蝉蜕对支气管哮喘模型大鼠肺组织形态学及血清中TXB_2、6-keto-PGF_(1α)的影响

蝉蜕（pellicula cicadae）治疗支气管哮喘，具有良好的平喘效果，我们在前期的实验中已进行了验证。但作用机制尚不清楚，故本实验进一步观察了蝉蜕对模型大鼠肺组织形态学及血清中TXB：及6-keto—PGF1α含量的影响，对其药理机制进行初步研究。     

早期肠内营养对休克后患者炎性反应的疗效研究

目的 研究早期肠内营养(EN)对休克患者内毒素及肿瘤坏死因子-α(TNF-α)的作用及全身炎性反应综合征(SIRS)的影响.方法 休克67例随机分为早期EN组和肠外营养(TPN)组,检测两组患者肠内营养治疗前、治疗后1、3、5 d血浆中内毒素与TNF-α水平;统计两组SIRS的持续时间与多器官功能障碍(MODS)的发生...     

常氧条件下姜黄素对肝癌Hep1细胞增殖及HIF-1α mRNA表达的影响

目的:研究常氧条件下姜黄素对Hep1细胞的增殖及HIF-1α mRNA表达的影响。方法CCK-8法检测常氧条件下不同浓度姜黄素(0、5、10、15、20μmol/L)对肝癌Hep1细胞增殖的影响;用终浓度为15μmol/L姜黄素对体外肝癌细胞系Hep1细胞进行干预,流式细胞术分析Hep1细胞凋亡的变化;常氧条件下不同浓度姜黄素(0、5、10、15、20μmol/L)对肝癌Hep1细胞作用24h后,RT-PCR检测Hep1细胞HIF-1α mRNA表达水平的变化。结果:5、10、15、20μmol/L的姜黄素在作用1周后,呈浓度依赖性抑制肝癌Hep1细胞增殖;流式分析显示15μmol/L的姜黄素使Hep1细胞凋亡率增高,差异具有统计学意义(P0.05);与空白对照组相比,10μmol/L姜黄素处理组的HIF-1α mRNA的表达水平升高,差异具有统计学意义(P0.05),15、20μmol/L姜黄素处理组的HIF-1α mRNA的表达水平升高更为显著(P0.01)。结论:常氧条件下,姜黄素呈浓度依赖性抑制肝癌Hep1细胞的增殖,促进Hep1细胞的凋亡和HIF-1α mRNA的表达,常氧条件下姜黄素抑制肝癌Hep1细胞增殖的机制可能与缺氧条件下姜黄素的抑瘤机制有所不同。     

茶属植物及茶多酚类成分对抗原诱导RBL-2H3细胞过敏反应的抑制作用

目的:研究茶属植物及茶多酚类和嘌呤碱类成分对抗原刺激RBL-2H3细胞脱颗粒及肿瘤坏死因子α(TNF-α)和白细胞介素4(IL-4)释放的抑制作用。方法:测定β-hexosaminidase的释放以评价脱颗粒反应的指标,酶联免疫吸附法测定TNF-α和IL-4的释放,评价茶中主要成分的抗过敏活性。结果:茶属植物均有抑制RBL-2H3细胞脱颗粒作用,其中花类表现出较叶类更强的抗过敏活性;EGCG对抗原刺激的RBL-2H3细胞即刻相(IC50:234μmol·L-1)和延缓相反应(IL4,IC50:158μmol·L-1),及钙离子载体A23187诱导的脱颗粒反应均有抑制作用(IC50:126μmol·L-1)。结论:茶属植物和EGCG具有明显的抗过敏作用。     

肠易激综合征大鼠炎性细胞因子水平及宁肠汤对其影响的研究

目的探讨应激法诱导的肠易激综合征（IBS）大鼠免疫功能的变化及宁肠汤对炎性细胞因子的调节作用。方法将实验动物随机分为正常组、模型组、匹维溴胺组及宁肠汤高、中、低剂量组，以慢性束缚＋夹尾刺激作为复合应激原诱导IBS大鼠模型。正常组、模型组给予生理盐水灌胃，中药组予不同剂量宁肠汤药液灌胃，匹维溴胺组予匹维溴胺水溶液灌胃，共用药4周。采用放免法检测大鼠血清肿瘤坏死因子-α（TNF-α）、白细胞介素-8（IL-8）含量，观察宁肠汤对IBS大鼠肠运动功能及免疫功能的调节作用。结果IBS大鼠免疫功能紊乱，血清TNF-α、IL-8含量增高（P〈0.01）。而宁肠汤能调节IBS大鼠肠运动功能，降低血清TNF-α、IL-8含量，改善其免疫功能。结论IBS存在免疫功能紊乱，宁肠汤可通过降低血清TNF-α、IL-8含量，调节免疫功能紊乱，从而发挥对IBS的治疗作用。     

