Accumulating evidence has indicated that intestinal microbiota is involved in the development of various human diseases, including cardiovascular diseases (CVDs). Both human and animal experiments have revealed that alterations in the composition and function of intestinal flora, recognized as gut microflora dysbiosis, can accelerate the progression of CVDs. Moreover, intestinal flora metabolizes the diet ingested by the host into a series of metabolites, including trimethylamine N-oxide, short chain fatty acids, secondary bile acid and indoxyl sulfate, which affects the host physiological processes by activation of numerous signalling pathways. The aim of a review was to summarize the role of gut microbiota in the pathogenesis of CVDs, including coronary artery disease, hypertension and heart failure, which may provide valuable insights into potential therapeutic strategies for CVD that involve interfering with the composition, function and metabolites of the intestinal flora 1).
Xu et al., explored the role of the intestinal microbiota on oxidative stress and autophagy in stroke, and Astragaloside IV (AS-IV) reversed the changes induced by intestinal microbiota. We determined the characteristics of the intestinal microbiota of AIS and transient ischaemic attack (TIA) patients by 16S sequencing and found that the structure and diversity of the intestinal microbiota in patients with AIS and TIA were significantly different from those in healthy subjects. Specifically, the abundance of genus Bifidobacterium, Megamonas, Blautia, Holdemanella, and Clostridium, content of homocysteine and triglyceride was increased significantly, thus it may be as a potential mechanism of AIS and TIA. Furthermore, germ-free mice were infused intracolonically with fecal supernatants of TIA and AIS with/without feed AS-IV for 12 weeks, and we found that the feces of AIS up-regulated the autophagy markers Beclin-1, light chain 3 (LC3)-II and autophagy-related gene (Atg)12, and the expression of reactive oxygen species (ROS) and NADPH oxidase 2/4 (NOX2/4), malondialdehyde (MDA), however, the expression of total antioxidant capacity (T-AOC) and activity of superoxide dismutase (SOD) and glutathione (GSH) was down-regulated in brain tissue, the content of homocysteine and free fatty acids (FFA) in serum of the mice. Meanwhile, AS-IV could reverse the above phenomenon, however, it does not affect the motor function of mice. AS-IV reversed these changes and it may be a potential drug for AIS therapeutics 2).
The gut microbiota has recently gained attention as a possible modulator of brain activity. A number of reports suggest that the microbiota may be associated with neuropsychiatric conditions such as major depressive disorder, autism, and anxiety. The gut microbiota is thought to influence the brain via vagus nerve signaling, among other possible mechanisms. The insula processes and integrates these vagal signals. To determine if microbiota diversity and structure modulate brain activity.
Curtis et al., collected fecal samples and examined insular function using resting state functional connectivity (RSFC). Thirty healthy participants (non-smokers, tobacco smokers, and electronic cigarette users, n=10 each) were studied.
They found that the RSFC between the insula and several regions (frontal pole left, lateral occipital cortex right, lingual gyrus right, and cerebellum and vermis) were associated with bacterial microbiota diversity and structure. In addition, two specific bacteria genera, Prevotella and Bacteroides, were specifically different in tobacco smokers and also associated with insular connectivity. In conclusion, they showed that insular connectivity is associated with microbiome diversity, structure, and at least two specific bateria genera. Furthemore, this association is potentially modulated by tobacco smoking, although the sample sizes for the different smoking groups were small and this result needs validation in a larger cohort. While replication is necessary, the microbiota is a readily accesible therapeutic target for modulating insular connectivity, which has previously been shown to be abnormal in anxiety and tobacco use disorders 3).