Emerging evidence implicates gut microbiota dysbiosis in Alzheimer's disease (AD) pathogenesis, suggesting probiotic interventions as a viable therapeutic strategy. This study systematically screened 18 Bifidobacterium strains, among which Bifidobacterium breve LE4 exhibited both potent antioxidant activity and lipopolysaccharide (LPS)-reducing capacity. Using APP/PS1 transgenic mice as an AD model, we comprehensively assessed the neuroprotective effects of B. breve LE4. The probiotic treatment significantly ameliorated cognitive impairments, particularly in spatial learning, and concurrently improving anxiety-like behaviors and locomotor activity. Notably, B. breve LE4 administration normalized metabolic disturbances, including body weight fluctuations, dyslipidemia, and glucose intolerance. At the molecular level, B. breve LE4 exerted potent anti-inflammatory effects by reducing systemic and hippocampal cytokine levels through modulation of the TLR4-NF-κB/NLRP3 signaling pathway. The probiotic intervention preserved intestinal barrier integrity, promoted beneficial gut microbiota remodeling, and enhanced short-chain fatty acids (SCFAs) production. These changes correlated with improved synaptic plasticity and reduced AD pathological markers, including Aβ deposition and tau hyperphosphorylation. Untargeted metabolomics revealed that B. breve LE4 administration significantly corrected AD-associated metabolic dysregulation, particularly affecting amino acid and lipid metabolism pathways. Our findings demonstrate that B. breve LE4 exerts multi-targeted protective effects against AD progression, providing compelling preclinical evidence for microbiota-based interventions in neurodegenerative diseases.
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Open Access
Review Article
Issue
Cholesterol is essential for cell membrane structure and steroid hormone synthesis, but elevated serum low-density lipoprotein cholesterol can lead to atherosclerosis. Although traditional drugs such as statins are effective, they carry a risk of hepatotoxicity and muscle injury. Gut microbiota regulates cholesterol metabolism through the gut-liver axis, providing a new direction for the intervention of hypercholesterolemia. Probiotics reduce serum cholesterol through bile saline hydrolase activity, secondary bile acid conversion, and cwholesterol adsorption. This article reviews the mechanism and clinical transformation prospects of probiotics in reducing serum cholesterol.
Open Access
Issue
To find a novel probiotic strain capable of effectively alleviating hyperuricemia (HUA) and to validate its inhibitory effect on HUA in an animal model.
All mice were randomly divided into four groups (n=6 per group): control (CON), HUA model, Bacillus paralicheniformis Q13 intervention (Q13), and allopurinol intervention (ADC). The modeling and administration lasted for a total of 14 days. One hour after the final administration, blood, kidney, liver, colon, and feces samples were collected from each group for subsequent analysis. The disc diffusion method was employed to evaluate the susceptibility of this strain to 13 antibiotics and the tolerance to gastric and intestinal fluids was assessed.
Q13 effectively alleviated the elevation of serum uric acid levels, inhibited the activity of xanthine oxidase in the liver (P＜0.01), and protected renal function in mice. Furthermore, Q13 significantly increased hepatic superoxide dismutase (SOD) activity (P＜0.01) and decreased hepatic malondialdehyde (MDA) content (P＜0.01) in mice. It helped maintain normal high-density lipoprotein cholesterol (HDL-C) levels while significantly reducing low-density lipoprotein cholesterol (LDL-C) levels (P＜0.05). Q13 also reduced endotoxin levels in the liver (P＜0.01) and inhibited the secretion of renal inflammatory cytokines such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) (P＜0.01), as well as ameliorating the histopathological changes of the kidney, liver, and colon. Moreover, it rectified the dysbiosis of gut microbiota induced by potassium oxonate, restoring the Bacteroidetes-to-Firmicutes ratio (Bac/Firm ratio) to the level of the CON group and decreasing the abundance of the inflammation-associated phylum TM7. Q13 was susceptible or moderately susceptible to all 13 antibiotics. The 4-h survival rate of Q13 was over 95% in artificial gastric juice and over 86% in artificial intestinal juice.
B. paralicheniformis Q13 significantly inhibited the elevation of uric acid and enhanced renal function. Moreover, it significantly down-regulated xanthine oxidase activity, mitigated renal, hepatic and colonic injury induced by potassium oxonate in mice, abated renal inflammation, boosted hepatic antioxidant function, and modulated the homeostasis of gut microbiota, ultimately alleviating HUA. This study provides scientific support for the development of probiotic products containing B. paralicheniformis Q13 for preventing and alleviating HUA.
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