Bifidobacterium pseudolongum TISTR 2737 Supplementation Alleviates High Fructose-Induced Vascular Injury and...

Excessive consumption of added fructose, rather than fructose naturally present in fruits, induces metabolic changes associated with atherosclerosis; however, specific probiotic supplementation has been documented to provide benefits in preventing cardiovascular diseases. This study investigated the protective effects of Bifidobacterium pseudolongum TISTR 2737 supplementation against high fructose-induced vascular injury in rats and the underlying mechanism. Male Sprague-Dawley rats received 20% fructose in their drinking water and were orally administered either vehicle, B. pseudolongum TISTR 2737 (2 × 10⁸ CFU/rat), or metformin for 12 weeks. Serum and aortic samples were collected and determined using biochemical assays, histological analysis, enzyme-linked immunosorbent assay (ELISA), and western blotting. Compared to the fructose-treated group, B. pseudolongum TISTR 2737 consumption significantly reduced serum glucose, total cholesterol, triglycerides, LDL-C, uric acid, and endothelin-1 levels, while increasing serum HDL-C and aortic nitric oxide (NO) levels. Histological analysis revealed that fructose-induced aortic structural changes were improved in the probiotic-treated group. B. pseudolongum TISTR 2737 downregulated the protein levels of oxidative stress markers (NADPH oxidase subunit p47^phox, 4-hydroxynonenal, and 3-nitrotyrosine) and inflammatory markers (vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and TNF-α). They also reduced the aortic expression of N∊-(Carboxymethyl) lysine (CML) and advanced glycation end products receptors (RAGE). Additionally, the eNOS dimer/monomer ratio and total antioxidant capacity were increased in the aortic tissues of the probiotic-supplemented group. This finding concludes that B. pseudolongum TISTR 2737 consumption ameliorates fructose-induced vascular injury and inflammation by lowering dyslipidemia, hyperglycemia, and hyperuricemia, and by reducing oxidative stress through the inhibition of NADPH oxidase, uncoupled eNOS, and the AGEs/RAGE pathway.