The present study was designed to evaluate the hepatoprotective potential of α-lactalbumin (αLA) against dimethylnitrosamine (DMN)-induced toxic insults in the rat liver. The liver damage was induced in rats by the repeated administration of DMN (10 mg/kg, i.p.) on three consecutive days per week for three weeks. The rats were maintained on either a standard AIN-93 M or αLA-enriched diet starting one week before the DMN injection until the termination of the experiment. The DMN treatment produced a progressive increase in the plasma markers (aspartate aminotransferase, alanine aminotransferase, total bililbin, hyarulonic acid, and matrix metalloproteinase-2) in 28 days after the first DMN injection. Dietary treatment with αLA significantly reduced the DMN-induced damage toward normalcy. N^Ｇ-nitro-L-arginine methyl ester, a nitric oxide synthase inhibitor, significantly attenuated the hepatoprotective effect of αLA. These findings show that αLA has a marked suppressive effect on hepetic fibrosis through a nitric oxide-mediated mechanism. Bovine milk-derived α-lactalbumin has a suppressive effect on dimethylnitrosamine-induced hepatic fibrosis by via nitric oxide pathway in rats.

We tested the hypothesis that α-lactalbumin inhibits the disruption of intestinal barrier function and liver cirrhosis by restoring gut-liver axis function in thioacetamide (TAA) -treated rats. Rat diets were supplemented with α-lactalbumin replacing 50% of dietary protein. After consuming α-lactalbumin for one week, rats were intraperitoneally injected with TAA twice a week for 14 weeks. The α-lactalbumin-enriched diet significantly inhibited the elevation of plasma alanine aminotransferase, aspartate aminotransferase, and hyaluronic acids. The supplement significantly reduced plasma lipopolysaccharide levels and increased occludin mRNA level. Hepatic fibrosis and regenerative nodules was developed and intestinal villi were shortened by TAA; α-Lactalbumin attenuated these histopathological changes. These results indicated that α-lactalbumin improved intestinal barrier function, suppressing endotoxin levels. These data also suggested that α-lactalbumin ameliorated the impairment of the gut-liver axis by TAA, inhibiting the development of liver cirrhosis.

Lactobacillus paragasseri OLL2809 has been shown to ameliorate stress. This study employed a randomized, placebo-controlled, double-blind, parallel-group design to assess the efficacy of continuous ingestion of OLL2809 for managing menstrual symptoms in healthy women. Eighty healthy adult women aged 25–40 years who experienced premenstrual and menstrual symptoms were randomly assigned to either the OLL2809 or placebo group (n = 40 each) and ingested tablets containing OLL2809 or placebo for three menstrual cycles. The OLL2809 group exhibited a significantly greater change in premenstrual ‘arousal’ scores on the menstrual distress questionnaire compared to the placebo group after the three menstrual cycles. Specifically, changes in the ‘activity’ subfactor were significantly higher in the OLL2809 group than in the placebo group. Additionally, the OLL2809 group reported significantly lower premenstrual irritability on the visual analog scale than the placebo group. These results suggest that OLL2809 may contribute to enhancing the quality of life of women.