姜黄素治疗炎症性肠病的研究进展

炎症性肠病(IBD)是一种病因不明的慢性非特异性肠道炎症性疾病,其发病与免疫系统功能紊乱密切相关。姜黄素是一种具有抗炎、抗纤维化、抗氧化、抗肿瘤作用的多酚类物质,近年研究表明其在IBD中通过免疫调节发挥明显抗炎作用。本文就姜黄素抗炎、抗纤维化的作用机制及其用于IBD治疗的研究进展作一综述。     

姜黄素在骨伤科的应用研究进展

<正>姜黄为姜科植物姜黄的根茎,味辛、苦,温,归肝、脾经。具有破血行气、通经止痛的功效,是中医学中用以活血疗伤的常用药物。姜黄素是从姜黄中提取的一种相对分子质量小的多酚类物质,是姜黄的主要有效成分,现代药理研究表明,姜黄素具有抗肿瘤、抗氧化、免疫调节及镇痛抗炎等作用~〔1,2〕,已被广泛用于临床并获得显著疗效。近年来许多学者开展了对姜黄素治疗骨伤科疾病的实验研究,取得了良好的成效,为姜黄素在骨伤科的应用提供了理论支持。本文对姜黄素在骨伤科的     

消化系炎性肌纤维母细胞瘤的研究进展

肝纤维化是多种病因所致慢性肝病的共同病理过程,如不及时控制最终将发展为肝硬化,目前尚无有效的抗肝纤维化的药物.姜黄素是一种酚类化合物,具有抗炎、抗肿瘤、抗脂质过氧化等多种药理作用.大量研究证实,姜黄素可通过多种途径发挥抗肝纤维化作用.此文旨在对近年来国内外有关姜黄素的抗肝纤维化作用及机制的研究进展作一综述.     

姜黄素抗肝损伤研究进展

姜黄素(curcumin)是姜黄的活性成分,是一种多酚类物质,有较强的抗氧化和抗炎等药理作用。姜黄素抗肝损伤作用的研究近年来已陆续展开,其作用机理主要表现在清除肝脏自由基、抑制肝脏炎症反应以及抑制肝星状细胞活化等几大方面。其中,有关姜黄素抑制自由基引起的氧化损伤及核因子-κB诱导的炎症反应的研究相对较广泛和深入。研究提示,姜黄素具有阻断、延缓肝损伤病理进程的作用,可能成为一种理想的抗肝损伤药剂,具有良好的应用开发前景。     

姜黄素抗肝纤维化作用及其机制的研究进展

肝纤维化是多种病因所致慢性肝病的共同病理过程,如不及时控制最终将发展为肝硬化,目前尚无有效的抗肝纤维化的药物.姜黄素是一种酚类化合物,具有抗炎、抗肿瘤、抗脂质过氧化等多种药理作用.大量研究证实,姜黄素可通过多种途径发挥抗肝纤维化作用.此文旨在对近年来国内外有关姜黄素的抗肝纤维化作用及机制的研究进展作一综述.     

姜黄素抗动脉粥样硬化作用研究进展

姜黄素是姜黄属中药的主要药理成分,是从姜黄属中药中提取的酚类物质。近年对其药理作用及相关机制进行的研究与探索发现,姜黄素能通过抗氧化、清除自由基、抗凝、抗炎等机制多途径发挥抗动脉粥样硬化作用。     

姜黄素抗肝损伤研究进展

姜黄素（curcumin）是姜黄的活性成分，是一种多酚类物质，有较强的抗氧化和抗炎等药理作用。姜黄素抗肝损伤作用的研究近年来已陆续展开，其作用机理主要表现在清除肝脏自由基、抑制肝脏炎症反应以及抑制肝星状细胞活化等几大方面。其中，有关姜黄素抑制自由基引起的氧化损伤及核因子-κB诱导的炎症反应的研究相对较广泛和深入。研究提示，姜黄素具有阻断、延缓肝损伤病理进程的作用，可能成为一种理想的抗肝损伤药剂，具有良好的应用开发前景。     

