白茶对烟雾诱导的小鼠慢性阻塞性肺病的改善研究

60只ICR小鼠随机等分成正常对照组、模型组、寿眉组、白牡丹组、白毫银针组和表没食子儿茶素没食子酸酯(EGCG)组。通过烟熏法建立小鼠慢性阻塞性肺病(Chronic obstructive pulmonary,COPD)模型,3个等级的白茶水提物和EGCG通过灌胃给予药物,5周后处死,收集血浆、支气管肺泡灌洗液、肺组织和肝组织,测定肺组织病理学变化和各样品的生化指标,研究白茶对小鼠COPD的改善作用及机制。结果显示:(1)模型组肺组织出现大量炎性浸润与杯状细胞化生等病理损伤,白茶提取物和EGCG处理均能明显改善肺组织病理性损伤,白毫银针效果最佳;(2)模型组出现明显的氧化应激和炎症反应,丙二醛(MDA)、白介素-6(IL-6)与肿瘤坏死因子-α(TNF-α)水平显著升高,超氧化物歧化酶(SOD)活性显著下降,白茶提取物和EGCG处理均能显著降低MDA、IL-6与TNF-α水平并上调SOD活性;(3)模型组血浆一氧化氮(NO)水平和肺组织髓过氧化物酶(MPO)活性显著升高,在支气管肺泡灌洗液和肺组织中NO水平降低,白茶提取物和EGCG组均能改善NO失调,降低MPO活性;(4)白茶提取物和EGCG均能上调COPD小鼠单磷酸腺苷依赖的蛋白激酶(AMPK)磷酸化水平的下降;上述处理过程中均未见白茶提取物和EGCG对小鼠的肝毒性。综上,白茶提取物能够通过抗氧化、抗炎和调节NO失常来明显改善香烟烟雾诱导的小鼠COPD。     

Bacteriophages with potential for inactivation of fish pathogenic bacteria: survival, host specificity and effect on bacterial community structure

Phage therapy may represent a viable alternative to antibiotics to inactivate fish pathogenic bacteria. Its use, however, requires the awareness of novel kinetics phenomena not applied to conventional drug treatments. The main objective of this work was to isolate bacteriophages with potential to inactivate fish pathogenic bacteria, without major effects on the structure of natural bacterial communities of aquaculture waters. The survival was determined in marine water, through quantification by the soft agar overlay technique. The host specificity was evaluated by cross infection. The ecological impact of phage addition on the structure of the bacterial community was evaluated by DGGE of PCR amplified 16S rRNA gene fragments. The survival period varied between 12 and 91 days, with a higher viability for Aeromonas salmonicida phages. The phages of Vibrio parahaemolyticus and of A. salmonicida infected bacteria of different families with a high efficacy of plating. The specific phages of pathogenic bacteria had no detectable impact on the structure of the bacterial community. In conclusion, V. parahaemolyticus and A. salmonicida phages show good survival time in marine water, have only a moderated impact on the overall bacterial community structure and the desired specificity for host pathogenic bacteria, being potential candidates for therapy of fish infectious diseases in marine aquaculture systems.     

L-茶氨酸改善热应激引起的小鼠组织损伤和氧化逆境

以SPF级Slca/KM雄性小鼠作为实验对象,在恒温恒湿模拟气候箱进行热处理,灌喂干预不同剂量L-茶氨酸,考察L-茶氨酸对小鼠采食量、体重变化、空肠切片病理情况、器官指数、血清谷丙转氨酶(ALT)与谷草转氨酶(AST)活性、血清肿瘤坏死因子(TNF-α)、白细胞介素6(IL-6)和干扰素-γ(IFN-γ)含量、肝组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)活性以及肝组织病理学变化的影响,以探讨L-茶氨酸改善热处理引起的小鼠组织损伤和氧化逆境作用。结果表明,L-茶氨酸能在一定程度上促进热处理小鼠采食量和体重的增加,降低肝脏和脾脏器官指数,降低血清ALT、AST酶活性,抑制血清炎症介质TNF-α、IL-6、IFN-γ的含量,降低肝组织MDA含量,提高SOD、GSH-Px、CAT酶活性,减轻热处理对空肠及肝脏组织的损伤,且以L-茶氨酸中剂量处理效果较好。说明L-茶氨酸具有改善热处理引起的小鼠组织损伤和氧化逆境的作用,主要表现为提高小鼠营养物质吸收能力、减少炎性细胞因子表达,以及降低氧化损伤。     

红茶延长秀丽线虫在环境氧化应激中寿命的研究

以秀丽隐杆线虫(Caenorhabditis elegans)为模型,研究了红茶在环境氧化应激中对秀丽线虫寿命的延长作用,并对相关蛋白与酶活力进行了测定.研究结果表明,在环境氧化应激条件下50 mg/L的红茶处理后的秀丽线虫存活时间显著延长;体内超氧化物歧化酶(SOD)活力升高40.8％,谷胱甘肽过氧化物酶(GSH-Px)活力升高340.8％; SKN-1::GFP蛋白表达上调了10％,DAF-16::GFP蛋白表达上调了18％.     

