肠道微生态参与功能性便秘发生机制的研究进展

功能性便秘(FC)是一种临床上常见的胃肠道动力障碍性疾病.近年来研究显示,FC患者肠道菌群的组成和数量与健康人群有显著差异,肠道微生态环境是FC发生和发展机制中的重要环节.目前对于FC与肠道菌群紊乱之间的因果关系尚未有定论,大量研究表明肠道菌群紊乱可通过多种途径参与FC的发生和发展机制.该文就肠道菌群通过神经系统、肠道...     

肠道微生态对骨骼的影响机制

近年来,肠道微生态对骨骼的影响引发人们关注。肠道菌群缺失可导致小鼠骨量增加,一些益生菌对性激素缺乏导致的骨量丢失有保护作用。肠道菌群可能通过以下机制影响骨代谢:调节免疫系统、产生相关代谢产物及酶类、调节钙吸收等。明确肠道微生态对骨骼的作用机制,可为肠道微生态用于骨质疏松骨折的风险预测和防治提供新思路。     

肠道微生态与高血压发生发展关系的研究进展

高血压作为心血管疾病的重要危险因素之一,其发病率、致残率及致死率居高不下。高血压是多因素作用的结果,发病机制尚不完全明确。肠道微生态作为人体内环境的重要部分,被认为与高血压有关。高血压影响肠道菌群组成、分布及肠屏障的特异性表达,肠道微环境产生短链脂肪酸、氧化三甲胺、类固醇激素、胆汁酸等代谢产物,最终通过介导免疫炎症、肾素-血管紧张素-醛固酮系统、自主神经系统、氧化应激、受体作用等方面实现肠道-高血压的交流通讯。因此,靶向肠道菌群的益生菌、高纤维饮食、中医中药对防治高血压有重要意义。     

肠道微生态与支气管哮喘发生发展相关性的研究进展

近年来,随着对微生物生态学的理解,人们逐渐认识到微生物群落在维持人类健康方面有着重要作用。肠道为人体中最大的微生物群提供环境,当肠道微生态失衡时,不仅对肠道系统产生影响,也会影响其他器官。研究表明,在支气管哮喘的进展过程中,肠道微生物群对疾病有一定影响。本文通过对人体微生态学的研究进展、肠道微生态与支气管哮喘发病机制及肠道微生态与支气管哮喘发展的关系进行综述,旨在为支气管哮喘的预防和治疗方向提供新思路。     

肠道菌群影响动脉粥样硬化免疫机制研究进展

动脉粥样硬化(As)与脂质代谢紊乱和炎症密切相关。目前研究发现,肠道菌群也参与As过程,是As独立的危险因素之一。人体肠道是机体最大的消化器官和"最大的免疫器官"。正常的肠道菌群参与胆汁酸代谢,菌群代谢产生的短链脂肪酸抑制炎症,从而抑制As。失衡的菌群通过影响宿主三甲胺代谢途径,扰乱机体胆固醇代谢,引发固有免疫应答和适应性免疫应答,减弱抗炎保护作用,从而促进As。因此,调节失衡的肠道菌群成为治疗As的新靶点。本文将对肠道菌群影响As的免疫机制进行综述。     

中医药对肠道微生态的影响

中医药(traditional Chinese medicine, TCM)治疗(中药治疗、针灸治疗、推拿治疗等)在临床上应用广泛、疗效显著,同时越来越多的研究表明众多疾病的预防、发生和治疗都与肠道微生态有关, TCM与肠道微生态关系的研究也越来越多. TCM治疗的基础理论与微生态学的很多理论和观点一致,从两者一致的基础理论出发,对TCM治疗与肠道微生态的关系进行综述,对从肠道微生态出发探讨TCM治疗临床疾病的机理具有重要意义.本文论述TCM治疗与肠道微生态的关系,以及TCM治疗对肠道微生态的影响,以此为中医治疗的传统手段治疗肠道微生态相关的疾病提供新的理论与依据.旨在促进TCM的现代化研究,促进TCM的临床应用和全球化.     

慢性胰腺炎和胰腺癌发生及发展中肠道微生态的研究进展

肠道微生态对于维持机体健康至关重要.越来越多的研究表明,肠道微生态失衡与胰腺疾病相关,肠道菌群失调在慢性胰腺疾病,如慢性胰腺炎、自身免疫性胰腺炎、慢性酒精性胰腺炎和胰腺癌的发生、发展中发挥着重要作用.重建肠道微生态对胰腺疾病有一定疗效,粪菌移植可能是胰腺疾病的新型治疗策略.     

微小分子核糖核酸与动脉粥样硬化发生发展的关系

微小分子核糖核酸是属内源性小分子核糖核酸,通过降解或抑制靶基因,在转录后水平调节基因表达.一些微小核糖核酸是动脉粥样硬化形成过程的调节器,包括内皮细胞损伤与修复、内皮祖细胞分化、炎症反应、脂质代谢和平滑肌细胞增殖等.另外一些微小核糖核酸可能是动脉粥样硬化新颖的诊断标志物或者治疗目靶.现就最近的研究阐述微小核糖核酸与动脉粥样硬化发生过程的关系.     

肠道微生态紊乱在HBV感染相关肝病发生发展中的研究

肠道微生态被认为是人体内最主要的虚拟器官,具有促进营养吸收、抵抗致病菌定植、免疫调节、抗肿瘤等作用.近年来研究证实,肠道微生态紊乱参与了人体多种疾病的发生和发展过程.HBV感染是慢性乙型肝炎、乙肝肝硬化、肝细胞癌(hepatocel-lular carcinoma,HCC)的最主要病因,在三者慢性、连续性的发展过程中,...     