姜黄素在心血管疾病中的应用

姜黄素是姜黄根茎中提取的活性成分。大量研究表明,姜黄素具有抗炎、抗氧化、降血糖、调脂、抑制血管生成、抗凝抗血栓等作用。研究证实,姜黄素在急性冠脉综合征、动脉粥样硬化、心力衰竭、代谢综合征治疗中具有良好的疗效和应用前景。     

中药莪术几种活性成分对肝脏疾病防治作用的机制

中药莪术几种主要活性成分如姜黄素、榄香烯、莪术醇、吉马酮对治疗肝脏疾病具有确定的疗效.研究发现姜黄素有抗肿瘤、抗炎、抗纤维化等作用,临床用于治疗慢性肝病、肿瘤等疾病;榄香烯能诱发肿瘤细胞凋亡,抑制肿瘤细胞的生长,提高机体免疫反应,降低放化疗不良反应;莪术醇可以通过抑制细胞因子表达发挥抗肝纤维化作用,并可以通过抑制基因表达诱导瘤细胞的凋亡,发挥抗肿瘤作用;吉马酮则在肝癌细胞的增殖、细胞周期及细胞凋亡等方面均有干预影响,从而呈现抗肝癌作用.     

姜黄素在消化系统疾病治疗中的新进展

姜黄素(CUR)是从植物姜黄中提取的一种天然多酚.近年来,姜黄素的抗肿瘤、抗炎症、抗氧化、促凋亡等药理作用已在消化系统疾病的研究中得到证实,特别是在信号通路转导水平中的作用,已经成为研究热点.文章就姜黄素的生物学特性及其在消化系统中疾病中的研究进展作一综述.     

Formulation Development of a Food-Graded Curcumin-Loaded Medium Chain Triglycerides-Encapsulated Kappa Carrageenan (CUR-MCT-KC) Gel Bead Based Oral Delivery Formulation

In recent years, curcumin has been a major research endeavor in food and biopharmaceutical industries owing to its miscellaneous health benefits. There is an increasing amount of research ongoing in the development of an ideal curcumin delivery system to resolve its limitations and further enhance its solubility, bioavailability and bioactivity. The emergence of food-graded materials and natural polymers has elicited new research interests into enhanced pharmaceutical delivery due to their unique properties as delivery carriers. The current study is to develop a natural and food-graded drug carrier with food-derived MCT oil and a seaweed-extracted polymer called k-carrageenan for oral delivery of curcumin with improved solubility, high gastric resistance, and high encapsulation of curcumin. The application of k-carrageenan as a structuring agent that gelatinizes o/w emulsion is rarely reported and there is so far no MCT-KC system established for the delivery of hydrophobic/lipophilic molecules. This article reports the synthesis and a series of in vitro bio-physicochemical studies to examine the performance of CUR-MCT-KC as an oral delivery system. The solubility of CUR was increased significantly using MCT with a good encapsulation efficiency of 73.98 ± 1.57% and a loading capacity of 1.32 ± 0.03 mg CUR/mL MCT. CUR was successfully loaded in MCT-KC, which was confirmed using FTIR and SEM with good storage and thermal stability. Dissolution study indicated that the solubility of CUR was enhanced two-fold using heated MCT oil as compared to naked or unformulated CUR. In vitro release study revealed that encapsulated CUR was protected from premature burst under simulated gastric environment and released drastically in simulated intestinal condition. The CUR release was active at intestinal pH with the cumulative release of >90% CUR after 5 h incubation, which is the desired outcome for CUR absorption under human intestinal conditions. A similar release profile was also obtained when CUR was replaced with beta-carotene molecules. Hence, the reported findings demonstrate the potencies of MCT-KC as a promising delivery carrier for hydrophobic candidates such as CUR.     

