Protective effect of Lactiplantibacillus pentosus CQZC01 in Kunming mice of subacute alcoholic liver injury

To decrease the climbing rate of alcoholic liver disease, the protective effect in subacute alcoholic liver injury of newly isolated Lactiplantibacillus pentosus CQZC01 has been investigated. Lactiplantibacillus pentosus CQZC01 (1 × 109 CFU/kgbw) administered orally could keep weight of mice at 30.54 ± 1.15 g; alleviate alcoholic damage on hepatic morphology; decrease the activities of hyaluronidase (147 ± 19 U/L), procollagen III (4.82 ± 0.54 ng/mL), alanine transaminase (10.66 ± 2.32 U/L), and aspartate aminotransferase (15.18 ± 1.98 U/L); enhance the activities of alcohol dehydrogenase (65.15 ± 3.2 U/mgprot), aldehyde dehydrogenase (16.50 ± 0.96 U/mgprot), superoxide dismutase (623 ± 39 U/mgprot), and glutathione (19.54 ± 2.46 µmol/gprot); and decrease liver total cholesterol (3.59 ± 0.50 mmol/gprot) and triglyceride (0.88 ± 0.24 mmol/gprot) (p < 0.05). Moreover, L. pentosus CQZC01 elevated the level of interleukin-10 (IL-10; 807 ± 44 pg/mL) but significantly decreased the levels of IL-1β (29.75 ± 5.27pg/mL), IL-6 (58 ± 8 pg/mL), and tumor necrosis factor-α (TNF-α, 564 ± 13 pg/mL). Liver malondialdehyde was also significantly decreased by treatment with L. pentosus CQZC01 from 3.61 ± 0.14 to 2.03 ± 0.49 nmol/mgprot. The relative expression of C-Jun N-terminal kinase, extracellular regulated protein kinases, and cyclooxygenase-1 was downregulated, and the SOD1, SOD2, peroxisome proliferator-activated receptor-α, glutathione peroxidase, catalase, nuclear factor erythroid-2-related factor 2, heme oxygenase-1 and nicotinamide adenine dinucleotide phosphate were upregulated by L. pentosus CQZC01. The overall protective effect of L. pentosus CQZC01 was comparable to commercial Lactobacillus delbrueckii subsp. Bulgaricus. Lactobacillus pentosus CQZC01 might be a suitable hepatoprotective measure for people who frequently ingest alcoholic drinks. PRACTICAL APPLICATION: L. pentosus CQZC01 can alleviate subacute alcoholic liver injury by raising the antioxidant status and upregulating the antioxidant-related genes.