A critical review on diet-induced microbiota changes and cardiovascular diseases

Abstract

Background: Cardiovascular diseases (CVDs) commonly denote the disorders that generally occur as a result of unhealthy food habits. Heart failure, cerebrovascular illness, rheumatic heart disease are the common CVDs. The prevalence of CVD is increased considerably in recent decades upon unhealthy food habits and varied alternative factors such as diabetes, smoking and excessive use of alcohol. A change into a healthy food habit can reverse the strategy during a course of time.

Objectives of the study: The objective of this review is to summarize the research findings and elaborate the relationship between the diet, gut microbiota, and CVD.

Results: The dietary products containing the least saturated, trans-fat and cholesterol have the tendency to scale back the burden of CVDs, for instance, vegetables and fruits. The potential reason for the cardioprotective activity of the diet ought to be its high-unsaturated fatty acid composition and less saturated fat. Recent studies have found that gut microbiota plays a key role in mediating disease prevention. The metabolism of dietary products into varied bioactive metabolites is regulated by gut microbiota. The contributory role of gut microbiota in dietary metabolism and CVD prevention studies are increasing with promising outcomes.

Conclusion: Hence, the review was proposed to reach the researchers within this field of study and share the available knowledge in gut microbiota-mediated CVD prevention. In our current review, we have updated all the research findings within the field of diet-mediated cardiovascular prevention through gut microbiota.     

Role of dietary proteins and peptides in cardiovascular disease

Cardiovascular disease (CVD) is the leading cause of death for both men and women in the United States and most other countries. Therefore, a disease of such wide-ranging impact calls for the development of multiple viable strategies for prevention. Diet plays an important role in the development of the major risk factors of CVD such as low-grade systemic inflammation, hypertension, obesity, diabetes and atherosclerosis, the most significant. Thus, diet-based methods of prevention would not only be more feasible, but ultimately more cost-effective than relying on drugs to combat this condition. In recent years, peptides derived from either animal or plant sources have been found to have various bioactive properties. Nevertheless, their potential impact on inflammation and prevention of atherosclerosis has not been fully explored, particularly at the molecular level. In this review, the most current scientific information from in vitro, in vivo and clinical studies on the role of dietary proteins and peptides on CVD has been summarized and discussed.     

阿昔莫司对RAW 264.7细胞三磷酸腺苷结合盒转运子A1表达及其调控的影响

目的研究阿昔莫司对巨噬细胞RAW264.7三磷酸腺苷结合盒转运子A1(ATP binding cassette transporterA1,ABCA1)及其上游调控因子肝脏X受体α(Liver X receptor,LXRα)的影响,探讨其促进胆固醇逆转运(Reversecholesterol transport,RCT)、抗动脉粥样硬化(Atherosclerosis,AS)的可能机制。方法体外培养RAW264.7细胞,将细胞分为空白对照组(不含阿昔莫司)和不同浓度的阿昔莫司干预组(分别含5、10、25μg/ml阿昔莫司),作用24 h后,采用RT-PCR法检测各组细胞中ABCA1和LXRα基因mRNA的转录水平;Western blot法检测各组细胞中ABCA1和LXRα蛋白的表达;闪烁计数法检测各组细胞内胆固醇的流出。结果阿昔莫司呈浓度依赖性地增加RAW264.7细胞中ABCA1和LXRα基因mRNA的转录水平和蛋白的表达水平(P<0.05或P<0.01)及细胞内胆固醇的流出率(P<0.01)。结论阿昔莫司可通过LXRα途径上调巨噬细胞ABCA1的表达,促使细胞内胆固醇流出,从而延缓AS的发生发展。     

肠道微生物代谢产物参与动脉粥样硬化的研究进展

肠道微生物群像一个内分泌器官,能产生多种生物活性代谢物,影响宿主的健康.近来研究发现,肠道微生物的代谢组成变化在肥胖、高血压、慢性心脏和肾脏疾病中起重要作用.多项研究表明,肠道微生物衍生的许多代谢物与动脉粥样硬化事件密切相关,如三甲胺N-氧化物(trimethylamine N-oxide,TMAO)、胆汁酸(bile...     

Plasma HDL Reduces Nonesterified Fatty Acid Hydroperoxides Originating from Oxidized LDL: a Mechanism for Its Antioxidant Ability

The antioxidant property of plasma high-density lipoprotein (HDL) is thought to be involved in potential anti-atherogenic effects but the exact mechanism is not known. We aimed to reveal the contribution of HDL on the elimination of lipid hydroperoxides (LOOH) derived from oxidized low-density lipoprotein (LDL). Oxidized LDL prepared by copper ion-induced oxidation contained nonesterified fatty acid hydroperoxides (FFA-OOH) and lysophosphatidylcholine (lysoPtdCho), in addition to cholesteryl ester hydroperoxides (CE-OOH) and phosphatidylcholine hydroperoxides (PtdCho-OOH). A platelet-activating factor-acetylhydrolase (PAF-AH) inhibitor suppressed formation of FFA-OOH and lysoPtdCho in oxidized LDL. Among LOOH species, FFA-OOH was preferentially reduced by incubating oxidized LDL with HDL. HDL exhibited selective FFA-OOH reducing ability if it was mixed with a liposomal solution containing FFA-OOH, CE-OOH and PtdCho-OOH. Two-electron reduction of the hydroperoxy group to the hydroxy group was confirmed by the formation of 13-hydroxyoctadecadienoic acid from 13-hydroperoxyoctadecadienoic acid in HPLC analyses. This reducing effect was also found in apolipoprotein A-1 (apoA-1). FFA-OOH released from PtdCho-OOH due to PAF-AH activity in oxidized LDL undergo two-electron reduction by the reducing ability of apoA1 in HDL. This preferential reduction of FFA-OOH may participate in the mechanism of the antioxidant property of HDL.     

细胞焦亡与动脉粥样硬化相关性的研究进展

细胞焦亡是一种促炎形式的细胞死亡方式,且依赖于半胱天冬酶-1(cysteinyl aspartate specific proteinase-1,caspase-1)的酶活性,在形态、机制和病理生理上均不同于细胞凋亡和坏死等其他细胞死亡方式,可能参与动脉粥样硬化,并在动脉粥样硬化病变中起重要作用。细胞焦亡包括依赖caspase-1的经典焦亡通路和非caspase-1依赖的非经典焦亡通路,其具有双向作用,中度细胞焦亡有助于细胞稳态,并可能有效防止细胞过度增殖,保护宿主;另一方面,高水平细胞焦亡可能导致炎症,不利于体内平衡的维持。本文主要对细胞焦亡产生机制及内皮细胞焦亡、巨噬细胞焦亡和平滑肌细胞焦亡与动脉粥样硬化相关性的最新研究进展作一综述。