丙泊酚对50例骨关节结核患者的炎症因子的影响

目的：探讨丙泊酚对骨关节结核患者的炎症因子的影响。方法：随机选取100例骨关节结核患者并分为丙泊酚组（接受丙泊酚治疗）和异氟烷组（接受异氟烷治疗）各50例,对比2组白细胞介素-1（IL-1）、肿瘤坏死因子-α（TNF-a）、细胞间黏附分子-1（ICAM-1）和白细胞介素-6（IL-6）、白细胞介素-10（IL-10）的变化。结果：丙泊酚组患者术后12和24 h的IL-1、TNF-a、ICAM-1及T2时间点的IL-6水平均明显低于、而T2～T4各时间点IL-10水平则明显高于异氟烷组（P<0.01）。2组患者IL-6水平均从T0时间点逐渐上升至T3、IL-10水平从T0时间点逐渐上升至T2（丙泊酚组）或T3（异氟烷组）达到峰值后逐渐下降。结论：丙泊酚能有效抑制炎症因子TNF-a,IL-1和ICAM-1的释放,降低患者炎症反应的强度,亦能调节细胞因子IL-6和IL-10水平的平衡,减轻患者对手术的应激反应。     

胶原诱导性关节炎大鼠在中药作用下对其关节炎指数、IL-1β、TNF-α、PGE2、 RANKL及OPG的影响探讨

目的 探讨胶原诱导性关节炎大鼠在中药作用下对其关节炎指数、白细胞介素1β(IL-1β)、肿瘤坏死因子(TNF-α)、前列腺素E2 (PGE2)、核因子-kB受体活化因子配体(RANKL)及护骨素(OPG)的影响.方法 取Wistar大鼠48只随机分为空白组、模型组、阳性组、A、B、C组.复制胶原诱导性关节炎大鼠模型,连续干预4周后,各组大鼠眼眶静脉取血,观察关节炎指数、IL-1β、TNF-α、PGE2、RANKL及OPG.结果 与空白组相比,其余各组大鼠关节炎指数均明显增加(P＜0.05).与模型组相比,阳性组、A、B、C组关节炎指数均明显降低(P＜0.05).与空白组相比,模型组血清IL-1β、TNF-α、PGE2、RANKL、OPG及RANKL/OPG水平均明显升高(P＜0.05).与模型组相比,阳性组、A、B、C组血清IL-1β、TNF-α、PGE2、RANKL、OPG及RANKL/OPG水平明显降低(P＜0.05),且A、B、C组大鼠血清IL-1β、TNF-α、PGE2水平抑制作用及对RANKL、OPG及RANKL/OPG的改善情况均优于阳性组(P＜0.05).组织病理学结果显示,A、B、C组可抑制CIA大鼠关节组织病理学改变.结论 自拟除痹汤可明显降低CIA模型大鼠的关节炎指数及关节组织病理学改变,下调IL-1β、TNF-α、PGE2水平,抑制RANKL、OPG,从而可以有效防治CIA.     

黄芪注射液对实验性大鼠脑出血灶周围TNF-a、IL-10表达的影响

目的研究黄芪注射液对大鼠脑出血灶周围TNF-a、IL-10含量变化的影响。方法 90只SD大鼠,随机分为假手术组、脑出血组(ICH)、黄芪组,应用肝素化Ⅶ型胶原酶建立大鼠ICH模型,免疫组化染色观察脑出血灶周围组织TNF-a、IL-10含量变化。结果 (1)ICH组和黄芪组术后6h出血灶周围有少量TNF-α阳性细胞,并逐渐增多,到24h时达高峰,以后逐渐下降,至7d表达量明显减少;黄芪组TNF-α阳性细胞数在6、24、48、72h、7d均较脑出血组同期明显减少,差异有统计学意义(P<0.05)。(2)ICH组和黄芪组术后6h出血灶周围有少量IL-10阳性细胞,并逐渐增多,到7d时达高峰;黄芪组IL-10阳性细胞数在6、24、48、72h、7d均较脑出血组同期明显增加,差异有统计学意义(P<0.05)。结论黄芪注射液可以减少出血灶周围TNF-α的表达,增加出血灶周围IL-10的表达。     

