In this study, lactic acid bacterium, Lactobacillus plantarum KFY04, was isolated from Xinjiang yogurt, and it was used to intervene in obese mice maintained on a 45% fat diet, and we compared its effects to those of a commercial strain, LDSB, and L-carnitine. The results showed that the LP-KFY04 intervention mice gained weight more slowly and had lower liver, epididymal adipose, and perirenal adipose tissue indices when compared to the other high-fat groups. Moreover, the LP-KFY04 can reduce the formation of fat vacuoles in the liver, while also reducing adipocyte differentiation and volume, and LP-KFY04 groups had the lowest liver and serum AST, ALT, TG, and TC levels and lowest serum LDL-C and highest HDL-C levels among the groups maintained on a high-fat diet. LP-KFY04 was also shown to mitigate obesity-associated oxidative damage and inflammatory responses. Additionally, quantitative real-time PCR and western blot analysis examining liver and adipose tissue expression of PPAR-α, CYP7A1, CPT1, and LPL showed an increased expression in the LP-KFY04 groups while decreased expression levels of PPAR-γ and C/EBPα relative to the other high-fat diet groups. These results show that of the different interventions, LP-KFY04 was the most effective at mitigating the effects of obesity than LDSB and L-carnitine. The results confirmed that LP-KEY04 has better anti-obesity, anti-oxidative, and anti-inflammatory effects than current fermentation strains. It indicates LP-KFY04 is a fermentation strain with potential practical value and high functionality, and it shows that a fermentation strain should not only have good fermentation performance, but, more importantly, it must provide more functionality on the basis of fermentation.

Background. It has been found that miR‐505‐5p is closely related to cardiovascular metabolic risk factors. Nonetheless, there is little research analyzing miR‐505‐5p for its role as well as molecular mechanism in myocardial injury caused by ischemia‐reperfusion (I/R). Methods. This work utilized quantitative reverse transcriptase PCR (qRT‐PCR) for detecting miR‐505‐5p and serum uromodulin (sUmod) levels. sUmod, interleukin‐1beta (IL‐1β), IL‐6, IL‐10, caspase7, caspase9, tumor necrosis factor‐alpha (TNF‐α), Bax, and Bcl‐xL expression was detected by western blot. Bioinformatics database was used for target prediction and miR‐505‐5’s target was determined by luciferase reporter gene assay. Results. Relative to sham group, sUmod was highly expressed within myocardial I/R injury (MIRI), whereas sUmod silencing significantly decreased the heart weight/body weight ratio, reduced serum myocardial enzymes expression, ameliorated I/R‐mediated myocardial apoptosis, and inflammation. TargetScan bioinformatics database and luciferase reporter genes confirmed that sUmod was miR‐505‐5p’s direct target gene, besides, miR‐505‐5p overexpression significantly improved the myocardial injury score, increased IL‐10, decreased TNF‐α, IL‐1β, IL‐6 expression, decreased caspase7, caspase9, Bax expression, and increased Bcl‐xL expression. More importantly, overexpression of sUmod abolished miR‐505‐5p overexpression’s role in I/R‐mediated myocardial apoptosis and inflammation. Conclusion. miR‐505‐5p can improve I/R‐mediated myocardial apoptosis and inflammation by targeting sUmod. In this study, miR‐505‐5p is related to MIRI pathogenesis, which provides the new possible targeted therapy in patients with MIRI.