Hongyuan Zhao,Xiaoyu Chen,Fanqiang Meng,Libang Zhou,Xinyi Pang,Zhaoxin Lu,Yingjian Lu
Hyperuricemia is a critical threat to human health, and a high inosine diet can increase the prevalence of it. Lacticaseibacillus rhamnosus Fmb14 was isolated from traditional fermented Chinese yogurt, and its inosine degradation rate reached 36.3 % at 10 9 CFU/mL for 24 h. LC-MS analysis revealed that high concentrations of inosine could activate compensatory metabolic pathways of L. rhamnosus Fmb14 to catalyse inosine as an energy source and produce intracellular folic acid and riboflavin. The contents of folic acid and riboflavin were 6.0 and 4.3 fold increased after inosine treatment in the cell-free extracts (CFE). L. rhamnosus Fmb14 CFE treatment ameliorates hyperuricemia through xanthine oxidase (XOD) inhibition and ATP-binding cassette subfamily G member 2 (ABCG2) promotion, both of which are responsible for uric acid (UA) synthesis and secretion in HepG2 and Caco2 cells, respectively. The in vivo results showed that the serum UA level decreased from 236.28 to 149.28 μmol/L after 8 weeks of oral administration of L. rhamnosus Fmb14 in inosine-induced hyperuricemia model mice. Our results revealed that L. rhamnosus Fmb14 has a potential as a biological therapeutic agent in hyperuricemia prevention.
Hongyuan Zhao,Xiaoyu Chen,Li Zhang,Fanqiang Meng,Libang Zhou,Zhaoxin Lu,Yingjian Lu
Hyperuricemia is a high-risk factor for the development of gout and renal fibrosis, but the adverse effects of hyperuricemia on the liver have been seriously neglected. This research investigated the ameliorating effect of Lacticaseibacillus rhamnosus Fmb14 on hyperuricemia induced liver dysfunction both in vitro and in vivo . Cell free extracts of high dose L. rhamnosus Fmb14 treatment reduced the death rate of HepG2 cell lines from 24.1 % to 14.9 % by inhibiting NLRP3 recruitment, which was mainly activated by reactive oxygen species release and mitochondrial membrane potential disorder. In purine dietary induced hyperuricemia (PDIH) mice model, liver oedema and pyroptosis were ameliorated after L. rhamnosus Fmb14 administration through downregulating the expression levels of NLRP3, caspase-1 and gasdermin-D from 1.61 to 0.86, 3.15 to 1.01 and 5.63 to 2.02, respectively. L. rhamnosus Fmb14 administration restored mitochondrial inner membrane protein (MPV17) and connexin 43 from 2.83 and 0.73 to 0.80 and 0.98 respectively in PDIH mice, indicating that dysbiosis of mitochondrial membrane potential was restored in liver. Intriguingly, PDIH pyroptosis stimulates the process of apoptosis, which leads to severe leakage of hepatocytes, and both of pyroptosis and apoptosis were decreased after L. rhamnosus Fmb14 treatment. Therefore, L. rhamnosus Fmb14 is a promising biological resource to maintain homeostasis of the liver in hyperuricemia and the prevention of subsequent complications.
Hongyuan Zhao,Zihan Zhang,Xiaoyu Chen,Chao Tang,Li Song,Zhaoxin Lu,Yingjian Lu
Fructose dietary intake is one of the most common risk factors for hyperuricemia, which is a critical threat to human health, and the lack of an effective biological intervention method is the main problem in preventing hyperuricemia caused by fructose intake.Lacticaseibacillus rhamnosusFmb14 (L. rhamnosusFmb14) has a fructose-metabolizing ability to produce extracellular polysaccharides (EPSs), and the yield of EPSs reached 0.50 and 0.42 g/L after 48 h of fermentation in liquid media of glucose-MRS and fructose-MRS. Six pure polysaccharide components were obtained after purification. A hyperuricemic mouse model was subsequently established by feeding a 60% high-fructose diet with potassium oxyazinate for 8 weeks, and the results revealed thatL. rhamnosusFmb14 and fructose-derived EPS (F-EPS) intervention significantly reduced the serum uric acid level of the model mice from 133.6 μmol/L to 106.7 to 111.0 μmol/L. The content of XOD in the liver decreased from 2188.1 ng/L in the model group to 1797.9 ng/L in the H-Fmb14 group and 1906.6 ng/L in the H-F-EPS group, alleviating fatty liver degeneration and improving intestinal barrier (increasing OCLN and ZO1 expression in colon). The abundances ofallobaculum,bacteroides,Lactobacilli prevotella, andclostridium, the new potential biomarkers of fructose-induced hyperuricemia, were found to be modulated after Fmb14 and F-EPS intervention. The effects of Fmb14 and F-EPS in reducing uric acid synthesis and protecting the intestinal tract are very promising as food intervention agents in the prevention of hyperuricemia caused by fructose dietary.
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