国内益生菌制剂清除幽门螺杆菌感染临床疗效的Meta分析

目的对益生菌制剂清除幽门螺杆菌（H.pylori）感染的临床疗效及其对治疗中抗生素相关的不良反应的改善情况进行系统评价。方法通过计算机检索CBMdisc、CNKI、VIP以及MEDLINE等数据库,全面收集中国地区应用益生菌制剂治疗且pylori感染的随机或半随机对照试验,并按Cochrane协作网推荐的方法对其进行Meta分析。并评价Meta分析结果的稳定性和发表偏倚。结果纳入15个试验包括1572例病人,对尼py／or／清除率和不良反应改善情况分别进行Meta分析显示,试验组Hpylori清除率（88．53％）明显高于对照组（82．73％）（合并OR为1．56,95％CI为1．17—2．08,总体效应检验,Z=2．99,P=0．003）;不良反应发生率分别为5．O％和24．3％,合并OR为0．16,95％cI为0．09—0．31,表明能显著改善治疗中的不良反应发生情况,且差异具有显著性。结论联合应用益生菌制剂可以提高抗皿pylori感染治疗中的清除率,单独应用益生菌制剂清除且pylori感染也有一定的疗效。同时,益生菌制剂对且pylori感染治疗中的不良反应有较显著的改善。益生菌制剂有可能对Hpylori感染及相关疾病的防治具有重要意义。     

益生菌的免疫调节作用及其相关应用研究进展

益生菌的定义来自希腊语,益生菌是指:当摄入足够的剂量时可以对宿主产生有益影响的活的微生物。目前,全球对益生菌及其相关制剂的研究日益受到重视,益生菌在食品、营养品及医药领域的研究也不断深入,益生菌的免疫调节机制主要包括黏膜屏障作用、增强单核—巨噬细胞的吞噬作用、促进sIgA生成等。此外,益生菌还应用于临床相关疾病的治疗,改善受损肝脏的功能,缓解肠易激综合征的临床症状,通过调节脂肪代谢及胰岛素敏感性预防2型糖尿病的发生,预防结直肠肿瘤细胞生长及减轻肠道炎症等。本文主要就益生菌的上述相关研究进展进行综述,为益生菌的研究及相关应用提供参考。     

三联疗法联合益生菌治疗小儿Hp相关性胃炎的有效性、安全性评价

目的观察三联疗法与益生菌联合治疗小儿Hp相关性胃炎的效果和安全性。方法选择2017年1月～2018年3月我院儿科门诊诊治的Hp相关性胃炎患儿88例,采用电脑随机双盲法分为实验组和对照组各44例,实验组实施三联疗法联合益生菌治疗,对照组采取三联疗法治疗,观察比较两组患儿的临床治疗总有效率、不良反应发生情况。结果实验组的临床治疗总有效率为95.45%,明显高于对照组的81.82%,组间差异有统计学意义(P0.05)。实验组的不良反应发生率为4.55%低于对照组的18.18%,差异有显著统计学意义(P0.05)。结论对Hp相关性胃炎患儿实施三联疗法与益生菌联合治疗能有效控制病情,Hp清除率高,不良反应低,值得临床应用。     

益生菌防治过敏性疾病的进展和展望

过敏是一种病理性的免疫反应。随着全球患病率逐年上升,它已成为困扰人类健康的常见疾病。目前针对过敏性疾病的疗法大都收效甚微。研究证实,益生菌可以刺激免疫细胞的免疫调节特性,维持免疫内环境平衡,调节胃肠道生态系统,是潜在的防治过敏性疾病的有效疗法。改变抗原提呈细胞的功能或调节Th1/Th2平衡是益生菌抗过敏的基本作用机制。目前益生菌防治过敏性疾病已经成为国内外研究的热点,未来有望利用益生菌实现过敏性疾病的个性化与精准化治疗。本文就益生菌防治过敏性疾病的最新进展以及该领域前沿作一综述,期望有助于我国益生菌治疗和预防过敏性疾病的普及和研究。     

二代益生菌嗜黏蛋白阿克曼菌与慢性疾病的研究进展

随着人们对肠道菌群研究的深入,越来越多的证据表明肠道菌群失调与许多慢性疾病的发生和进展密切相关。目前,采用益生菌治疗疾病已成为国际热点,而嗜黏蛋白阿克曼菌(Akkermansia muciniphila,A. muciniphila)作为人类肠道黏液层中的常见定植菌,逐渐被认为是二代益生菌中有前途的候选者。本文综述了A. muciniphila对慢性疾病的改善作用及其可能机制,从而为疾病治疗提供新思路。     