电针对角叉菜胶致炎大鼠的抗炎效应及对白细胞介素-1β、肿瘤坏死因子-α的影响

目的:观察电针对角叉菜胶致炎大鼠的治疗作用,并探讨电针抗急性炎症的部分机理。方法:正常Wistar大鼠分别在电针、消炎痛和罗非昔布预处理5 d后致角叉菜胶急性炎症模型。电针刺激"曲池"穴,刺激参数为:连续波,频率2 Hz,强度5 mA,时间30 min,每天1次,连续5 d;消炎痛和罗非昔布预处理分别以7.5 mg/kg灌胃,每天1次,连续5 d;另一组大鼠在相同造模后进行即刻电针处理(参数同电针预处理组)。以毛细管放大法检测足跖肿胀度,ELISA法检测炎症足爪PGE2、IL-1β和TNF-α水平,RT-PCR法检测足爪炎症组织IL-1βmRNA、TNF-αmRNA表达。结果:电针可有效抑制角叉菜胶致炎大鼠足跖肿胀,尤以造模后2、3 h最为显著;可降低大鼠炎症足爪组织中的PGE2水平;不同时段电针介入治疗均能下调炎症足爪组织中IL-1β和TNF-α水平,但以造模后治疗为佳;电针对足爪炎症组织IL-1βmRNA、TNF-αmRNA表达产生不同程度的下调作用。结论:电针对角叉菜胶致炎大鼠急性炎症具有良好的抗炎效应,并通过抑制局部促炎症因子(如IL-1β、TNF-α)的生成与表达而控制炎症的发展。     

舒郁散对慢性应激抑郁大鼠行为及海马糖皮质激素受体表达的影响

目的观察舒郁散对慢性不可预见性应激（CUMS）抑郁大鼠的行为变化及对大鼠脑组织肿瘤坏死因子-α（TNF—α）含量、海马内糖皮质激素受体表达的影响。方法50只Wistar大鼠随机分为正常对照组、模型组、百忧解组、舒郁散小剂量组、舒郁散大剂量组。对大鼠进行21d的CUMS刺激,采用糖水实验、悬尾实验观察大鼠的行为改变．用ELISA法测大鼠脑组织TNF-α含量,免疫组化观察大鼠海马GR表达。结果百忧解组、舒郁散大剂量组大鼠的尾悬不动时间明显延长、糖水消耗百分率明显下降,与模型组比差异显著（P〈0．01）。百忧解、舒郁散大剂量治疗组大鼠悬尾不动时间明显减少,糖水消耗量明显增加,与模型组比差异显著（P〈0．05）。百忧解、舒郁散大剂量治疗组大鼠脑组织TNF—α含量显著降低,与模型组比差异显著（P〈0．05）。模型组海马GR免疫反应阳性神经元数目明显减少,百忧解组、舒郁散大剂量组海马GR免疫反应阳性神经元数目明显增加,平均光密度明显增强,与模型组比差异显著（P〈0．05）。结论动物行为学显示舒郁散具有抗抑郁作用,这种作用与降低CUMS抑郁大鼠脑组织TNF一仪含量,增强海马糖皮质激素受体表达有关,上述作用与其剂量呈正相关。     

Evidence of anti-inflammatory effects of Passiflora edulis in an inflammation model

