EXCLI Journal : Experimental and Clinical Sciences (Jul 2022)

Ameliorative effects of high intensity interval training and Lactobacillus rhamnosus GG against tetracycline-induced fatty liver in rats

  • Hamideh Mahmoodzadeh Hosseini,
  • Hossein Shirvani,
  • Fariba Aghaei,
  • Ehsan Arabzadeh,
  • Martin Hofmeister

DOI
https://doi.org/10.17179/excli2022-4791
Journal volume & issue
Vol. 21
pp. 991 – 1006

Abstract

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Exercise training and probiotics have been suggested as a treatment for the prevention of chronic liver damage such as non-alcoholic fatty liver disease (NAFLD). Lactobacillus rhamnosus Gorbach‐Goldin (LGG) is one of the most widely used probiotic strains that decreases liver damage. Thus, this study aims to consider the ameliorative effects of high intensity interval training (HIIT) and LGG against tetracycline-induced fatty liver in rats. Eighty male Wistar rats were randomly divided into 8 groups of (n=10 each group): control, LGG, HIIT, LGG+HIIT, NAFLD, NAFLD+LGG, NAFLD+HIIT, and NAFLD+LGG+HIIT. The rats are treated by intraperitoneal injection with 140 mg/kg−1 tetracycline, an antibiotic previously known to induce steatosis. The exercise training groups performed HIIT 5 days/week for 5 weeks. 107 colony-forming units (cfu) of LGG were gavaged for LGG groups 5 days/week for 5 weeks. Probiotic supplementation in combination with interval training significantly decreased tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) mRNA and matrix metalloproteinase-2 (MMP-2) mRNA in the liver (p<0.05), while the levels of lysosomal acid lipase (LIPA) mRNA was significantly increased compared to NAFLD group. Also, compared with NAFLD group, NAFLD+LGG, NAFLD+HIIT and NAFLD+LGG+HIIT groups showed a significant decrease in hepatic monocyte chemoattractant protein-1 (MCP-1). Compared to LGG and LGG+HIIT groups, all NAFLD groups showed a significant decrease in apolipoprotein C3 (APOC3) in liver tissue (p<0.05). The results suggested that interval exercise with LGG supplementation minimizes cell destruction and inflammation in liver tissue due to NAFLD by improving gene expression profiles.

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