Journal of Medicinal Food

Periodontal disease results from dysbiotic oral biofilms and the host’s inflammatory response. Given the limitations of conventional therapies, this study aimed to evaluate the efficacy and safety of Weissella cibaria CMU (OraCMU) in improving gingival inflammation in individuals with gingivitis and incipient periodontitis. In this randomized, double-blind, placebo-controlled trial, 80 participants received either OraCMU tablets (2.0 × 10⁸ CFU/g; n = 40) or placebo (n = 40) twice daily for 8 weeks. The primary outcome was the gingival index (GI), and secondary outcomes included bleeding on probing (BOP), probing depth, clinical attachment level, gingival recession, plaque index, inflammation-related proteins, and oral microbiota. Clinical parameters were assessed at six preselected index teeth (#16, 12, 24, 32, 36, and 44). At week 8, the probiotic group showed significantly greater reductions in GI (−0.19 ± 0.03 vs. −0.08 ± 0.04; P = .035) and BOP (−7.74 ± 1.54 vs. −2.82 ± 1.60; P = .030) compared with the placebo group. Inflammatory markers, including fibroblast growth factor-5 (P = .003), thymic stromal lymphopoietin (P = .017), and the receptor activator of nuclear factor κB ligand/osteoprotegerin ratio (P = .021), were significantly decreased. The levels of Porphyromonas gingivalis (P = .001), Treponema denticola (P = .005), and Prevotella intermedia (P = .046) were also significantly reduced, while Weissella increased (P < .001) in the probiotic group. Eight-week supplementation with OraCMU improved gingival health and modulated the oral microbiota and inflammatory response. No serious adverse events were reported during the study period. These findings support the potential clinical utility of OraCMU as a probiotic adjunct for managing gingivitis.

Helicobacter pylori (H. pylori) is a major pathogen that colonizes the human gastric surface and induces chronic inflammation and mucosal damage, leading to various gastric diseases. This study examined the gastroprotective effects of Lacticaseibacillus paracasei HP7 in an H. pylori-infected animal model. Male C57BL/6 mice were divided into four groups: normal control, H. pylori-infected control (HP), H. pylori-infected group treated with live L. paracasei HP7 for 4 weeks (L-HP7), and H. pylori-infected group treated with heat-killed L. paracasei HP7 for 4 weeks (HK-HP7). The results showed that serum histamine and gastrin levels, as well as gastric mucosal inflammatory cytokine mRNA levels, including interleukin (IL)-1β, IL-6, IL-8, IL-18, interferon gamma, and tumor necrosis factor alpha, were significantly reduced in both the L-HP7 and HK-HP7 groups. Histopathological scoring of hematoxylin & eosin-stained gastric mucosal tissues also showed significant improvements in both groups. Serum anti-H. pylori immunoglobulin G (IgG) and CCK2R mRNA levels decreased in the L-HP7 group, whereas MUC1 mRNA levels increased. Collectively, these findings indicate that L. paracasei HP7, in both live and heat-killed forms, protects gastric surface epithelial and mucosal cells and alleviates inflammatory status by reducing the expression of pro-inflammatory cytokines. L. paracasei HP7 may serve as a promising adjunct to antibiotics in the management of H. pylori-associated diseases.

This study investigated the effects of nasal inhalation of Osmanthus fragrans var. aurantiacus (OFA) extract in lipopolysaccharide (LPS)-challenged rats. Electronic nose analysis of the OFA extracts identified 25 volatile organic compounds. Gas chromatography–mass spectrometry–olfactometry (GC–MS–O) analysis revealed that β-ionone, linalool, and related derivatives are the primary odor-active compounds in the OFA extract. LPS exposure increased pro-inflammatory markers like tumor necrosis factor-alpha, caused organ hypertrophy in the liver, lungs, and spleen, and altered transcriptional profiles linked to nuclear factor-kappa B (NF-κΒ) and immune pathways. RNA sequencing of brain tissues showed that while LPS strongly elevated NF-κΒ and cytokine pathways, this effect was less pronounced in OFA-treated rats, indicating reduced LPS-driven inflammation at the transcriptome level. Overall, these findings highlight the potential of OFA extract, abundant in β-ionone and linalool, to mitigate inflammatory signaling and improve select metabolic markers in an LPS-induced inflammatory model.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic liver condition with a rising global incidence, closely linked to metabolic risk factors such as dyslipidemia. Apolipoprotein E-deficient (ApoE⁻/⁻) mice fed a Paigen diet are an established model for MASLD and atherosclerosis research. This study investigated the effects of ellagic acid (EA) on MASLD progression in ApoE⁻/⁻ mice fed a Paigen diet. Wild-type (WT) and ApoE⁻/⁻ mice were fed a Paigen diet for 10 weeks to induce metabolic dysregulation. ApoE⁻/⁻ mice were concurrently administered either EA (10 mg/kg/day orally) or no treatment. After 10 weeks, ApoE⁻/⁻ mice exhibited significant hepatic lipid accumulation, confirmed by increased Oil Red O staining. EA treatment significantly reduced hepatic lipid accumulation and lipid peroxidation. Furthermore, EA administration decreased hepatic expression of lipogenic proteins, including sterol regulatory element-binding protein 1, fatty acid synthase, and CCAAT/enhancer-binding protein alpha. The hepatic fibrogenic marker, α-smooth muscle actin (α-SMA), was significantly elevated in ApoE⁻/⁻ mice compared with WT, and was significantly reduced by EA. In addition, transforming growth factor-β (TGF-β) protein levels and downstream SMAD signaling components, including phosphorylated SMAD2 and total SMAD2, SMAD3, and SMAD4, were significantly attenuated by EA treatment. In conclusion, EA effectively ameliorated MASLD and hypercholesterolemia in ApoE⁻/⁻ mice fed a Paigen diet. The beneficial effects of EA may be mediated through downregulating lipogenic pathways and suppressing TGF-β/SMAD signaling.

This study examined the effects of coffee berry pulp (CBP) extract on hepatic lipid accumulation and blood lipid levels in mice fed on a high-fat, high-fructose (HFHF) diet. Male C57BL/6J mice were divided into the following four groups and fed their respective diets for 15 weeks: normal diet, HFHF diet, and HFHF diet supplemented with 100 or 200 mg/kg body weight CBP extract. CBP inhibited weight gain and normalized blood glucose and insulin levels. CBP supplementation also inhibited lipid and lipoprotein accumulation in the liver, thereby effectively regulating triglyceride (TG) levels in both the blood and liver. Analysis of liver lipid metabolism revealed that CBP suppressed the increased messenger RNA (mRNA) expression of sterol regulatory element-binding protein-1C induced by HFHF and downregulated both mRNA and protein levels of peroxisome proliferator-activated receptor-γ. Liver X receptor regulation occurred at the mRNA level, and the adenosine monophosphate-activated protein kinase (AMPK)/phosphorylated AMPK ratio was modulated at the protein level. Among the lipid catabolic enzymes, adipose TG lipase expression was specifically modulated by CBP treatment. These findings suggest that CBP supplementation modulates key hepatic lipid regulators and reduces blood and liver TG accumulation. Although CBP shows promise in regulating TG synthesis and storage in a mouse model, further studies, including clinical validation, are required to confirm its potential as a treatment for human non-alcoholic fatty liver disease.