茶及其提取物对肺癌等恶性肿瘤的预防治疗作用研究

茶叶中富含茶多酚等抗氧化成分,对肺癌等恶性肿瘤有良好的预防治疗作用。本文综述了茶叶及其提取物对吸烟和被动吸烟诱发的肺癌及相关肿瘤预防治疗作用研究,对比分析茶多酚的抗癌作用机理,提出通过将不同茶类的茶多酚提取物用于吸烟与被动吸烟诱发的肺部损伤及肺癌治疗对比,与防癌、抗癌开发热点的茶多酚单体——EGCG比较,获取防癌、抗癌活性相对较强的茶多酚混合体,并为广大烟民饮用合适的茶类提供参考。     

茶叶减轻吸烟危害相关产品的开发探讨

茶叶中的抗氧化成分,可抑制香烟的致突变作用,还能在体内阻断致癌物的合成,有助于防止由于吸烟而发生的DNA损伤以及辐射的污染,还可有效预防烟民白内障的发生和补充维生素C等。本文对茶叶减轻吸烟危害相关产品的开发作了介绍,并对其进行探讨,以期找到一条利用茶叶减轻吸烟危害的有效途径。     

茶多酚对实验性肿瘤的治疗作用

茶多酚是从传统饮料茶叶中提取的一类多酚类化合物,主要成分为儿茶素(约占茶多酚总量的80％) 对茶叶及其提取物的药效药理研究表明,茶叶及其提取物能明显抑制有致癌作用的亚硝基化合物在体外及动物和人体内的合成,能抑制多种致癌物对动物的致癌作用,也能抑制或减少某些肿瘤的发生和生长等。研究结果还表明,茶叶提取物的防癌抗癌作用主要的有效物质是茶多酚类化合物。本文报道茶多酚对动物实验性肿瘤的治疗和对荷瘤小鼠的细胞免疫的影响,并对其作用机制进行探讨。     

茶多酚抑癌变作用研究进展

本文从自由基学说和化学致癌因素出发，综合近几年国内外茶学界、医学界就自由基在癌变中的作用及茶多酚对自由基清除作用的研究成果，论述了茶叶有机成份──茶多酚对肿瘤的预防和辅助治疗作用，便于进一步了解自由基与肿瘤病的关系及茶多酚抑制癌变作用的机制，为茶多酚开发成天然的预防癌症和癌症辅助治疗用药药物报供依据。     

浅谈茶叶的肿瘤防治作用

茶,作为一种有治愈性的饮品,它的治愈性绝不仅仅体现在它提神醒脑的功能上,更体现在它对身体的治愈作用上。近年来,已经有不少的研究发现,茶叶中含有的茶多酚对身体的各项机理都是非常有益的作用。因此,对其功能的利用可以帮助我们调节身体内部的系统,改善身体的状况,对身体上的某些重大疾病,它也有一定的治疗和控制的效果。也有研究表明,茶多酚可以有效的控制细胞的癌变,因此,在对肿瘤的防治上,茶叶有着较高的研究价值。本文首先对茶叶中茶多酚的组成做出了大体的介绍,对茶多酚的功能进行了具体的分解,最后对茶叶在肿瘤防治上的作用做了深入的研究,希望能够为目前的肿瘤防治工作提供新的研究方向。     

茶多酚感官性质及其对茶叶涩味的影响

茶叶中含有的大量茶多酚对茶叶涩味有重要作用。涩味是茶叶滋味中极重要的感官性质,对茶叶总体质量至关重要。本文就茶叶中茶多酚的感官性质、茶汤涩味分析及茶多酚对茶叶涩味的影响等方面进行综述。     

吸附色谱法用于茶多酚的分离提取

茶多酚是茶叶中具保保健功能的重要化学物质,研究表明,茶多酚具有诸多生理活性和药理作用,如抗氧化、清除自由基、降血脂、降血压、预防心血管疾病、抗突变、抗辐射、抗癌防癌、抑菌、防龋等.茶多酚已开始工厂化生产并应用于食品、化妆品和医药品等领域,因此,安全、有效地从茶叶中提取和制备茶多酚产品具有重要的意义.     

