Advances in Experimental Studies on Treatment of Psoriasis by Traditional Chinese Medicine

Traditional Chinese medicine has demonstrated its strength in treating psoriasis, which is characterized by a variety of methods of treatment, flexible use of drugs, high efficacy, low recurrence, and few side-effects. Experimental studies on the mechanism governing the TCM treatment of psoriasis have been conducted at the cellular level and the molecular level. The studies on proliferation and differentiation of keratinocytes and the inhibitory effect against them, apoptosis, intercellular adhesion molecules, cytokine, and haemorheology indicate that the laboratory studies on the treatment of psoriasis have now entered a very high stage since the eighties. The studies on relationship between typing of psoriasis based on TCM differentiation of symptoms and signs and changes in some laboratory indexes have been carried out by some researchers to explore the inherent pathological changes in typing of psoriasis based on TCM differentiation of symptoms and signs and to provide scientific basis for the differentiation and typing under a unified standard. However, the present studies lack depth and scope in the methods. In future, the laboratory studies should be enhanced to go further into the principles governing the TCM treatment of psoriasis and to seek new drugs that will be even more effective for psoriasis and can bring its relapse under control.     

肠道微生态与银屑病的中医研究

银屑病是一种常见的以慢性炎性反应为特征的全身心身疾病,与肠道菌群紊乱密切相关。中医的整体观和恒动观与肠道微生态的整体性、动态性特征相契合;"肺与大肠相表里"、"肺主皮毛"、"肠-脑-皮轴"学说,及已有有关中医药维持肠道微生态稳态的研究,为从肠道微生态角度探索银屑病的中医诊治机制提供了依据。将传统中医证候与客观的微生态学相结合,明确不同中医证型肠道微生态的特征性变化,探究可调节此类肠道微生态失调的中药复方制剂或单味药物,通过肠道菌群与中医"方"和"证"结合研究以寻找中医药治疗银屑病的新思路及新方法。     

腺病毒介导的SOCS3对银屑病小鼠模型治疗的实验研究

目的研究腺病毒介导的SOCS3对银屑病小鼠模型的治疗作用。方法获得重组腺病毒Ad—SOCS3,用WesternBlot分析Ad—SOCS3在TC-1细胞中的表达。用流式细胞仪检测对TC-1的细胞凋亡。腹腔注射Ad-SOCS3小鼠银屑病模型,观察小鼠阴道上皮有丝分裂,用ELISA检测血清中IL-6和TNF-α浓度。结果SOCS3在TC-1能有效表达。与Ad—SOCS3的感染复数相关。Ad-SOCS3能显著抑制TNF-α介导的细胞凋亡（P〈0．01）。Ad—SOCS3能抑制雌激素期小鼠阴道上皮有丝分裂（P〈0．01）,较Ad—EGFP,Ad-SOCS3降低血清中IL-6和TNF-α浓度（P〈0．01）。结论Ad-SOCS3能抑制炎性因子诱导的细胞凋亡和炎症,其对银屑病具有潜在的治疗价值。     

Bcl-2、Caspase-3、Survivin与银屑病的研究进展

Bcl-2、caspase-3、survivin是细胞凋亡过程中重要的调控基因,在银屑病角质形成细胞凋亡中,三种蛋白起着非常重要的作用。Bcl-2是一种凋亡抑制基因,可延长细胞的生存期,caspase-3可促进细胞凋亡,survivin是迄今发现最强的凋亡抑制因子,具有抑制细胞凋亡、促进细胞增殖的作用,在银屑病皮损中Bcl-2呈低表达,caspase-3、survivin呈高表达,三种蛋白的相互作用,可能导致银屑病角质形成细胞的生存期缩短、凋亡速度加快,同时细胞增殖明显,从而维持银屑病表皮的良性增生状态。     

Effect of Cytokines Secreted by Human Adipose Stromal Cells on Endothelial Cells

Recently, several observations have pointed to the presence of a population named adipose-derived adult stem cells (ADAS) or adipose stromal cells (ASCs) in human adipose tissue. Subsequent studies revealed that ASCs were multipotent, differentiating along the cardiac myocyte, endothelial, neuronal, and other cells lineages[1, 2], and could secrete cytokines such as HGF and VEGF[3]. Since adipose tissue is an abundant, accessible, and re- plenishable source of adult stem cells that can b…     