Oral Administration of Curcumin Emulsified in Carboxymethyl Cellulose Has a Potent Anti-inflammatory Effect in the IL-10 Gene-Deficient Mouse Model of IBD

Curcumin is a tumeric-derived, water-insoluble polyphenol with potential beneficial health effects for humans. It has been shown to have preventive as well as therapeutic effects in chemically induced murine models of colitis. To investigate whether curcumin exerts a similar effect on the spontaneous colitis in interleukin (IL)-10 gene-deficient mice, we gavaged these mice daily for 2 weeks with 200 mg/kg per day curcumin emulsified in carboxymethyl cellulose, a food additive generally used as a viscosity modifier. Mice fed the curcumin/carboxymethyl cellulose mixture and those receiving carboxymethyl cellulose alone demonstrated similar reductions in histological injury score and colon weight/length ratio compared to water-fed controls. However, significant reductions in pro-inflammatory cytokine release in intestinal explant cultures were only seen in mice treated with the curcumin mixture. Our data demonstrate that in IL-10 gene-deficient mice, both oral curcumin and carboxymethyl cellulose, appear to have modifying effects on colitis. However, curcumin has additional anti-inflammatory effects mediated through a reduced production of potent pro-inflammatory mucosal cytokines.     

髓样分化因子88对姜黄素诱导肝星状细胞凋亡的影响

目的观察髓样分化因子88在姜黄素促进肝星状细胞(HSC)凋亡中的作用。方法体外培养大鼠肝星状细胞株HSCT6,并分为空白对照组、Control siRNA组、MyD88 siRNA干扰组、姜黄素组、姜黄素+Control siRNA组、姜黄素+MyD88 siRNA干扰组,siRNA处理组给予siRNA干扰48 h后,姜黄素组加入姜黄素作用24 h,各组均在收集细胞前12 h给予LPS诱导,收集各组细胞,Western blotting法检测MyD88蛋白表达;流式细胞术检测细胞凋亡。结果 MyD88 siRNA干扰、姜黄素均可降低MyD88蛋白的表达(P0.05),同时给予MyD88 siRNA干扰和姜黄素作用时与单独给予姜黄素比较,MyD88蛋白下降更明显(P0.05)。MyD88siRNA干扰后HSCs凋亡率无明显增加(P0.05),给予姜黄素处理HSCs凋亡率增加(P0.05),且姜黄素+MyD88 siRNA干扰组的凋亡率升高更明显。结论降低MyD88表达可加强姜黄素促进HSCs凋亡的作用。     

Curcumin (diferuloylmethane) inhibits cell proliferation, induces apoptosis, and decreases hormone levels and secretion in pituitary tumor cells

Prolactinomas are the most prevalent functional pituitary adenomas. Dopamine D2 receptor (D2R) agonists, such as bromocriptine are the first line of therapy; however, drug intolerance/resistance to D2R agonists exists. Apart from D2R agonists, there is no established medical therapy for prolactinomas; therefore, identifying novel therapeutics is warranted. Curcumin, a commonly used food additive in South Asian cooking, inhibits proliferation of several tumor cell lines; however, its effect on pituitary tumor cell proliferation has not been determined. Our objectives were to: 1) determine whether curcumin inhibits proliferation of pituitary tumor cell lines; 2) identify the signaling intermediaries that mediate the effect of curcumin; 3) examine whether curcumin inhibited pituitary hormone production and release; and 4) examine whether curcumin could enhance the growth-inhibitory effect of bromocriptine. Using rat lactotroph cell lines, GH3 and MMQ cells, we report that curcumin had a robust dose and time-dependent inhibitory effect on GH3 and MMQ cell proliferation. Inhibitory effects of curcumin persisted, even on removal of curcumin, and curcumin also blocked colony formation ability of pituitary tumor cells. The growth-inhibitory effect of curcumin was accompanied by decreased expression of cyclin D3 and ser 780 phosphorylation of retinoblastoma protein. In addition, curcumin also induced apoptosis in both GH3 and MMQ cells. Furthermore, curcumin suppresses intracellular levels and release of both prolactin and GH. Finally, we show that low concentrations of curcumin enhanced the growth-inhibitory effect of bromocriptine on MMQ cell proliferation. Taken together we demonstrate that curcumin inhibits pituitary tumor cell proliferation, induces apoptosis, and decreases hormone production and release, and thus, we propose developing curcumin as a novel therapeutic tool in the management of prolactinomas.     