乌龙茶预防食管癌的流行病学研究

已有流行病学和实验室研究资料表明,茶叶中的主要组分茶多酚、儿茶素可能对多种化学致癌物引起的肿瘤(特别是上消化道肿瘤)具有预防作用[1￣4]。福建省安溪县是全国乌龙茶的主要产地,每年产量为3万t,为了探讨饮用乌龙茶与食管癌的关系,并为今后食管癌的预防提供依据,我们与安溪     

茶多酚作为保健型香烟添加剂的综合开发

从中低档茶中提取茶多酚,将其添加到香烟中,降低香烟燃烧时产生自由基对人体的毒害,开发新型保健型香烟投放市场,既为广大烟民提供一种相对保健的香烟产品,还可提高中低档茶产品附加值。本文论述了香烟吸食社会化流行的成因、毒害发生机理;茶多酚降低香烟中自由基的产生机理,茶多酚作为添加剂在中式香烟中的开发形式。发挥茶多酚抗氧化功能、开发出新型保健型香烟,以降低香烟对人体的危害。     

茶多酚的抗低密度脂蛋白氧化作用

低密度脂蛋白(LDL)的氧化是动脉粥样硬化的特征之一，在脂肪沉着性动脉硬化斑块中有氧化修饰的LDL，但是正常的动脉壁没有。LDL颗粒的氧化修饰可以决定动脉粥样硬化的发生和发展。流行病学研究显示，茶叶和茶叶提取物茶多酚的摄入，与动脉粥样硬化引起的冠心病、心肌梗塞和中风导致的死亡呈负相关，其机制在于作为天然饮料的茶叶中的茶多酚能在体内抑制铜催化的、紫外线诱导的和巨噬细胞介导的LDL氧化。……     

Cytotoxic Effects of Fascaplysin against Small Cell Lung Cancer Cell Lines

Fascaplysin, the natural product of a marine sponge, exhibits anticancer activity against a broad range of tumor cells, presumably through interaction with DNA, and/or as a highly selective cyclin-dependent kinase 4 (CDK4) inhibitor. In this study, cytotoxic activity of fascaplysin against a panel of small cell lung cancer (SCLC) cell lines and putative synergism with chemotherapeutics was investigated. SCLC responds to first-line chemotherapy with platinum-based drugs/etoposide, but relapses early with topotecan remaining as the single approved therapeutic agent. Fascaplysin was found to show high cytotoxicity against SCLC cells and to induce cell cycle arrest in G1/0 at lower and S-phase at higher concentrations, respectively. The compound generated reactive oxygen species (ROS) and induced apoptotic cell death in the chemoresistant NCI-H417 SCLC cell line. Furthermore, fascaplysin revealed marked synergism with the topoisomerase I-directed camptothecin and 10-hydroxy-camptothecin. The Poly(ADP-ribose)-Polymerase 1 (PARP1) inhibitor BYK 204165 antagonized the cytotoxic activity of fascaplysin, pointing to the involvement of DNA repair in response to the anticancer activity of the drug. In conclusion, fascaplysin seems to be suitable for treatment of SCLC, based on high cytotoxic activity through multiple routes of action, affecting topoisomerase I, integrity of DNA and generation of ROS.     

茶多糖对阿霉素抑制肺癌A549细胞增殖作用的影响

肺癌是全世界目前发病率和死亡率最高的癌症之一,当前治疗恶性肿瘤的主要手段之一是化疗,阿霉素是临床常用的化疗药物,然而该药物毒性较大,长期使用可发生剂量依赖性的不可逆的心肌病变、骨髓抑制等,同时其多药耐药性的存在也使它在临床应用受到一定限制。为了减少阿霉素的毒副作用,通过体外培养人肺癌A549细胞,将茶叶提取物茶多糖与阿霉素联用,加入A549细胞,24 h后以噻唑蓝(MTT)法检测细胞存活率。结果表明,当阿霉素质量浓度为3 mg·L~(-1)时,对肺癌A549细胞的抑制效果最明显;不同浓度茶多糖与1、2、3 mg·L~(-1)阿霉素联用,以2 mg·L~(-1)阿霉素与6 mg·L~(-1)茶多糖联用时对肺癌A549细胞的抑制效果最明显,且优于单独使用3 mg·L~(-1)阿霉素的效果。阿霉素可诱导A549细胞凋亡,茶多糖与阿霉素联用可减少阿霉素的使用剂量,增强阿霉素对肺癌A549细胞的增殖抑制作用。     

