Impact of Probiotic Lactobacillus plantarum ATCC 14917 on atherosclerotic plaque and its mechanism

Abstract

Abstract Background: Atherosclerosis is viewed as not just as a problem of lipid build-up in blood vessels, but also as a chronic inflammatory disease involving both innate and acquired immunity. The most important feature of atherosclerosis is inflammation of the vessel walls, which play a vital role in both plaque instability and thrombotic blockage of arteries, which then cause stroke and acute coronary syndrome. Probiotics are living microorganisms that, when ingested in appropriate amounts, provide health benefits. Aim: The main goal of this research was to explore the impact of Lactobacillus plantarum ATCC 14917 (L. p ATCC 14917) on atherosclerosis plaque formation and its mechanism in Apo lipoprotein E-knockout (ApoE−/−) mice. Methodology: In this study ApoE−/− mice around 08-weeks old were randomly divided into three groups as; Normal group provided with normal chow, high fat diet group, gavage with PBS and Lactobacillus plantarum group provided high fat diet and gavage with L. plantarum ATCC 14917 (2 ×109 CFU/mL). Results: Our strain significantly reduced the plaque size of ApoE−/− mice by modulating the expression of inflammatory maker, immune cell markers and chemokine/chemokine receptors and tight junction proteins (TJP); concisely by down-regulating inflammatory marker (ICAM-1, CD-60 MCP-1, F4/80, ICAM-1 and VCAM-1) in thoracic aorta, (Ccr7, cd11c, cd4, cd80, IL-1β, TNF-α) in colon and by inducing ROS-scavenging enzymes (SOD-1 and SOD-2.), TJP's (occuldin. ZO-1, claudin-3 and MUC-3). Furthermore L. P ATCC 14917 administrations statistically lessened lipopolysaccharide (LPS) level in mesenteric adipose tissue. Conclusion Our results exhibited that our strain could reduce atherosclerotic plaque size by regulating inflammation, oxidative stress, intestinal integrity, and intestinal immunity.