Acetyl-11-Keto-Beta-Boswellic Acid Has Therapeutic Benefits for NAFLD Rat Models That Were Given a High Fructose Diet by Ameliorating Hepatic Inflammation and Lipid Metabolism

Inflammation. 2023 Oct;46(5):1966-1980. doi: 10.1007/s10753-023-01853-y. Epub 2023 Jun 13.

Abstract

Acetyl-11-keto-beta-boswellic acid (AKBA), a potent anti-inflammatory compound purified from Boswellia species, was investigated in a preclinical study for its potential in preventing and treating non-alcoholic fatty liver disease (NAFLD), the most common chronic inflammatory liver disorder. The study involved thirty-six male Wistar rats, equally divided into prevention and treatment groups. In the prevention group, rats were given a high fructose diet (HFrD) and treated with AKBA for 6 weeks, while in the treatment group, rats were fed HFrD for 6 weeks and then given a normal diet with AKBA for 2 weeks. At the end of the study, various parameters were analyzed including liver tissues and serum levels of insulin, leptin, adiponectin, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor beta (TGF-β), interferon gamma (INF-ϒ), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α). Additionally, the expression levels of genes related to the inflammasome complex and peroxisome proliferator-activated receptor gamma (PPAR-ϒ), as well as the levels of phosphorylated and non-phosphorylated AMP-activated protein kinase alpha-1 (AMPK-α1) protein, were measured. The results showed that AKBA improved NAFLD-related serum parameters and inflammatory markers and suppressed PPAR-ϒ and inflammasome complex-related genes involved in hepatic steatosis in both groups. Additionally, AKBA prevented the reduction of the active and inactive forms of AMPK-α1 in the prevention group, which is a cellular energy regulator that helps suppress NAFLD progression. In conclusion, AKBA has a beneficial effect on preventing and avoiding the progression of NAFLD by preserving lipid metabolism, improving hepatic steatosis, and suppressing liver inflammation.

Keywords: AMP-activated protein kinase (AMPK); Acetyl-11-keto-beta-boswellic acid (AKBA); Inflammasome; Non-alcoholic fatty liver disease (NAFLD); Peroxisome proliferator-activated receptor gamma (PPAR-ϒ).

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Animals
  • Diet
  • Fructose / metabolism
  • Fructose / pharmacology
  • Fructose / therapeutic use
  • Inflammasomes / metabolism
  • Inflammation / metabolism
  • Lipid Metabolism
  • Liver / metabolism
  • Male
  • Non-alcoholic Fatty Liver Disease* / drug therapy
  • Non-alcoholic Fatty Liver Disease* / metabolism
  • Peroxisome Proliferator-Activated Receptors / metabolism
  • Rats
  • Rats, Wistar

Substances

  • acetyl-11-ketoboswellic acid
  • AMP-Activated Protein Kinases
  • Inflammasomes
  • Fructose
  • Peroxisome Proliferator-Activated Receptors