益生菌提高幽门螺杆菌根除率的随机对照双盲试验

目的了解益生菌制剂(双歧三联杆菌活检胶囊)增加标准四联根除幽门螺旋杆菌(H.pylori)方案的临床疗效及其对根除H.pylori过程的不良反应的改善情况。方法对H.pylori阳性患者采用随机双盲试验,随机分为益生菌组:埃索美拉唑钠肠溶片20mg+果胶铋200mg(2次/d,餐前0.5h)+阿莫西林1 000mg+克拉霉素500mg(2次/d,餐后即服)+益生菌(培菲康,双歧三联杆菌活菌胶囊)420mg(3次/d,与抗生素间隔2h以上);150例患者纳入安慰剂组:标准四联(同上)+安慰剂,各方案疗程均为14d,治疗结束并所用药物停药后4周对患者进行13 C呼气试验(13 C-UBT)检查,了解H.pylori根除率,治疗期间第7、14、30天对患者进行随访观察了解不良反应情况。结果 ITT分析益生菌组H.pylori根除率为85.6%,安慰剂组为75.1%;PP分析益生菌组H.pylori根除率为87.4%,安慰剂组为76.7%;益生菌组较安慰剂组不良反应发生率下降。结论联合应用益生菌制剂可提高H.pylori根除率且对治疗过程中不良反应有明显改善作用。     

益生菌在根除幽门螺杆菌中的应用

随着幽门螺杆菌耐药率的上升,幽门螺杆菌根除率逐渐下降,如何提高根除率是目前临床治疗上遇到的重要问题。益生菌不但能提高幽门螺杆菌根除率,还能降低根除幽门螺杆菌治疗的不良反应,益生菌在根除幽门螺杆菌中的应用越来越引起重视。     

益生菌治疗结肠癌患者术后化疗相关性腹泻的效果观察

目的:探讨益生菌对结肠癌术后患者化疗相关性腹泻(CID)的治疗效果,为临床提供依据。方法:选择我院2011年1月-2013年6月结肠癌术后化疗并有CID患者85例,根据治疗方法分为对照组和观察组,其中对照组41例,按照常规治疗,观察组44例,在对照组基础上应用益生菌治疗;观察指标主要为患者平均腹泻持续时间、腹泻治疗效果以及不良反应。结果:观察组总有效率为93.18%(41/44),高于对照组78.05%(32/41)(P0.05);观察组腹泻持续时间为2.91±0.17d,低于对照组4.86±0.24d(P0.05);两组治疗后不良反应比较差异无统计学意义(P0.05)。结论:采用益生菌可以缩短CID持续时间,提高疗效,改善患者生活质量。     

益生菌与肠道疾病

益生菌是一类消化时能对宿主的健康和生理功能产生积极影响的非病原微生物.他们由酵母菌和细菌,特别是乳酸菌组成,其在肠道中的命运及作用因菌株而异.益生菌的作用可直接或间接地通过调节内源性菌群或免疫系统来实现.虽然益生菌的使用对其他疾病也有减轻作用,但通常被用来治疗与胃肠道相关的疾病.尽管如此,只有少数益生菌菌株在随机取样、安慰剂作对照的临床试验中被认为是有益生作用的.本文就目前益生菌在治疗人类胃肠道疾病中的应用效果进行了综述.     

基于益生菌治疗帕金森病的研究进展

帕金森病是常见的神经退行性疾病,其发病原因至今尚未明确,目前的治疗方法价格昂贵、效果差且副作用大。帕金森病患者常见胃肠道功能障碍,帕金森病和肠道菌群之间的关联已得到实验证实,患者有望通过益生菌改善肠道菌群达到治疗的目的。工程益生菌的出现使得人们可以按照自己的意愿改造益生菌,提高其稳定性和靶向性,展现出其特有的应用潜力。本文将从益生菌治疗帕金森病的研究现状出发,阐述益生菌治疗帕金森病的可能机制,进一步分析工程益生菌治疗帕金森病的可行性,为该疾病的安全治疗提供新的思路。     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.