Effects of Baicalin on Expression of Inducible Nitric Oxide Synthase in Cultured Fibroblasts Stimulated by Cytokines

Objective: To investigate the effects of baicalin on expression of inducible nitric oxide synthase (iNOS) in fibroblasts and its mechanisms in treating psoriasis. Methods: Fibroblasts cultured in vitro were stimulated with tumor necrosis factor-α(TNF-α), interferon-γ (IFN-γ), interleukin-8 (IL-S) in different groups. iNOS was detected by western blot and immunocytochemistry assay, and in addition, the effects of baicalin on its expression were investigated. Results: Fibroblasts did not express iNOS without cytokine stimulation. When treated for 24 h with 1. 0× 106 U/L TNF-α, 0.2× 106U/L IFN-γ, 0.2× 106 pg/L IL-8 alone or in combinations indicated, fibroblasts produced iNOS when stimulated by TNF-α alone while neither IFN-γ nor IL-8 could induce the production of iNOS. The combination of TNF-α and IL-8 induced a strong expression of iNOS, the combined exposure of three kinds of cytokines showed an even stronger effects. The strongly stained area was in the cytoplasm near the nuclei. Expression of iNOS induced by TNF-α and IL-8 was inhibited by 50 μg/ mi of baicalin. Conclusion: Fibroblasts might express iNOS when stimulated by certain cytokines. Baicalin decreased production of nitric oxide through inhibiting the expression of iNOS, furthermore it reduced inflammation, which might be part of its mechanisms in treating psoriasis.     

Antitumor Effect of Interferon-α on U937 Human Acute Leukemia Cells in vitro and Its Molecular Mechanism

In order to investigate the antitumor effect and molecular mechanism of interferon-α(IFN-α) on human acute myeloid leukemia cell line U937 cells in vitro,the proliferation of U937 cells was determined by MTT assay,the apoptosis rate was analyzed by flow cytometry(FCM),and the mRNA expression of cell cycle regulatory protein cyclin E was detected by RT-PCR.The results showed that IFN-α could inhibit the proliferation of U937 cells significantly in a dose-and time-dependent way(P<0.01),and induce the apoptosis of U937 cells also in a dose-and time-dependent manner at the concentration of 1000-4000 U/L(P<0.01).The apoptosis rate of U937 cells was even over 50% when cultured with IFN-α for 36-48 h at the concentration of 2000-4000 U/L.Moreover,the expression of cyclin E mRNA was markedly inhibited by the addition of IFN-α,and the inhibition was time-dependent(P<0.01).It was concluded that the anti-leukemia mechanism of IFN-α might be correlated with its antiproliferative and apoptotic inducing effects,and the down-regulation of the cyclin E expression might be one of its molecular mechanisms.     

中药保护关节软骨的作用机制研究进展

通过文献整理,从组织形态学、细胞因子、软骨细胞凋亡等多方面概述了近些年来中药在保护关节软骨方面的作用机制及研究进展,中药治疗骨关节炎主要通过减轻损伤、延缓退变及促进软骨分化和修复起作用,其机制包括:1)抑制软骨细胞炎性因子的表达及产生;2)抑制关节软骨基质金属蛋白酶表达;3)促进生长因子表达;4)促进胶原蛋白形成;5)促进关节软骨细胞增殖;6)抑制关节软骨细胞凋亡等方面。     

Triptolide-induced apoptosis by inactivating nuclear factor-kappa B apoptotic pathway in multiple myeloma <Emphasis Type="Italic">in vitro</Emphasis>

The effect of triptolide on proliferation and apoptosis of human multiple myeloma RPMI-8226 cells in vitro,as well as the roles of nuclear factor-kappa B(NF-κB) and IκBα was investigated.The effect of tritptolide on the growth of RPMI-8226 cells was studied by MTT assay.Apoptosis was detected by Hoechest 33258 staining and Annexin V/PI double staining assay.The expression of NF-κB and IκBα was observed by Western blot and confocal microscopy.The results showed that triptolide inactivated NF-κB apoptotic pathway in human multiple myeloma RPMI-8226 cells.Triptolide at nM range induced proliferation inhibition in a dose-and time-dependent manner and apoptosis in a dose-dependent fashion in RPMI-8226 cells.Besides,we observed the inhibition of NF-κB /p65 in the nuclear fraction was correlated with the increase in the protein expression of IκBα in the cytosol.These results suggested that triptolide might exhibit its strong anti-tumor effects via inactivation of NF-κB/p65 and IκBα.     