Targeting EGFR in Combination with Nutritional Supplements on Antitumor Efficacy in a Lung Cancer Mouse Model

Selenium (Se) and fish oil (FO) exert anti-epidermal growth factor receptor (EGFR) action on tumors. This study aimed to compare the anti-cancer efficacy of EGFR inhibitors (gefitinib and erlotinib) alone and in combination with nutritional supplements of Se/FO in treating lung cancer. Lewis LLC1 tumor-bearing mice were treated with a vehicle or Se/FO, gefitinib or gefitinib plus Se/FO, and erlotinib or erlotinib plus Se/FO. The tumors were assessed for mRNA and protein expressions of relevant signaling molecules. Untreated tumor-bearing mice had the lowest body weight and highest tumor weight and volume of all the mice. Mice receiving the combination treatment with Se/FO and gefitinib or erlotinib had a lower tumor volume and weight and fewer metastases than did those treated with gefitinib or erlotinib alone. The combination treatment exhibited greater alterations in receptor signaling molecules (lower EGFR/TGF-β/TβR/AXL/Wnt3a/Wnt5a/FZD7/β-catenin; higher GSK-3β) and immune checkpoint molecules (lower PD-1/PD-L1/CD80/CTLA-4/IL-6; higher NKp46/CD16/CD28/IL-2). These mouse tumors also had lower angiogenesis, cancer stemness, epithelial to mesenchymal transitions, metastases, and proliferation of Ki-67, as well as higher cell cycle arrest and apoptosis. These preliminary results showed the Se/FO treatment enhanced the therapeutic efficacies of gefitinib and erlotinib via modulating multiple signaling pathways in an LLC1-bearing mouse model.     

Regulatory Effect of let-7f Transfection in Non-Small Cell Lung Cancer on its Candidate Target Genes

Background:Let-7f has essential impacts on biological processes; however, its biological and molecular functions in lung cancer pathogenesis have yet been remained unclear. We aimed to investigate the expression level of let-7f and its candidate target genes both in lung cancer tissues and A549 cell line. Methods:Bioinformatics databases were first used to select candidate target genes of let-7f. Then the relative gene and protein expressions of let-7f and its target genes, including HMGA2, ARID3B, SMARCAD1, and FZD3, were measured in lung tissues of Non-Small Cell Lung Cancer (NSCLC) patients and A549 cell line using quantitative real-time PCR and Western blotting. The electroporation method was used to transfect A549 cells with let-7f mimic and microRNA inhibitor. The impact of let-7f transfection on the viability of A549 cells was assessed using MTT assay. The expression data of studied genes were analyzed statistically Results:Results indicated significant downregulated expression level of let-7f-5p (p = 0.0013) and upregulated level of the HMGA2 and FZD3 in NSCLC cases (p < 0.05). In A549 cells, after transfection with let-7f mimic, the expression of both mRNA and protein levels of HMGA2, ARID3B, SMARCAD1, and FZD3 decreased. Also, the overexpression of let-7f significantly inhibited the A549 cell proliferation and viability (p = 0.017). Conclusion:Our findings exhibited the high value of let-7f and HMGA2 as biomarkers for NSCLC. The let-7f, as a major tumor suppressor regulatory factor via direct targeting genes (e.g. HMGA2), inhibits lung cancer cell viability and proliferation and could serve as a marker for the early diagnostic of NSCLC.Key Words: MicroRNAs, Biomarkers, Carcinoma, Non-Small-Cell Lung     

Antiproliferative Activity of Cyanophora paradoxa Pigments in Melanoma,Breast and Lung Cancer Cells

