ArticleExperimental and therapeutic medicine2016
Effects of lactadherin on plasma D-lactic acid and small intestinal MUC2 and claudin-1 expression levels in rats with rotavirus-induced diarrhea.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- CLDN3 inhibits rotavirus attachment by targeting residue 74 of VP7.PLoS pathogens · 2026Article
- The role of gut microbiota in diarrhea and its alleviation through microbiota-targeted interventions.Frontiers in microbiology · 2025Review
- Qiweibaizhu Decoction Treats Diarrheal Juvenile Rats by Modulating the Gut Microbiota, Short-Chain Fatty Acids, and the Mucus Barrier.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Impaired intestinal barrier function in a mouse model of hyperuricemia.Molecular medicine reports · 2019Article
- Protective effect of aplysin on liver tissue and the gut microbiota in alcohol-fed rats.PloS one · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the effects of lactadherin on plasma D-lactic acid and small intestinal mucin (MUC) 2 and claudin-1 expression levels in rats with diarrhea induced by rotavirus (RV) infection. A total of 75 seven-day-old healthy Sprague-Dawley rats were randomly divided into the following five groups: Control (C), RV infection (RVI), lactadherin before rotavirus infection (LBRI), lactadherin after rotavirus infection (LARI), and blank (B). On day 4 of artificial feeding, the rats in groups RVI, LBRI and LARI were intragastric administered 1×106 PFU RV; whereas the rats in groups C and B were intragastrically administered an equal volume of maintenance solution from the RV supernatant and normal saline, respectively. In the LBRI and LARI groups, rats received daily intragastric administration of 0.25 mg lactadherin for three days prior to and following infection with RV, respectively. The course of diarrheal symptoms was observed in each group and samples were collected on days 1, 4, and 7 post-infection in order to determine the mucosal morphology, plasma D-lactic acid levels and the expression levels of MUC2 and the intracellular junction protein, claudin-1, in the small intestine. On day 4 post-infection, the rats in group RVI demonstrated severely damaged small intestines and typical diarrheal characteristics, as detected by light microscopy; whereas rats in groups LBRI and LARI demonstrated intact small intestinal villi with partial vacuolation of epithelial cells and changes in the position of their nuclei. Electron microscopy demonstrated that the rats in the RVI group had sparse, shortened, disordered intestinal microvilli and widened intercellular junctions; whereas those in groups LBRI and LARI had long intestinal microvilli sparser compared with groups B and C and slightly widened intercellular junctions. Plasma D-lactic acid levels were increased in groups RVI, LBRI and LARI, as compared with groups B and C, and the greatest levels were detected in the RVI group on days 1, 4 and 7 post-infection. In addition to maintaining intestinal permeability, lactadherin enhanced the expression levels of MUC2 and reduced the expression of claudin-1; therefore, further protecting the intestinal epithelial barrier, which may contribute to the prevention and treatment of diarrhea induced by infection with RV.
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