted by TargetScan and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The expression level of miR-92b-3p was decreased and TRAF3 expression was increased in AR42J cells stimulated with caerulein. Moreover, the protein levels of pro-inflammatory cytokines (TNF-α and IL-6) were markedly elevated, and the expression levels of autophagy-related markers Beclin1 as well as the ratio of LC3-II/I were obviously increased in AR42J cells treated with caerulein. In addition, overexpression of miR-92b-3p or knockdown of TRAF3 significantly suppressed the release of pro-inflammatory cytokines and autophagy in caerulein-induced AR42J cells. Furthermore, TRAF3 was a direct target of miR-92b-3p and its upregulation reversed the effects of miR-92b-3p overexpression on inflammatory response and autophagy. Besides, overexpression of miR-92b-3p inhibited the activation of the MKK3-p38 pathway by affecting TRAF3 expression. In conclusion, miR-92b-3p attenuated inflammatory response and autophagy by downregulating TRAF3 and suppressing MKK3-p38 pathway in caerulein-induced AR42J cells, providing a novel avenue for treatment of AP.