狭叶茶提取物对小鼠氧化应激性肝损伤的保护作用

研究狭叶茶(Camellia angustifolia Chang)提取物对拘束负荷诱发小鼠应激性肝损伤的保护作用。采用拘束负荷小鼠应激性肝损伤模型,18h拘束负荷诱发小鼠应激性肝损伤,分别用赖氏法测定小鼠血浆和肝组织丙氨酸转移酶(ALT)活性、硫代巴比妥酸法测定丙二醛(MDA)含量、HPLC法测定谷胱甘肽(GSH)水平、比色法测定黄嘌呤氧化酶(XOD)、谷胱甘肽过氧化物酶(GPX)和谷胱甘肽S转移酶(GST)活性,荧光酶标仪测定血浆、肝组织及狭叶茶提取物体外抗氧化能力指数(ORAC)。与拘束模型组相比,狭叶茶提取物可以明显提高拘束负荷小鼠血浆与肝组织匀浆的ALT活性和抗氧化能力指数,提高GSH水平,增强GPX和GST活性,有效降低肝组织中MDA含量和XOD活性,并在体外显示出较强的抗氧化能力。说明狭叶茶提取物对拘束应激引起的小鼠肝损伤具有一定的保护作用,其作用机制可能部分来自于减少拘束负荷小鼠氧化应激水平,清除自由基和抑制脂质过氧化过程。     

外源 NO 对干旱胁迫下茶树生理特性的影响

研究外源 NO 对干旱胁迫生理生化反应。以15％聚乙二醇（PEG 6000）模拟干旱胁迫,0．5 mmol·L－1的外源 NO 供体（SNP）处理对茶树幼苗叶片游离脯氨酸、丙二醛（MDA）的含量及保护酶活性的影响。结果表明,一定浓度的 SNP 缓解干旱胁迫伤害的效果较好,显著提高了受干旱胁迫茶树幼苗叶片的保护酶（CAT）活性和游离脯氨酸含量,并降低了 MDA 的含量。表明外源 NO 通过提高干旱胁迫下渗透调节物质含量和保护酶活性,降低 MDA 的含量,缓解干旱胁迫对茶树幼苗的损伤,增强植株的抗旱性。     

Marine Carotenoids against Oxidative Stress: Effects on Human Health

Carotenoids are lipid-soluble pigments that are produced in some plants, algae, fungi, and bacterial species, which accounts for their orange and yellow hues. Carotenoids are powerful antioxidants thanks to their ability to quench singlet oxygen, to be oxidized, to be isomerized, and to scavenge free radicals, which plays a crucial role in the etiology of several diseases. Unusual marine environments are associated with a great chemical diversity, resulting in novel bioactive molecules. Thus, marine organisms may represent an important source of novel biologically active substances for the development of therapeutics. In this respect, various novel marine carotenoids have recently been isolated from marine organisms and displayed several utilizations as nutraceuticals and pharmaceuticals. Marine carotenoids (astaxanthin, fucoxanthin, β-carotene, lutein but also the rare siphonaxanthin, sioxanthin, and myxol) have recently shown antioxidant properties in reducing oxidative stress markers. This review aims to describe the role of marine carotenoids against oxidative stress and their potential applications in preventing and treating inflammatory diseases.     

Towards the Small and the Beautiful: A Small Dibromotyrosine Derivative from Pseudoceratina sp. Sponge Exhibits Potent Apoptotic Effect through Targeting IKK/NFκB Signaling Pathway

A dibromotyrosine derivative, (1′R,5′S,6′S)-2-(3′,5′-dibromo-1′,6′-dihydroxy-4′-oxocyclohex-2′-enyl) acetonitrile (DT), was isolated from the sponge Pseudoceratina sp., and was found to exhibit a significant cytotoxic activity against leukemia K562 cells. Despite the large number of the isolated bromotyrosine derivatives, studies focusing on their biological mechanism of action are scarce. In the current study we designed a set of experiments to reveal the underlying mechanism of DT cytotoxic activity against K562 cells. First, the results of MTT cytotoxic and the annexin V-FITC/PI apoptotic assays, indicated that the DT cytotoxic activity is mediated through induction of apoptosis. This effect was also supported by caspases-3 and -9 activation as well as PARP cleavage. DT induced generation of reactive oxygen species (ROS) and the disruption of mitochondrial membrane potential (MMP) as indicated by flow cytometric assay. The involvement of ROS generation in the apoptotic activity of DT was further corroborated by the pretreatment of K562 cells with N-acetyl-cysteine (NAC), a ROS scavenger, which prevented apoptosis and the disruption of MMP induced by DT. Results of cell-free system assay suggested that DT can act as a topoisomerase II catalytic inhibitor, unlike the clinical anticancer drug, etoposide, which acts as a topoisomerase poison. Additionally, we found that DT treatment can block IKK/NFκB pathway and activate PI3K/Akt pathway. These findings suggest that the cytotoxic effect of DT is associated with mitochondrial dysfunction-dependent apoptosis which is mediated through oxidative stress. Therefore, DT represents an interesting reference point for the development of new cytotoxic agent targeting IKK/NFκB pathway.