Abstract The reduction of nitric oxide (NO) bioavailability in the endothelium induces endothelial dysfunction, contributing to the development of hypertension. Although Lactobacillus consumption decreases blood pressure, intracellular signaling pathways related to hypertension have not been well elucidated. Thus, this study examined the effect of spray-dried Lactiplantibacillus plantarum K79 (LpK79) on NO production, intracellular signaling pathways, and inflammatory responses related to vascular function and hypertension. NO production was assessed in human umbilical vein endothelial cells (HUVECs) treated with LpK79. Endothelial NO synthase (eNOS) and intracellular signaling molecules were determined using Western blot analysis. LpK79 dose-dependently increased NO production and activated eNOS via the phosphoinositide 3-kinase/Akt signaling pathway HUVECs. Moreover, LpK79 mitigated the activation of crucial factors pivotal for vascular contraction in smooth muscle cells, such as phospholipase Cγ, myosin phosphatase target subunit 1, and Rho-associated kinase 2. When HUVECs were treated with LpL79 in the presence of Escherichia coli lipopolysaccharide (LPS), LpK79 effectively suppressed mRNA and protein expression of pro-inflammatory mediators induced by E. coli LPS. These results suggest that LpK79 provided a beneficial effect on the regulation of vascular endothelial function.

Regulatory effect of spray-dried Lactiplantibacillus
 plantarum K79 on the activation of vasodilatory factors and
 inflammatory responses

Screening efficient strains by cell platform is cost-effective, but to date, no screening experiments have been performed for targeted lactic acid bacteria with hypoxic/reoxygenation (H/R)-treated cardiomyocytes, and their effects on the phosphoinositide 3-kinase (PI3K)/protein kinase b (Akt)/endothelial nitric oxide synthase (eNOS) pathway in myocardial infarction (MI) are unclear. Here we activated 102 strains of lactic acid bacteria and inoculated them into MRS medium for fermentation. The fermentation supernatants of the lactic acid bacteria were incubated with an H/R model of H9C2 cells. We found that Bifidobacterium longum ZL0210 had the greatest potential for inhibiting the apoptosis of H/R-induced H9C2 cells. Furthermore, it significantly increased the expression of heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO1) in H9C2 cardiomyocytes, as well as the Bcl-2/Bax protein ratio, protecting damaged myocardial cells via an anti-apoptotic pathway. Intragastric administration of B. longum ZL0210 to mice for one week before and after establishment of an MI model drastically attenuated the myocardial cell hypertrophy and fibrosis of the MI mice. Meanwhile, B. longum ZL0210 significantly reduced the secretion of myocardial enzymes, increased the activity of antioxidant enzymes, and inhibited lipid-oxidative malondialdehyde (MDA) levels. Moreover, it upregulated the expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protein and the phosphorylation levels of PI3K, Akt, and eNOS, resulting in increased NO contents. In summary, we screened 102 strains of lactic acid bacteria with a cell platform and determined that B. longum ZL0210 was a favorable candidate for protecting the myocardium. We are the first to reveal the protective effects of B. longum ZL0210 for MI via activation of the PI3K/Akt/eNOS pathway through TRAIL.

https://www.jstage.jst.go.jp/article/bmfh/42/1/42_2021-044/_pdf

Screening of the most efficacious lactic acid bacteria strain for myocardial infarction recovery and verification and exploration of its functions and mechanisms

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Screening of the most efficacious lactic acid bacteria strain for myocardial infarction recovery and verification and exploration of its functions and mechanisms