The Probiotic Lactobacillus fermentum Prevents Dysbiosis and Vascular Oxidative Stress in Rats with Hypertension Induced by Chronic Nitric Oxide Blockade

다국어 초록 (Multilingual Abstract)

Whether the probiotic Lactobacillus fermentum CECT5716 (LC40) ameliorates hypertension in rats with chronic nitric oxide (NO) synthase inhibition is tested.
Rats are randomly divided into four different groups and treated for 4 weeks: a) vehicle (control), b) vehicle plus NG‐nitro‐l‐arginine methyl ester (l‐NAME; 50 mg 100 mL−1 in drinking water), c) LC40 (109 colony‐forming units d–1 by gavage), and d) LC40 plus l‐NAME. l‐NAME induces gut dysbiosis, characterized mainly by an increased Fimicutes/Bacteroidetes (F/B) ratio and reduced Bifidobacterium content, increased Th17 cells and reduced Treg in mesenteric lymph nodes (MLN), increased aortic Th17 infiltration and reactive oxygen species, reduced aortic endothelium‐dependent relaxant response to acetylcholine, and hypertension. LC40 prevents gut dysbiosis, alters the Th17/Treg balance in MLN, vascular oxidative stress, and inflammation, slightly improves endothelial dysfuncion but do not inhibit the development of l‐NAME‐induced hypertension.
Chronic LC40 treatment, in this model of chronic inhibition of NO synthesis, reduces early events involved in atherosclerosis development, such as vascular oxidative stress and pro‐inflammatory status, as a result of prevention of gut dysbiosis and immune changes in MLN, but not hypertension, confirming the critical role of NO in the antihypertensive effects of LC40 in genetic hypertension.
In this model of chronic inhibition of nitric oxide synthesis, chronic Lactobacillus fermentum (LC40) treatment reduces early events involved in atherosclerosis development, such as vascular oxidative stress and pro‐inflammatory status, as a result of prevention of gut dysbiosis and immune changes in mesenteric lymph nodes, but not hypertension, confirming the critical role of nitric oxide in the antihypertensive effects of LC40 in genetic hypertension.