藿香正气片增强镇静催眠药的镇静与催眠作用的研究

目的研究藿香正气片增强镇静催眠药对小鼠的镇静催眠作用.为临床增添了一个中西药结合的镇静催眠合剂提供药理依据.方法应用抖笼换能器法观察藿香正气片对小鼠的自发活动的影响.由此观察藿香正气片与镇静催眠药的协同作用.测定藿香正气片与镇静催眠药对小鼠的入睡时间及睡眠持续时间的作用.两个实验均分成四组,生理水组、藿香正气片组、安定组、安定+藿香正气片组.结果1.对小鼠自发活动的影响.(1)藿香正气片组与生理盐水组比较,具有极显著性差异(P＜0.01).(2)安定组与安定+藿香正气片组比较具有显著性差异(P＜0.05).2.藿香正气片增强镇静催眠药对小鼠的睡眠作用.(1)藿香正气片组与生理盐水组比较具有显著性差异(P＜0.05).(2)藿香正气片+安定组与安定组比较具有极显著性差异(P＜0.01).结论藿香正气片与安定合用对镇静及催眠确有协同作用.     

阿斯匹林对胃癌细胞株SGC-7901的细胞毒作用及体外增效作用

目的：观察阿斯匹林（ASA）对胃癌细胞株SGC－7901的细胞毒作用以及联用其它抗肿瘤药的增效作用。方法：应用流式细胞仪（FCM）测定细胞周期,噻唑蓝（MTT）法测定药物细胞的抑制率。结果：MTT显示体外ASA对SGC－7901有细胞毒作用,与ASA的浓度和作用时间有显著的相关性。同时可使SGC－7901细胞周期中S期及G2／M期比例升高,G1期比例下降,呈一定的剂量效应关系。低浓度ASA与5－氟脲噻啶（5－Fu)、阿霉素（DOX）和丝列霉素（MMC）合用,可增强它们对SGC－7901的杀伤作用,与各药物有相加或协同作用。结论：ASA体外对SGC－7901有细胞毒作用,可明显阻断SGC－7901细胞在S期和G2／M期;增强上述药物对SGC－7901的杀伤作用。鉴于所试药物对细胞周期的影响不同,提示ASA的体外增效作用可能与此相关。     

姜黄素与羟基脲对K562细胞的体外联合作用

目的 了解姜黄素与羟基脲合用对人白血病Ｋ５６２细胞的体外作用。方法 采用ＭＴＴ法测定药物的体外杀伤作用,应用ＡＯ／ＥＢ荧光染料染色观察药物诱导细胞凋亡,金氏公式进行联合用药分析。结果 姜黄素５,１０ｕｇ／ｍｌ,羟基脲２５,５０ｕｇ／ｍｌ同时给药,对Ｋ５６２细胞可产生单纯相加的协同杀伤效果。姜黄素与羟基脲同时给药诱导Ｋ５６２细胞凋亡率高于羟基脲单独用药,低于姜黄素单独用药。结论 姜黄素与羟基脲同时联     

工程化纳米囊泡结合化疗用于增强肿瘤免疫治疗

目的：结合免疫治疗与化疗,以改善肿瘤的治疗效果,为安全有效的肿瘤免疫治疗策略的发展提供更多见解。方法：使用工程化纳米囊泡,囊泡膜上表达PD-1受体,可以靶向肿瘤细胞表面的PD-L1,通过破坏PD-1/PD-L1免疫抑制通路增强抗肿瘤反应。同时,囊泡包裹的化疗药物阿霉素可以进入肿瘤细胞核,抑制DNA与RNA的合成,诱导肿瘤细胞死亡。结果：实验证实,制备的PD1-阿霉素材料具备良好的稳定性、安全性,能准确靶向肿瘤部位,阿霉素在细胞核部位起作用,能有效地进行肿瘤杀伤。结论：本研究首次将PD-1免疫检查点抑制与化疗药物阿霉素相结合,利用PD-1囊泡安全性高、长循环的特点作为包裹化疗药物阿霉素的载体,这种方法可以进行肿瘤细胞的有效靶向与治疗,实现肿瘤的有效清除。     

骆驼蓬总碱抗肿瘤及其协同抗瘤作用

用小鼠移植性肿瘤和裸鼠异体移植人肿瘤模型研究骆驼蓬总碱（TAH）抗肿瘤作用及其协同抗瘤作用。结果表明：TAH对小鼠S-180、LⅡ、肝癌以及裸鼠移植人鼻咽癌（CNE2）和人（BEL-7402）肝癌均有抗肿瘤作用，并发现TAH与顺铂（DDP）或阿霉素（ADM）合用，具有协同抗肿瘤作用。     

金属离子对果胶酶的协同作用研究

以香蕉皮为原料,在固定pH值、温度、加热时间的实验条件下,采用酸醇沉淀的实验工艺,探讨不同金属离子(铜、铅、镁)及同种离子不同浓度对果胶提取率的影响,从而确定金属离子对果胶酶的协同作用。     