基质金属蛋白酶及其抑制物与子宫内膜异位症的研究进展

子宫内膜异位症是妇科的常见疾病,其发病机制至今未明。近年来研究发现,基质金属蛋白酶（MMPs）及其抑制物（TIMPs）在该病的发生及发展中起了重要作用,现就MMPs及其抑制物TIMPs在子宫内膜异位症中的研究进展做一综述。     

沙利度胺对结节性痒疹患者血清TNF-α、IL-12的影响

目的:观察沙利度胺治疗结节性痒疹患者前后血清中肿瘤坏死因子-α(TNF-α)及白介素-12(IL-12)的变化。方法:50例结节性痒疹患者给予口服沙利度胺片治疗,测定治疗前后患者血清中TNF-α及IL-12水平,并与正常对照组比较。结果:治疗总有效率为78%。治疗前TNF-α及IL-12水平分别为(4.16±1.68)μg/m L及(65.74±19.58)pg/m L,均较正常对照者增高,差异有统计学意义(t值分别为3.78、4.05,P值均<0.05);治疗后分别下降至(2.78±1.24)μg/m L及(51.43±13.47)pg/m L,与治疗前比较差异均具有统计学意义(t值分别为2.52、2.38,P值均<0.05)。结论:沙利度胺可能通过降低血清TNF-α及IL-12水平起到治疗作用。     

核转录因子kappaB在急性心肌梗死后心室重塑中作用研究

目的:探讨外周血单个核细胞(PBMCs)核因子-kappaB(NF-κB)活化程度对急性心肌梗死(AMI)后左心室重塑(LVRM)作用及其与血浆肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)分泌的相关性。方法:选取首次AMI患者58例,进行超声心动图检查,按simpson法计算出的左心室舒张末期容积,并计算出左心室舒张末期容积指数增加率(ΔLVEDVI),以△LVEDVI>20%将患者分为心室重塑组33例和无心室重塑组25例;另取20例体检正常者为对照组。三组PB-MCs的NF-κB活性用细胞免疫化学染色检测,血浆细胞因子TNF-α,IL-1β含量由放射免疫法测定。结果:①AMI重塑组血浆外周血PBMCs的NF-κB核染色阳性百分率、TNF-α、IL-1β分泌表达均显著增加,高于无重塑组及健康对照组(P<0.01),差异有统计学意义。②左心室重塑组患者外周血PBMCs的NF-κB核染色阳性百分率与TNF-α、IL-1β表达均显著正相关(P<0.05)。结论:AMI后心室重塑患者外周血PBMCs的NF-κB活性是明显升高的,可能是通过促进细胞因子(TNF-α、IL-1β)的分泌来参与心室重塑的发病机制。     

Correlation of cytotoxic effect of transmembrane and secretory TNF-α to cell cycle

This study was aimed to examine the correlation of the cytotoxic effects induced by two types of TNF-α to cell cycle. Hoechst 33342 and PI were used to detect the morphological changes in the cell death induced by the two types of TNF-α. TdT and PI co-staining was performed to determine the phase of cell cycle of apoptotic cells. L929 cells in different phases of cell cycle were further synchronized and their sensitivity to the two types of TNF-α was observed. Our results showed that the apoptosis of HepG2 cells triggered by tm-TNF-α mainly occurred in G1 phase while in HL-60, Raji and K562 cell lines it mainly took place in S phase. The apoptosis of L929 cells induced by tm-TNF-α mainly occurred in S phase while the apoptosis induced by s-TNF-α mainly appeared in G1 phase. L929 cells were sensitive to s-TNF-α when synchronized in G1 phase (cytotoxicity 49.8%) while their sensi-tivity to tm-TNF-α was highest in S phase (45.7%) and G1/S phase (cytotoxicity 40.6%). It was concluded that tm-TNF-α-induced apoptosis of different target cells took place in different phases of cell cycle. The apoptosis of the specific cell line induced by the two types of TNF-α occurred in different phases of cell cycle. The sensitivity of the specific cell line to the two types of TNF-α was correlated with the phase of cell cycle.     

