Effects of Lactobacillus plantarum on gut barrier function in experimental obstructive jaundice.
OBJECTIVE
To investigate the mechanisms of Lactobacillus plantarum (L. plantarum) action on gut barrier in preoperative and postoperative experimental obstructive jaundice in rats.


METHODS
Forty rats were randomly divided into groups of sham-operation, bile duct ligation (BDL), BDL + L. plantarum, BDL + internal biliary drainage (IBD), and BDL + IBD + L. plantarum. Ten days after L. plantarum administration, blood and ileal samples were collected from the rats for morphological examination, and intestinal barrier function, liver function, intestinal oxidative stress and protein kinase C (PKC) activity measurement. The distribution and expression of the PKC and tight junction (TJ) proteins, such as occludin, zonula occludens-1, claudin-1, claudin-4, junction adhesion molecule-A and F-actin, were examined by confocal laser scanning microscopy, immunohistochemistry, Western blotting, real-time fluorescent quantitative polymerase chain reaction assay.


RESULTS
L. plantarum administration substantially restored gut barrier, decreased enterocyte apoptosis, improved intestinal oxidative stress, promoted the activity and expression of protein kinase (BDL vs BDL + L. plantarum, 0.295 ± 0.007 vs 0.349 ± 0.003, P < 0.05; BDL + IBD vs BDL + IBD + L. plantarum, 0.407 ± 0.046 vs 0.465 ± 0.135, P < 0.05), and particularly enhanced the expression and phosphorylation of TJ proteins in the experimental obstructive jaundice (BDL vs BDL + L. plantarum, 0.266 ± 0.118 vs 0.326 ± 0.009, P < 0.05). The protective effect of L. plantarum was more prominent after internal biliary drainage ( BDL + IBD vs BDL + IBD + L. plantarum, 0.415 ± 0.105 vs 0.494 ± 0.145, P < 0.05).


CONCLUSIONS
L. plantarum can decrease intestinal epithelial cell apoptosis, reduce oxidative stress, and prevent TJ disruption in biliary obstruction by activating the PKC pathway.
Department of Hepatobiliary Surgery, No. 455 Hospital of People's Liberation Army, Shanghai 200052, China.
Yu-Kun
YK
Zhou
Huan-Long
HL
Qin
Ming
M
Zhang
Tong-Yi
TY
Shen
Hong-Qi
HQ
Chen
Yan-Lei
YL
Ma
Zhao-Xin
ZX
Chu
Peng
P
Zhang
Zhi-Hua
ZH
Liu
D000410:Alanine Transaminase / Q000097:blood; D006631:Amine Oxidase (Copper-Containing) / Q000097:blood; D000818:Animals; D017209:Apoptosis; D001663:Bilirubin / Q000097:blood; D004731:Endotoxins / Q000097:blood; D020895:Enterocytes / Q000382:microbiology / Q000502:physiology; D005978:Glutathione / Q000097:blood; D007082:Ileum / Q000473:pathology; D007413:Intestinal Mucosa / Q000201:enzymology* / Q000382:microbiology / Q000473:pathology; D041781:Jaundice, Obstructive / Q000097:blood / Q000382:microbiology / Q000601:surgery; D019344:Lactic Acid / Q000097:blood; D048191:Lactiplantibacillus plantarum; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D019936:Probiotics / Q000627:therapeutic use*; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D013482:Superoxide Dismutase / Q000378:metabolism; D062725:Tight Junction Proteins / Q000378:metabolism*; D019108:Tight Junctions / Q000378:metabolism* / Q000648:ultrastructure
D004731:Endotoxins; D062725:Tight Junction Proteins; D019344:Lactic Acid; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D006631:Amine Oxidase (Copper-Containing); D000410:Alanine Transaminase; D011493:Protein Kinase C; D005978:Glutathione; D001663:Bilirubin