黄芪注射液对缺血性心肌病大鼠心肌的保护作用*

目的: 探究黄芪注射液对缺血性心肌病大鼠心肌保护作用及其机制。方法: 将36只雄性鼠随机分成:对照组(12只)、缺血性心肌病组(12只)及黄芪注射液组(12只);缺血性心肌病组和黄芪注射液组的大鼠开胸结扎冠状动脉,建立缺血心肌病大鼠模型;建立心肌缺血模型后,黄芪注射液组术后注射黄芪注射液(每周一次,剂量:10 g/kg体重),共注射4次,其他两组腹腔均注射相同剂量的生理盐水;4周后给予3组大鼠麻醉后行心电图及心脏彩超后,处死大鼠取心肌标本行电镜检查,观察其心肌病理超微结构的变化,检测大鼠心肌细胞线粒体Ca²⁺浓度和心肌细胞线粒体融合蛋白mitofusin 1(Mfn1)及凋亡因子C/EBP 同源蛋白(chop)表达,以及黄芪注射液对大鼠心肌细胞ATP敏感钾通道电流的作用。结果: 与对照组比较,缺血性心肌病组中大鼠出现心律失常现象;心室扩大,EF值降低;心肌排列紊乱,线粒体空泡化严重;线粒体Ca²⁺浓度增加(P＜0.01);Mfn1表达减低(P＜0.05),chop表达增加(P＜0.01); 与缺血性心肌病组比较,黄芪注射液组中大鼠心律失常发生率明显减少,心肌细胞动作电位时程缩短,心脏彩超及心肌病理明显改善并存在大量线粒体融合,心肌线粒体Ca²⁺浓度和chop表达明显减少(P＜0.01),而Mfn1表达明显增加(P＜0.01),心肌细胞ATP敏感钾电流明显增加(P＜0.01),该作用可被ATP敏感钾通道特异性阻断剂格列本脲阻断。结论: 黄芪注射液明显减少缺血性心肌病大鼠心律失常的发生率,继而改善缺血性心肌病大鼠心脏功能、减轻心肌病理损伤,其作用机制可能通过心肌细胞ATP敏感钾通道所介导。     

光对种子萌发的影响机理研究进展

种子萌发是植物成功实现天然更新的关键环节, 需要适宜的温度、水分或光照条件。对于需光性种子, 光照是决定其萌发与否或萌发率高低的主要因素。光对植物种子萌发的影响不仅是一个复杂的生理过程, 也是受到调控的信号传递和基因表达过程。该文系统总结了影响种子萌发的光照属性、光与水/热耦合作用和种子的光属性(光敏色素)与种子萌发的关系, 明确了光调控种子萌发的生态意义; 重点综述了种子内光敏色素调控种子萌发的生理反应模式和光敏色素的光信号转导途径。试图为全面评估光对种子萌发的影响和将来开展更深入的研究提供参考。     

雌激素的非基因组途径在哺乳动物雌性生殖过程中的作用机制

雌激素的非基因组调节模式在雌性生殖系统中广泛存在．雌激素通过基因组、非基因组及两种调节模式的整合在不同组织中行使多种生理功能．卵巢中雌激素能通过非基因组效应对卵细胞起到保护作用．子宫中雌激素对多种基因的表达都是通过非基因组模式．对雌激素非基因组效应的研究将有利于进一步了解雌激素的作用机制．     

两株芽孢杆菌在苎麻纤维复合脱胶中的应用

【背景】苎麻纤维细长、强韧、洁白、有光泽,被誉为"天然纤维之王",应用广泛。但其被以半纤维素和果胶为主要成分的胶质所包裹,脱胶是生产精干麻工艺的核心工序。利用单一菌株脱胶,往往因其脱胶酶系不全,存在胶质去除率低的问题,导致后期仍需要大量的碱和漂白剂处理。【目的】丰富苎麻脱胶过程中关键酶系,从而提高苎麻胶质去除率,并降低脱胶后期化学试剂的用量,推进苎麻生物脱胶的工艺应用。【方法】选用2株芽孢杆菌HG-9 (高果胶酶和甘露聚糖酶)和HG-25(高木聚糖酶)建立了复合微生物脱胶技术,并对其进行了优化。【结果】当2株菌接种量均为6%,水料比16:1,初始pH值5.9,在温度37.6°C下脱胶处理14 h时脱胶效果最佳,与菌株HG-9单独脱胶相比,脱胶时间减少2 h,胶质去除率、半纤维素去除率和木质素去除率分别提高9.32%、21.24%和17.93%,次氯酸钠用量减少20%。通过电子显微镜分析其形貌特征发现,混合脱胶获得的纤维表面更加平滑,无明显扭曲和损伤且纤维分散度较高。【结论】通过复合微生物协同作用,丰富脱胶过程中关键酶系,提高了苎麻纤维胶质去除率,缩短了脱胶时间,而且减少了脱胶后期漂白剂的用量,为苎麻生物脱胶工业化应用的进一步发展提供了指导。     

