The mechanisms of baicalin ameliorate obesity and hyperlipidemia through a network pharmacology approach

Eur J Pharmacol. 2020 Jul 5:878:173103. doi: 10.1016/j.ejphar.2020.173103. Epub 2020 Apr 9.

Abstract

Obesity is one of the main causes of human cardiovascular and cerebrovascular diseases. Baicalin, a bioactive flavonoid isolated from the herbal medicine Scutellaria baicalensis Georgi, is reported to ameliorate obesity and hyperlipidemia. However, its mechanism remains unclear. Here, we used network pharmacology to explore the potential mechanism of baicalin on a system level. First, we predicted the targets of baicalin and diseases, and then protein-protein interaction (PPI) networks were constructed. Moreover, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment was performed via the Database for Annotation, Visualization, and Integrated Discovery (DAVID) server. Lastly, we confirmed the results of the network analysis by palmitic acid (PA) treated human hepatoma cells (HepG2) in vitro. The results indicated that 37 targets related to obesity treated by baicalin were predicted by network pharmacology, and top 10 related pathways were extracted by the KEGG database. Baicalin treatment could reduce triglyceride (TG) contents and lipid droplet accumulation in PA-treated HepG2 cells. The anti-obesity effects of baicalin might be due to the up-regulation of solute carrier family 2 member 1 (SLC2A1) and down-regulation of tumor necrosis factor (TNF), nuclear factor kappa B subunit 1 (NFKB1), sterol regulatory element binding transcription factor 1 (SREBF1), peroxisome proliferator activated receptor gamma and caspase 3 (CASP3). Our results indicated that baicalin may regulate key inflammatory markers, adipogenesis process, and apoptosis for treatment of obesity.

Keywords: Baicalin; Hyperlipidemia; Network pharmacology; Obesity.

MeSH terms

  • Amino Acid Sequence
  • Anti-Obesity Agents / pharmacology*
  • Caspase 3 / genetics
  • Caspase 3 / metabolism
  • Drug Discovery
  • Flavonoids / pharmacology*
  • Gene Expression Regulation
  • Glucose Transporter Type 1 / genetics
  • Glucose Transporter Type 1 / metabolism
  • Hep G2 Cells
  • Herbal Medicine
  • Humans
  • Hyperlipidemias / drug therapy*
  • Hypolipidemic Agents / pharmacology*
  • Models, Molecular
  • Molecular Structure
  • NF-kappa B p50 Subunit / genetics
  • NF-kappa B p50 Subunit / metabolism
  • Obesity / drug therapy*
  • Plant Extracts / pharmacology*
  • Protein Binding
  • Protein Conformation
  • Scutellaria baicalensis
  • Signal Transduction
  • Sterol Regulatory Element Binding Protein 1 / genetics
  • Sterol Regulatory Element Binding Protein 1 / metabolism
  • Structure-Activity Relationship
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Obesity Agents
  • Flavonoids
  • Glucose Transporter Type 1
  • Hypolipidemic Agents
  • NF-kappa B p50 Subunit
  • NFKB1 protein, human
  • Plant Extracts
  • SREBF1 protein, human
  • Scutellaria baicalensis extract
  • Sterol Regulatory Element Binding Protein 1
  • Tumor Necrosis Factor-alpha
  • baicalin
  • CASP3 protein, human
  • Caspase 3