中药影响炎症免疫反应的机制研究进展

炎症免疫反应是血管系统的活体组织对损伤因子的防御反应,是由损伤因子引起的组织损伤。临床药理学对炎症免疫反应的研究集中于作用机制方面,而中药影响炎症免疫反应的机制包括影响下丘脑-垂体-肾上腺皮质轴的功能、炎性介质的作用、核因子的功能、活性氧的生成、细胞功能而导致凋亡以及神经内分泌激素的生成等。因许多化学药物在影响炎症免疫反应过程中存在严重不良反应,而中药的不良反应少,故中药影响炎症免疫反应的机制已受到广泛的关注。     

核因子-κB在皮肤病中的研究进展

核因子-κB是一种具有多项转录调节作用的蛋白质,通过调节免疫和炎症相关因子及炎症递质的表达,在炎症和免疫反应中起枢纽作用,此外在细胞增殖和凋亡相关基因的调控中也起关键作用。多种皮肤病,如银屑病、结缔组织病、特应性皮炎、皮肤肿瘤等与核因子-κB途径的失调有关,本文就核因子-κB的组成、功能及在皮肤病发病机制中的研究进展作一综述。     

趋化因子在银屑病发病机制中的作用

银屑病是一种免疫诱导的慢性炎性反应性皮肤病,多种细胞及细胞因子在疾病的不同阶段分别发挥着主导作用,炎性反应细胞浸润皮肤并释放各种细胞因子启动及加重银屑病皮损的发生。趋化因子是一大类具有控制炎性反应细胞定向迁移的细胞因子,多种趋化因子参与了银屑病的发病:CCL17及CCL27在T淋巴细胞归巢至皮肤的过程中发挥作用;CCL2、CXCL8等参与了角质细胞增生及新生血管的形成;此外,CCL2、CX3CR1的单核苷酸多态性与银屑病的发病密切相关。     

Dual Effect of 3, 4-Dihydroxyacetophenone on LPS-induced Apoptosis in RAW264.7 Cells by Modulating the Production of TNF-α

To explore the pharmacological effect of 3,4-dihydroxyacetophenone (DHAP) on the apoptosis of RAW264. 7 macrophage cells and the mechanism, RAW264. 7 macrophage cells were treated with 100 or 500 mg/L lipopolysaccharide (LPS), with or without 10^-5 mol/L DHAP for 24 h. Trypan blue dye exclusion assay was used to assess cell viability. Cell apoptosis was morphological studied and flow cytometric assay was used. Tumor necrosis factor-α (TNF-α) level was measured by ELISA methods. IκB protein was determined by Western blotting. Our results showed that in 100 mg/L LPS stimulated macrophages, DHAP enhanced the cell apoptosis while in 500 mg/L LPS-stimulated macrophages, DHAP significantly inhibited the cell apoptosis. In both groups, DHAP increased the level of IκB but decreased the level of TNF-α. It is concluded that DHAP has dual effect on the apoptosis of RAW 264.7 cells treated with different concentrations of LPS. This effect may be due to the inhibition of activation of NF-κB and autocrine production of TNFα. Our study suggests that DHAP may have anti-inflammatory effect on LPS-activated macrophages.     