The popular medicine Passiflora edulis has been used as a sedative, tranquilizer, against cutaneous inflammatory diseases and intermittent fever. Most of the pharmacological investigations of Passiflora edulis have been addressed to its Central Nervous System activities, such as anxiolytic, anticonvulsant and sedative actions. Otherwise, there are few reports about the anti-inflammatory activity of the Passiflora species. The aim of this study was to investigate the mechanism of the anti-inflammatory effect of aqueous lyophilized extract obtained from leaves of Passiflora edulis var. flavicarpa Degener (Passifloraceae) in the mouse model of pleurisy induced by carrageenan (Cg), bradykinin, histamine or substance P, observing the effects upon leucocytes migration, myeloperoxidase (MPO), nitric oxide (NO) concentrations and tumor necrosis factor-alpha (TNFalpha) and interleukin-1 beta (IL-1beta) levels. RESULTS: Passiflora edulis (250mg/kg) administered by intraperitoneal route (i.p.) inhibited the leukocyte, neutrophils, myeloperoxidase, nitric oxide, TNFalpha and IL-1beta levels (P<0.01) in the pleurisy induced by carrageenan. Passiflora edulis (250-500mg/kg, i.p.) also inhibited total and differential leukocytes in the pleurisy induced by bradykinin, histamine or substance P (P<0.05). CONCLUSION: Several mechanisms, including the inhibition of pro-inflammatory cytokines (TNFalpha, IL-1beta), enzyme (myeloperoxidase) and mediators (bradykinin, histamine, substance P, nitric oxide) release and/or action, appear to account for Passiflora edulis's actions.     

TNF-α+308、TNF-α+489基因态性与慢性阻塞性肺疾病的相关性研究

目的探讨TNF-α+308、TNF-α+489基因态性及环境因素与慢性阻塞性肺疾病(COPD)发生的相关性。方法根据患者的年龄、性别,病例组与对照组按1∶2配对设计的病例对照研究方法,调查180例住院COPD患者和360例健康体检者的基本信息,并应用PCR-RFLP技术检测研究对象的TNF-α+308、TNF-α+489的基因型,采用Logistic回归分析TNF-α+308、TNF-α+489基因型和吸烟因素与COPD的关系及其两者间的交互作用。结果①病例组与对照组患者的年龄、性别差异无统计学意义,吸烟、肺癌家族史、FEV1/Pre、FEV1/FVC 2组间差异有统计学意义。②病例组TNF-α+308的等位基因A频率为15.6%,对照组为8.2%,等位基因A发生COPD的风险OR值为2.06(95%CI(1.39,3.05));病例组与对照组的TNF-α+489的等位基因A频率分别为16.1%和6.9%,TNF-α+489等位基因A发生COPD的风险OR值为2.55(95%CI(1.71,3.09))。③以显性遗传模式估计,TNF-α+308(+)联合吸烟因素发生COPD的OR值5.36(95%CI(2.81,10.23)),TNF-α+489(+)联合吸烟因素发生COPD的OR值为8.18(95%CI(4.08,16.38))。④TNF-α+308联合TNF-α+489(+)发生COPD的OR值为4.02(95%CI(1.89,8.52)),高于TNF-α+308、TNF-α+489基因型独立作用。结论 TNF-α+308、TNF-α+489基因多态性与COPD相关,与吸烟因素存在相加正交互作用。TNF-α+308、TNF-α+489基因多态性可增加吸烟患者发生COPD的风险。     

Attenuation of diabetic nephropathy by Chaihuang-Yishen granule through anti-inflammatory mechanism in streptozotocin-induced rat model of diabetics

Ethnopharmacological relevance

Traditional Chinese medical herbs have been used in China for a long time to treat different diseases. Based on traditional Chinese medicine (TCM) principle, Chaihuang-Yishen granule (CHYS) was developed and has been employed clinically to treat chronic kidney disease including diabetic nephropathy (DN). The present study was designed to investigate its mechanism of action in treatment of DN.

Materials and methods

Diabetic rats were established by having a right uninephrectomy plus a single intraperitoneal injection of STZ. Rats were divided into four groups of sham, diabetes, diabetes with CHYS and diabetes with fosinopril. CHYS and fosinopril were given to rats by gavage for 20 weeks. Samples from blood, urine and kidney were collected for biochemical, histological, immunohistochemical and molecular analyses.

Results

Rats treated with CHYS showed reduced 24 h urinary protein excretion, decreased serum TC and TG levels, but CHYS treatment did not affect blood glucose level. Glomerular mesangial expansion and tubulointerstitial fibrosis in diabetic rats were significantly alleviated by CHYS treatment. Moreover, CHYS administration markedly reduced mRNA levels of NF-κB p65 and TGF-β1, as well as decreased protein levels of NF-κB p65, MCP-1, TNF-α and TGF-β1 in the kidney of diabetic rats.

Conclusions

CHYS ameliorates renal injury in diabetic rats through reduction of inflammatory cytokines and their intracellular signaling.