Chloride channel involved in the regulation of curcumin-induced apoptosis of human breast cancer cells

Objective: To investigate the role of ClC-3 chloride channel in the proliferation of breast cancer cell line Mcf-7 treated with curcumin and its specific mechanism. Methods: MTT assay was used to detect the effect of chloride channel blocker(DIDS) and curcumin on Mcf-7 and human normal cell viability. Patch-clamp technique was used to determine the current density before and after drug treatment. Apoptosis assay by flow cytometry was performed for further examination of cell apoptosis. Results: Curcumin had toxicity on Mcf-7 and HUVEC cells and DIDS reduced the survival rate of Mcf-7 cells by inhibiting proliferation. Curcumin could activate the chloride ion current on MCF-7 cell membrane, which would be inhibited by DIDS.Finally, curcumin in low concentration combined with DIDS could significantly promote the MCF-7 cells apoptosis. Conclusions: Our results suggest that ClC-3 protein is involved in the regulation of curcumin induced proliferation inhibiting in breast cancer cells through inducing cell apoptosis. ClC-3 may be a potential target of tumor therapy.     

Interactions between the intestinal microbiota and innate lymphoid cells

The mammalian intestine must manage to contain 100 trillion intestinal bacteria without inducing inappropriate immune responses to these microorganisms. The effects of the immune system on intestinal microorganisms are numerous and well-characterized, and recent research has determined that the microbiota influences the intestinal immune system as well. In this review, we first discuss the intestinal immune system and its role in containing and maintaining tolerance to commensal organisms. We next introduce a category of immune cells, the innate lymphoid cells, and describe their classification and function in intestinal immunology. Finally, we discuss the effects of the intestinal microbiota on innate lymphoid cells.     

Curcumin as a potential therapeutic candidate for Helicobacter pylori associated diseases

Curcumin, a yellow pigment and principal polyphenolic Curcuminoid obtained from the turmeric rhizome Curcuma longa, is commonly used as a food-coloring agent. Studies suggest that curcumin has a wide range of beneficial properties e.g., anti-inflammatory, anti-oxidant, anti-cancer, anti-proliferative, anti-fungal and anti-microbial. These pleiotropic activities prompted several research groups to elucidate the role of curcumin in Helicobacter pylori (H. pylori) infection. This is the first review with this heading where we discussed regarding the role of curcumin as an anti-H. pylori agent along with its potential in other gastrointestinal diseases. Based on several in vitro, early cell culture, animal research and few pre-clinical trials, curcumin projected as a potential therapeutic candidate against H. pylori mediated gastric pathogenesis. This review sheds light on the anti-H. pylori effects of curcumin in different models with meticulous emphasis on its anti-oxidant, anti-inflammatory and anti-carcinogenic effects as well as some critical signaling and effecter molecules. Remarkably, non-toxic molecule curcumin fulfills the characteristics for an ideal chemopreventive agent against H. pylori mediated gastric carcinogenesis but the foremost challenge is to obtain the optimum therapeutic levels of curcumin, due to its low solubility and poor bioavailability. Further, we have discussed about the possibilities for improving its efficacy and bioavailability. Lastly, we concluded with the anticipation that in near future curcumin may be used to develop a therapeutic drug against H. pylori mediated gastric ailments through improved formulation or delivery systems, facilitating its enhanced absorption and cellular uptake.