Probiotics Prevent Cardiovascular Diseases (CVD) via Decrease Reactive Oxygen Species(ROS)

2023-07-12

The gut microbiota is a broad symbiotic community ofnonpathogenic microorganisms composed primarily ofanaerobic bacteria and fungi, which areessential barrier for an effective mechanism of defenseagainst pathogens in the host.Gut dysbiosis is a confirmedcause of increased oxidative stress in the body. Infact, frequent consumption of fats and refined sugars inthe Western-type diet produces an increase in reactive oxygenspecies (ROS) production and inflammatory processes. In recent years, variousstudies have revealed that gut dysbiosis may contribute tothe development and progression of CVD (Cardiovascular Diseases) and other relateddiseases. Several clinical studies in humans have also demonstratedthe ability of probiotics to reduce abnormally highBP levels. In view of these reports, it will still be necessary to carryout more studies to verify the possible role of probiotic foodsas coadjuvants in the treatment of hypertension.

 

The vascular endothelium contributes to the regulation of vascular tone by synthesizing and releasing a huge number of vasodilating substances, both vasodilators such as nitric oxide (NO), prostacyclin, angiotensin II , and ROS.Due to this multifunctional role of the vascular endothelium, it is easy to understand that its alterations may induceto development of various diseases. Therefore, its dysfunction is recognized as a risk factor for the onset of CVD and appears in the early stages and during the development of hypertension, cardiac ischemia, atherosclerosis, stroke, or peripheral vascular disease.In fact, the generation of ROS caused by hypertension,hypercholesterolemia, diabetes, or other cardiovascularrisk factors causes a decrease in the release of endothelialNO.

 

Some studies in humans or human cells have also shown an improvement in endothelial function due to probiotic treatment. In endothelial cells, soy milk fermented with Lactobacillus plantarum or Streptococcus thermophilus stimulated NO production and eNOS activity, suggesting their effectiveness for the improvement of endothelial function. A 6-week supplementation with Lactobacillus plantarum in men with stable coronary artery disease improved endothelial function via increasing NO bioavailability while concomitantly reducing systemic inflammation. These results suggest that the intestinal microbiota is mechanistically linked to systemic inflammation and vascular endothelial function. There is an important relationshipbetween gut dysbiosis and the development of hypertension, which could involve the impaired endothelialfunction due to alterations of the gut microbiota duringthe chronic rise in BP. In fact, fecal microbiota transplantationfrom hypertensive SHR to normotensive WKY rats caused achronic impairment of endothelial function, accompaniedby greater vascular oxidative stress and increased systolicBP. In contrast, transplantation of fecal microbiota fromWKY to SHR provoked the opposite effects with animprovement of endothelial dysfunction in hypertensiveanimals.

 

Heart failure (HF) patients experience some changes in the gut microbiome during disease. Some reports have described increased levels of pathogenic microbes that could have potential deleterious effects on cardiac function.The association between gut dysbiosis and CVD was highlighted when 60 stable HF patients were selected to test whether the characteristics of the gut microbiota would correlate with their cardiovascular functional status. Evidenced showedthat HF patients had more colonies of pathogenic bacteria than control participants, along with an increased intestinal permeability that favored bacterial translocation. Using a rat model of acute myocardial infarction by permanent coronary occlusion, Gan et al. showed improved ventricular function and structure after treatment with the probiotic Lactobacillus rhamnosus, in which the probiotic decreased the leptin levels and, thus, reduced the infarct size in rats.

 

Other exciting findings in recent years has been the demonstration of a marked association between the effects of probiotics and decreased production of intravascular ROS and augmented NO bioavailability. It seems that the mechanisms underlying the beneficial actions of probiotics on cardiac autonomic control could occur through its capability to decrease the production of ROS. Many evidences indicating that a habitual consumption of probiotics, which restore the balance of the intestinal microbiota, could present cardiovascular benefits based, at least in part, on its ability to reduce oxidative stress. Although many points remain to be clarified and many of the published results are contradictory, it is evident that consumption of probiotics constitutes a promising complement to more conventional cardiovascular therapies, as well as to nonpharmacological measures that are commonly used to counteract the onset and progression of CVD.

 

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