The glaucophyte Cyanophora paradoxa (Cp) was chemically investigated to identify pigments efficiently inhibiting malignant melanoma, mammary carcinoma and lung adenocarcinoma cells growth. Cp water and ethanol extracts significantly inhibited the growth of the three cancer cell lines in vitro, at 100 µg·mL⁻¹. Flash chromatography of the Cp ethanol extract, devoid of c-phycocyanin and allophycocyanin, enabled the collection of eight fractions, four of which strongly inhibited cancer cells growth at 100 µg·mL⁻¹. Particularly, two fractions inhibited more than 90% of the melanoma cells growth, one inducing apoptosis in the three cancer cells lines. The detailed analysis of Cp pigment composition resulted in the discrimination of 17 molecules, ten of which were unequivocally identified by high resolution mass spectrometry. Pheophorbide a, β-cryptoxanthin and zeaxanthin were the three main pigments or derivatives responsible for the strong cytotoxicity of Cp fractions in cancer cells. These data point to Cyanophora paradoxa as a new microalgal source to purify potent anticancer pigments, and demonstrate for the first time the strong antiproliferative activity of zeaxanthin and β-cryptoxanthin in melanoma cells.     

Regioselective Synthesis of 6-O-Acetyl Dieckol and Its Selective Cytotoxicity against Non-Small-Cell Lung Cancer Cells

Dieckol, a phlorotannin from Ecklonia cava, has shown potential for use as an anticancer agent that selectively kills cancer cells. However, it is necessary to amplify its potency without damaging its inherent safety in order to develop it as a competitive chemotherapeutic. Here, we explored the controlled O-acylations of dieckol. Acyl groups could be consistently introduced to the 6-O position of dieckol with a high regioselectivity, which was confirmed by NOESY, HMBC and HSQC spectroscopies. In cytotoxicity studies on the newly synthesized 6-O-acetyl, 6-O-benzoyl dieckols and previously synthesized 6-O-alkyl dieckols against A549 vs. normal cells, all of the derivatives showed low cytotoxicity in normal cells with an IC₅₀ of 481–719 μM, and highly structure-dependent cytotoxicity in A549 cells with an IC₅₀ of 7.02 (acetyl)−842.26 (benzyl) μM. The selectivity index also showed a large structure dependency in the range of 0.67 (benzyl)–68.58 (acetyl). An analysis of the structure–activity relationship indicated that the activity was dramatically reduced in the presence of a benzene ring and was highly increased in the presence of small polar substituents. Conclusions: Controlled mono-O-modifications of dieckol could be a powerful tool to enhance the anticancer activity of dieckol, thus contributing to the development strategy for dieckol-based chemotherapeutics.     

Fish Oil,Se Yeast,and Micronutrient-Enriched Nutrition as Adjuvant Treatment during Target Therapy in a Murine Model of Lung Cancer

Despite the effectiveness of primary treatment modalities for cancer, the side effects of treatments, medication resistance, and the deterioration of cachexia after disease progression lead to poor prognosis. A supportive treatment modality to overcome these limitations would be considered a major breakthrough. Here, we used two different target drugs to demonstrate whether a nutraceutical formula (fish oil, Se yeast, and micronutrient-enriched nutrition; NuF) can interfere with cancer cachexia and improve drug efficacy. After Lewis lung cancer (LLC) tumor injection, the C57BL/6 mice were orally administered targeted therapy drugs Iressa and Sutent alone or combined with NuF for 27 days. Sutent administration effectively inhibited tumor size but increased the number of lung metastases in the long term. Sutent combined with NuF had no significant difference in tumor weight and metastasis compare with Sutent alone. However, NuF slightly attenuated metastases number in lung may via mesenchymal marker N-cadherin suppression. NuF otherwise increased epithelial-like marker E-cadherin expression and induce NO-mediated intrinsic apoptotic pathway in tumor cells, thereby strengthening the ability of the targeted therapy drug Iressa for inhibiting tumor progression. Our results demonstrate that NuF can promote the anticancer effect of lung cancer to targeted therapy, especially in Iressa, by inhibiting HIF-1α and epithelial-mesenchymal transition (EMT) and inducing the apoptosis of lung cancer cells. Furthermore, NuF attenuates cancer-related cachectic symptoms by inhibiting systemic oxidative stress.