Striatal dopamine signals are region specific and temporally stable across action-sequence habit formation

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Evaluating perceptions of risk in mosquito experts and identifying undocumented pathways for the introduction of invasive mosquito species into Europe

In several reported cases of the entry of invasive mosquito species (IMSs) into Europe, the introduction was associated with a specific pathway of introduction or dispersal. The identification of potential pathways for the introduction of IMSs and evaluations of the importance of the different pathways are key to designing proper surveillance strategies to promptly detect and control introductions in non‐infested areas. The main goals of the present study were to identify other, previously undocumented, pathways of introduction into Europe, and to identify mosquito experts' perceptions regarding control measures against IMS introductions via different documented pathways. At the European Mosquito Control Association (EMCA) conference in Montenegro in March 2017, a questionnaire was distributed among meeting participants to collect expert data. Results showed that ground transportation (by cars, trucks, etc.), passive natural dispersal and the shipping of used tyres are perceived as the most likely pathways. Introduction via aircraft did not appear to be well known and was not perceived as probable. This study shows that there were no pathways unknown to European experts that could lead to cryptic introductions into the experts' countries. Furthermore, the findings demonstrated that the perceived efficacy of surveillance and control is key to overcoming the constraints experienced and to supporting the implementation of actions against introductions.     

Antioxidant therapeutics: Pandora′s box

Evolution has favored the utilization of dioxygen (O₂) in the development of complex multicellular organisms. O₂ is actually a toxic mutagenic gas that is highly oxidizing and combustible. It is thought that plants are largely to blame for polluting the earth′s atmosphere with O₂ owing to the development of photosynthesis by blue-green algae over 2 billion years ago. The rise of the plants and atmospheric O₂ levels placed evolutionary stress on organisms to adapt or become extinct. This implies that all the surviving creatures on our planet are mutants that have adapted to the “abnormal biology” of O₂. Much of the adaptation to the presence of O₂ in biological systems comes from well-coordinated antioxidant and repair systems that focus on converting O₂ to its most reduced form, water (H₂O), and the repair and replacement of damaged cellular macromolecules. Biological systems have also harnessed O₂′s reactive properties for energy production, xenobiotic metabolism, and host defense and as a signaling messenger and redox modulator of a number of cell signaling pathways. Many of these systems involve electron transport systems and offer many different mechanisms by which antioxidant therapeutics can alternatively produce an antioxidant effect without directly scavenging oxygen-derived reactive species. It is likely that each agent will have a different set of mechanisms that may change depending on the model of oxidative stress, organ system, or disease state. An important point is that all biological processes of aerobes have coevolved with O₂ and this creates a Pandora′s box for trying to understand the mechanism(s) of action of antioxidants being developed as therapeutic agents.     

Naftopidil reduced the proliferation of lung fibroblasts and bleomycin‐induced lung fibrosis in mice

Naftopidil, an α‐1 adrenoceptor antagonist with few adverse effects, is prescribed for prostate hyperplasia. Naftopidil inhibits prostate fibroblast proliferation; however, its effects on lung fibroblasts and fibrosis remain largely unknown. Two normal and one idiopathic pulmonary fibrosis human lung fibroblast lines were cultured with various naftopidil concentrations with or without phenoxybenzamine, an irreversible α‐1 adrenoceptor inhibitor. We examined the incorporation of 5‐bromo‐2?‐deoxyuridine into DNA and lactic acid dehydrogenase release by enzyme‐linked immunosorbent assay, cell cycle analysis by flow cytometry, scratch wound‐healing assay, and mRNA expressions of type IV collagen and α‐smooth muscle actin by polymerase chain reaction. Effects of naftopidil on bleomycin‐induced lung fibrosis in mice were evaluated using histology, micro‐computed tomography, and surfactant protein‐D levels in serum. Naftopidil, dose‐dependently but independently of phenoxybenzamine, inhibited 5‐bromo‐2?‐deoxyuridine incorporation in lung fibroblasts. Naftopidil induced G1 cell cycle arrest, but lactic acid dehydrogenase release and migration ability of lung fibroblasts were unaffected. Naftopidil decreased mRNA expressions of type IV collagen and α‐smooth muscle actin in one normal lung fibroblast line. Histological and micro‐computed tomography examination revealed that naftopidil attenuated lung fibrosis and decreased serum surfactant protein‐D levels in bleomycin‐induced lung fibrosis in mice. In conclusion, naftopidil may have therapeutic effects on lung fibrosis.