三联疗法根除幽门螺杆菌治疗对肠道微生态的影响

目的 探讨抗幽门螺杆菌(Hp)治疗对患者肠道菌群状态(肠道微生态)及耐药性的影响。方法 分别称取60例患者治疗前后新鲜粪便0．5g，选择肠道菌群中具代表性的4种需氧菌和6种厌氧菌分别进行需氧和厌氧培养，从培养出的菌落中挑选相同的菌株进行治疗前后药敏试验。结果 (1)治疗后肠道菌群中肠杆菌、葡萄球菌、拟杆菌、双歧杆菌、消化球菌、梭菌、乳杆菌、真杆菌均较治疗前明显降低(P＜0．05)；(2)治疗后肠道菌群中大肠埃希氏菌、消化链球菌、赛氏葡萄球菌、普氏梭杆菌、肺炎致病性链球菌群、产气真杆菌等对庆大霉素、红霉素、环丙沙星、特美丁、头孢噻肟钠等药耐药率明显增加，且存在多重耐药(P＜0．05)；(3)治疗后超广谱β—内酰氨酶阳性的消化链球菌、表皮葡萄球菌、普氏梭杆菌、肺炎致病性链球菌群、赛氏葡萄球菌等较治疗前分别增加26．2％、33．3％、28．6％、35．3％、28．6％。结论 三联抗Hp治疗后肠道菌群失调、耐药菌株的增加、传播与扩散对广大人群存在潜在危险。     

微生态制剂的临床应用

微生态学 (ｍｉｃｒｏｅｃｏｌｏｇｙ)是一门新的生命科学分支 ,在保健医学、疾病预防和治疗方面具有重要的理论和实践意义。近年来 ,由于临床上一些治疗手段的应用 ,如大量新的高效抗生素和免疫抑制剂的广泛使用、放疗等 ,使人体正常菌群发生改变和失衡 ,从而导致临床疾病的发生。为了使微生物菌群重新获得平衡 ,治疗或治愈疾病 ,微生态制剂(益生菌、益生元、合生元 )的临床应用受到了关注和重视。本文仅就这一方面的研究近况作一介绍。1　肠道微生态1 1　肠道微生态平衡　正常菌群在人体表构成一个生物层 ,形成生物屏障。在粘膜层的细菌称…     

Dietary effects on oxidation of low-density lipoprotein and atherogenesis

Oxidization of low-density lipoprotein (LDL) particles leads to formation of atherosclerotic lesions and increased risk of cardiovascular disease (CVD) via a complex cascade of biochemical events occurring mostly within the arterial wall. Multiple dietary factors impact LDL oxidation levels, such as fat-rich meals, hyper- and hypocaloric diets, and specific nutrients (vitamins E, C, and beta-carotene; mono- and polyunsaturated fatty acids; and polyphenolic compounds). These basic nutrients are naturally present at high concentrations, individually or in combinations, in common foods (fruits/vegetables, vegetable oils, red wine, soy, fish, tea); in turn, these foods are the main components of well-defined diets (Mediterranean, East Asian, balanced vegetarian) that display protective action against LDL oxidation and potentially against CVD. For most nutrients, however, both positive and negative evidence exists as to the extent of their antioxidant properties and protection against risk of CVD, prompting caution in the interpretation of data reports and health claims of advertised antioxidant products.     

硝苯吡啶,硫氮zuo酮和赤芍对家兔动脉粥样硬化形成的影响

The effects of nifedipine, diltiazem, and Paeonia lactiflora Pall (PLP) on serum lipids. Plasma lipid peroxides (LPO), TXB2, and 6-keto-PGF1 alpha in cholesterol-fed rabbits have been investigated. Oral administration of nifedipine (15 mg/kg.d), diltiazem (30 mg/kg.d), and PLP (5 g/kg.d) caused 60.8%, 45.2%, and 74.2% reduction in the area of atherosclerosis in the aorta respectively. The levels of plasma LPO and TXB2 and the contents of cholesterol, phospholipid, and calcium in the intimal-media of the aorta in the treated groups were significantly lower than those in the cholesterol group, but the level of plasma 6-keto-PGF1 alpha in the treated groups was significantly higher. The appearance of cholesterol-induced TXB2 elevation and 6-keto-PGF1 alpha decrease in the treated groups was delayed. There are positive correlation between plasma TXB2 and the followings: serum lipids, plasma LPO, and the content of calcium in the intimal-media of the aorta, and the percentage of area of lesion in the aorta, while plasma 6-keto-PGF1 alpha showed significantly negative correlation with the above data. TXB2/6-keto-PGF1 alpha was found to be positively correlated with the percentage of lesion area of the aorta. It was shown that Ca2+ metabolism plays an important role in thromboxane, prostaglandin, and LPO metabolism. In conclusion, the inhibition of LPO production and regulation of TXA2-PGI2 balance may be one of the main mechanisms of the antiatherogenic effects of calcium antagonists and PLP.     

Metabolic effects of carbon monoxide in relation to atherogenesis.

The acute and chronic effects of carbon monoxide (CO) are reviewed. Direct effects of CO-induced hypoxia on arterial metabolism may facilitate deposition of cholesterol in the intimal surface and exacerbate existing atherosclerosis. Other studies indicate that CO may alter hepatic metabolism so as to inhibit both the secretion of very low density lipoproteins and the clearance of chylomicron remnants. The former change would diminish and the latter enhance atherogenesis. These findings are considered and avenues of future investigation suggested.