独活寄生汤加减治疗风湿性关节炎的研究概况

多项研究表明关节腔滑膜炎症、软骨和骨组织破坏、免疫反应、微循环障碍等是引起风湿性关节炎的关键因素。独活寄生汤加减在风湿性关节炎的中药治疗中应用广泛,近年的研究表明独活寄生汤具有抑制炎症反应、镇痛、抑制软骨细胞凋亡、促进软骨细胞增殖、调节免疫平衡、改善血管循环等作用,故推断出独活寄生汤加减治疗风湿性关节炎与上述机制有关,对其研究进行综述如文。     

Heat-Clearing Chinese Medicines in Lipopolysaccharide-Induced Inflammation

Lipopolysaccharide (LPS)-induced inflammation causes massive threatening diseases, such as sepsis, acute lung injury and multiple organ dysfunction syndrome. Efficient treatment to prevent inflammation is crucial in LPS-induced inflammatory diseases. Heat-clearing Chinese medicines (CMs) have been used to ameliorate LPS-induced inflammation in China for centuries. Heat-clearing CMs regulate inflammatory pathways, thereby inhibiting the release of inflammatory factors. This review aimed to introduce promising heat-clearing CMs countering LPS-induced inflammation in the last 5 years, exploring the underlying molecular mechanisms.     

Mechanism of traditional Chinese medicine in the treatment of allergic rhinitis

Objective To review the major progress in mechanism of traditional Chinese medicine (TCM) in the treatment of allergic rhinitis (AR).Methods Contents about the treatment mechanism of TCM in the therapy...     

中医药抗乳腺癌细胞实验研究进展

对近年来中医药抗乳腺癌细胞的机理进行综述,实验研究表明主要通过抑制细胞增殖,促进凋亡,发挥细胞毒,去甲基化等作用达到抗癌效应,并针对细胞实验研究中存在的某些问题予以探讨。     

他汀类药物对血管平滑肌细胞的影响及机制

心血管疾病尤其是冠状动脉硬化性心脏病具有很高的死亡率和发病率,对这些冠脉疾病的病因分析,认为动脉粥样硬化是主要原因。动脉壁脂质沉积和血管平滑肌细胞的异常迁移与增殖是动脉粥样硬化形成的两个关键步骤。目前抗动脉粥样硬化以调脂药物如三羟基三甲基戊二酰辅酶A（HMG-COA）还原酶抑制剂（即他汀类药物）为主,临床实验和基础研究表明：他汀类药物不仅具有调控血浆胆固醇的主要作用,而且还涉及其非调脂的抗动脉粥样硬化作用,如抗炎症反应、抑制血小板聚集、抑制血管平滑肌细胞增殖与迁移、促进血管平滑肌细胞凋亡和改善内皮功能等。本文主要就他汀类药物对血管平滑肌细胞增殖、迁移、凋亡的影响及其机制做如下综述。     

NF—κB信号通路在脑缺血再灌注损伤中的作用及中药有效组（成）分的干预研究

脑缺血／再灌注损伤（cerebral ischemia reperfusion injury,CIRI）是一种机制复杂的级联反应性疾病,在其机制中炎症反应最为关键。核因子-κB（nuclear factor—κappa B,NF—κB）信号通路作为炎症反应的主要环节,通过调节多种细胞因子及下游基因表达启动炎症反应与细胞凋亡。目前研究显示,部分中药有效成分对CIRI具有保护作用,为明确中药有效成分在CIRI中的作用机理,就近年来NF-κB信号通路在CIRI后炎症反应及细胞凋亡方面可能相关作用作一综述。     

The Role of IκBα in TNF-α-induced Apoptosis in Hepatic Stellate Cell Line HSC-T6

To investigate the role of NF-κB in TNF-α induced apoptosis in HSC-T6, a mutant IκBα was transfected into HSC-T6 cells by lipofectin transfection technique and its transient effect was examined 48 h after the transfection. The activation of NF-κB was detected by immune fluorescence cytochemistry and Western blotting with anti-p65 antibody. The apoptosis and the rate of inhibition by TNF-α in both transfected and untransfected HSC-T6 cells were measured respectively by FAC-Scan side scatter analysis and MTF methods. Our results showed that TNF-α could activate NF-κB in untransfected cells but not in transfected HSC-T6 cells. The percentage of apoptosis in transfected cells were significantly higher than that in the untransfected ones （P〈0.01） and it was also true of the inhibition rate （P〈0.01）. It is concluded that the resistance of HSC-T6 towards apoptosis induced by TNF-α can be mediated by NF-κB activation. The inhibition of NF-κB activation by mutant IκBα can attenuate the resistance of HSC-T6 cells and increase its sensitivity to TNF-α.