Prevention and management of diabetic retinopathy in STZ diabetic rats by Tinospora cordifolia and its molecular mechanisms

We investigated the potential of Tinospora cordifolia (TC) in treatment of diabetic retinopathy in STZ-induced rats due to its antihyperglycemic, angiogenic, antiinflammatory and antioxidant effects. The diabetic rats, treated for 24 weeks with TC extract (250 mg/kg), were evaluated for lenticular and fundus changes. Biochemical parameters were estimated and histopathological studies performed. TC significantly reduced blood glucose and glycated hemoglobin in treated rats. It prevented cataract development in treated group. Angiogenic markers VEGF and PKC increased in diabetic retina, which reduced significantly with TC. Anti-inflammatory parameters TNF-α and IL-1β elevated in diabetic group unlike that in treated group. TC also provided defense against depletion of antioxidant enzymes- glutathione and catalase. Histopathological studies revealed thickening of basement membrane of the retinal and glomerular vasculature of diabetic rat, but no basement membrane widening was seen in treated animals. Destruction of pancreatic islet structure was observed in diabetic group, but not in treated. Thus, TC reduces blood glucose and inhibits overexpression of angiogenic and inflammatory mediators, which are distinct markers of diabetic retinopathy. It also prevents retinal oxidative stress and restores antioxidant enzyme levels. These data provide evidence for the safety and potential effect of TC in the management of experimental diabetic retinopathy.     

核苷类药物治疗乙型肝炎肝硬化患者IL-6、TNF-α及TGF-β1的变化研究

目的 观察乙型肝炎（乙肝,HBV）相关失代偿期肝硬化患者接受核苷类药物治疗后细胞因子白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）、转化生长因子β1（TGF-β1）水平的变化及意义.方法 应用ELISA法对52例HBV相关失代偿期肝硬化患者进行血清IL-6、TNF-α及TGF-β1的水平含量进行测定,并与28例健康对照组进行比较;对接受核苷类药物抗病毒治疗患者与未接受抗病毒治疗的患者以上细胞因子的变化进行比较.结果 HBV相关失代偿期肝硬化患者血清IL-6、TNF-α及TGF-β1的含量显著高于健康对照组（P〈0.01）,接受核苷类药物抗病毒治疗1年后,抗病毒治疗组的细胞因子水平较治疗前明显降低（P〈0.01）,且优于未抗病毒治疗组（P〈0.05）.结论 HBV相关失代偿期肝硬化患者血清IL-6、TNF-α及TGF-β1的含量变化对了解核苷类药物抗病毒治疗临床疗效及明确机体免疫状态有重要意义.     

薯蓣皂苷元对肿瘤坏死因子诱导的单核细胞组织因子表达的抑制作用研究

目的：研究薯蓣皂苷元对肿瘤坏死因子（TNF-α）诱导的THP-1细胞中组织因子（TF）促凝活性及表达的作用,并探讨其可能的作用机制。方法：采用TNF-α（10ng．mL^-1）诱导THP-1细胞活化,采用改良的发色底物法测定TF的促凝活性;应用逆转录聚合酶链式反应（RT-PCR）及荧光定量聚合酶链式反应（qPCR）测定TF的mRNA表达;Westernblotting分析TF蛋白及相关信号通路激酶表达水平。结果：薯蓣皂苷元（0．01,0．1和1μm01．L^-1）预处理,可浓度依赖性地抑制TNF．6c诱导的TF促凝活性,经计算其Ic50为0．25μm01．L^-1;薯蓣皂苷元明显抑制TNF-d诱导的TFmRNA和蛋白表达。同时,著蓣皂苷元1gm01．L^-1对于TNF-α诱导的5～30minNF-κB／p65、IKKB、Akt、ERK和JNK的激活,也有一定的抑制作用。结论：薯蓣皂苷元可明显抑制TNF-α诱导的THP-1细胞TF的活性及表达,其机制可能与下调NF-κB／p65,IKKβ、Akt、ERK和JNK的磷酸化有关。