联合新型Bcl-2反义核酸与足叶乙苷抑制人小细胞肺癌细胞的增殖

目的　研究一种新型Bcl 2反义寡核苷酸 F95 1在与足叶乙苷 (VP16 )联合使用时 ,对人小细胞肺癌细胞增殖的影响。方法　分别单独及联合应用F95 1、VP16于人小细胞肺癌细胞株NCI H4 4 6 ,通过MTT法检测细胞存活率 ,通过集落形成法检测集落生存率 ,按Welander法计算联合应用组的预测值 ,通过实测值与预测值的比较进行效应分析。结果　细胞存活率 (MTT法 )和集落生存率 (集落形成法 )均显示联合应用F95 1、VP16组的实测值明显低于预测值。结论　联合应用F95 1与VP16对人小细胞肺癌细胞的增殖有协同的抑制作用。     

Inorganic Nanoparticle-Modified Poly(Phenylene Sulphide)/Carbon Fiber Laminates: Thermomechanical Behaviour

Carbon fiber (CF)-reinforced high-temperature thermoplastics such as poly(phenylene sulphide) (PPS) are widely used in structural composites for aerospace and automotive applications. The porosity of CF-reinforced polymers is a very important topic for practical applications since there is a direct correlation between void content and mechanical properties. In this study, inorganic fullerene-like tungsten disulphide (IF-WS₂) lubricant nanoparticles were used to manufacture PPS/IF-WS₂/CF laminates via melt-blending and hot-press processing, and the effect of IF-WS₂ loading on the quality, thermal and mechanical behaviour of the hybrid composites was investigated. The addition of IF-WS₂ improved fiber impregnation, resulting in lower degree of porosity and increased delamination resistance, compression and flexural properties; their reinforcement effect was greater at temperatures above the glass transition (T_g). IF-WS₂ contents higher than 0.5 wt % increased T_g and the heat deflection temperature while reduced the coefficient of thermal expansion. The multiscale laminates exhibited higher ignition point and notably reduced peak heat release rate compared to PPS/CF. The coexistence of micro- and nano-scale fillers resulted in synergistic effects that enhanced the stiffness, strength, thermal conductivity and flame retardancy of the matrix. The results presented herein demonstrate that the IF-WS₂ are very promising nanofillers to improve the thermomechanical properties of conventional thermoplastic/CF composites.     

The synergistic antitumor activity of 3-(2-nitrophenyl) propionic acid-paclitaxel nanoparticles (NPPA-PTX NPs) and anti-PD-L1 antibody inducing immunogenic cell death

Cancer immunotherapy is a strategy that is moving to the frontier of cancer treatment in the current decade. In this study, we show evidence that 3-(2-nitrophenyl) propionic acid-paclitaxel nanoparticles (NPPA-PTX NPs), act as immunogenic cell death (ICD) inducers, stimulating an antitumor response which results in synergistic antitumor activity by combining anti-PD-L1 antibody (aPD-L1) in vivo. To investigate the antitumor immunity induced by NPPA-PTX NPs, the expression of both ICD marker calreticulin (CRT) and high mobility group box 1 (HMGB1) were analyzed. In addition, the antitumor activity of NPPA-PTX NPs combined with aPD-L1 in vivo was also investigated. The immune response was also measured through quantitation of the infiltration of T cells and the secretion of pro-inflammatory cytokines. The results demonstrate that NPPA-PTX NPs induce ICD of MDA-MB-231 and 4T1 cells through upregulation of CRT and HMGB1, reactivating the antitumor immunity via recruitment of infiltrating CD3+, CD4+, CD8+ T cells, secreting IFN-γ, TNF-α, and the enhanced antitumor activity by combining with aPD-L1. These data suggest that the combined therapy has a synergistic antitumor activity and has the potential to be developed into a novel therapeutic regimen for cancer patients.     

AZT and emodin exhibit synergistic growth-inhibitory effects on K562/ADM cells by inducing S phase cell cycle arrest and suppressing MDR1 mRNA/p-gp protein expression

Abstract

Context: Previous studies have demonstrated that both 3′-azido-3′-deoxythymidine (AZT) and emodin, a traditional chemotherapy agent, can inhibit the growth of many types of cancer cells.

Objective: This study aimed to evaluate the effect of AZT and emodin on adriamycin-resistant human chronic myelogenous leukemia (K562/ADM) cells, determine the expression of multidrug resistance 1 (MDR1) mRNA/p-glycoprotein (p-gp) protein, a protein known to induce resistance to anticancer agents, and to elucidate the underlying molecular mechanisms.

Materials and methods: K562/ADM cells were treated with AZT (10–160?μM) or emodin (5–80?μM) for 24,?48 and 72?h and cell viability was measured using the MTT assay. The effect of AZT (16.5, 33 and 66?μM) and emodin (6.1,?17.6 and 33.2?μM) on K562/ADM cell cycle distribution was determined by flow cytometry, and MDR1 mRNA/p-gp protein expression was determined by real time RT-PCR and western blotting.

Results: The growth suppression of emodin was dramatically enhanced by AZT in K562/ADM cells. The IC₅₀ of AZT and emodin was lower than that of emodin alone. All examined combinations of AZT and emodin yielded a synergetic effect (CI?<?1). Furthermore, AZT and emodin altered the cell cycle distribution and led to an accumulation of cells in S phase. Meanwhile, the expression of MDR1 mRNA/p-gp protein was markedly decreased.

Discussion and conclusion: These results show a synergistic growth-inhibitory effect of AZT and emodin in K562/ADM cells, which is achieved through S phase arrest. MDR1 might ultimately be responsible for these phenomena.