title: Protective effects of Lactobacillus paracasei F19 in a rat model of oxidative and metabolic hepatic injury.
abstract: The liver is susceptible to such oxidative and metabolic stresses as ischemia-reperfusion (I/R) and fatty acid accumulation. Probiotics are viable microorganisms that restore the gut microbiota and exert a beneficial effect on the liver by inhibiting bacterial enzymes, stimulating immunity, and protecting intestinal permeability. We evaluated Lactobacillus paracasei F19 (LP-F19), for its potential protective effect, in an experimental model of I/R (30 min ischemia and 60 min reperfusion) in rats fed a standard diet or a steatogen [methionine/choline-deficient (MCD)] diet. Both groups consisted of 7 sham-operated rats, 10 rats that underwent I/R, and 10 that underwent I/R plus 8 wk of probiotic dietary supplementation. In rats fed a standard diet, I/R induced a decrease in sinusoid perfusion (P < 0.001), severe liver inflammation, and necrosis besides an increase of tissue levels of malondialdehyde (P < 0.001), tumor necrosis factor-alpha (P < 0.001), interleukin (IL)-1beta (P < 0.001), and IL-6 (P < 0.001) and of serum levels of transaminase (P < 0.001) and lipopolysaccharides (P < 0.001) vs. sham-operated rats. I/R also induced a decrease in Bacterioides, Bifidobacterium, and Lactobacillus spps (P < 0.01, P < 0.001, and P < 0.001, respectively) and an increase in Enterococcus and Enterobacteriaceae (P < 0.01 and P < 0.001, respectively) on intestinal mucosa. The severity of liver and gut microbiota alterations induced by I/R was even greater in rats with liver inflammation and steatosis, i.e., MCD-fed animals. LP-F19 supplementation significantly reduced the harmful effects of I/R on the liver and on gut microbiota in both groups of rats, although the effect was slightly less in MCD-fed animals. In conclusion, LP-F19 supplementation, by restoring gut microbiota, attenuated I/R-related liver injury, particularly in the absence of steatosis.
authors.affiliation: Dept. of Clinical and Experimental Medicine, University "Federico II" of Naples, Italy. nardone@unina.it
authors.forename: Gerardo
authors.initials: G
authors.lastname: Nardone
authors.forename: Debora
authors.initials: D
authors.lastname: Compare
authors.forename: Eleonora
authors.initials: E
authors.lastname: Liguori
authors.forename: Valentina
authors.initials: V
authors.lastname: Di Mauro
authors.forename: Alba
authors.initials: A
authors.lastname: Rocco
authors.forename: Michele
authors.initials: M
authors.lastname: Barone
authors.forename: Anna
authors.initials: A
authors.lastname: Napoli
authors.forename: Dominga
authors.initials: D
authors.lastname: Lapi
authors.forename: Maria Rosaria
authors.initials: MR
authors.lastname: Iovene
authors.forename: Antonio
authors.initials: A
authors.lastname: Colantuoni
mesh_terms: D000818:Animals; D002794:Choline / Q000378:metabolism*; D004032:Diet; D004731:Endotoxins; D007778:Lactobacillus; D008099:Liver / Q000098:blood supply / Q000473:pathology; D008107:Liver Diseases / Q000188:drug therapy* / Q000473:pathology; D008715:Methionine / Q000172:deficiency*; D008856:Microscopy, Fluorescence; D018384:Oxidative Stress; D019936:Probiotics / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury; D000637:Transaminases / Q000097:blood
chemical_list: D004731:Endotoxins; D008715:Methionine; D000637:Transaminases; D002794:Choline