Effect of Chlorogenic Acid via Upregulating Resolvin D1 Inhibiting the NF-κB Pathway on Chronic Restraint Stress-Induced Liver Inflammation

J Agric Food Chem. 2022 Aug 31;70(34):10532-10542. doi: 10.1021/acs.jafc.2c04593. Epub 2022 Aug 17.

Abstract

Chronic stress can cause chronic inflammatory injury to the liver. Chlorogenic acid (CGA) is known to have a wide range of biological activities and anti-inflammatory effects. Resolvin D1 (RvD1) is a polyunsaturated fatty acid derivative that has inhibitory effects on a variety of inflammatory diseases. However, whether CGA can inhibit liver inflammation in chronic stress through RvD1 remains unclear. In this work, male rats were subjected to restraint stress for 6 h every day and built a chronic stress model for 21 days. CGA (100 mg/kg) was administered intragastrically 1 h before restraint, with intraperitoneal injection of RvD1 inhibitor WRW4 (antagonist of FPR2, 0.1 mg/kg) or WRW4 solution every 2 days for 30 min before CGA administration. CGA reduced hepatic hemorrhage and inflammatory cell infiltration, alleviated hepatic injury, decreased the activation of the NF-κB pathway and the expression of interleukin 1β, interleukin 6, and tumor necrosis factor α in the liver, and increased RvD1 in the serum and liver. The therapeutic effect of CGA was blocked after WRW4 intervention. These results suggest that the protective effects of CGA mediate the NF-κB pathway by upregulating the generation of RvD1. Above all, this research demonstrates the liver protective effect of CGA and provides a potential treatment strategy for chronic inflammatory disease.

Keywords: NF-κB pathway; RvD1; chlorogenic acid; chronic restrain stress; liver inflammation.

MeSH terms

  • Animals
  • Chlorogenic Acid*
  • Docosahexaenoic Acids / pharmacology
  • Inflammation / drug therapy
  • Inflammation / pathology
  • Liver / metabolism
  • Male
  • NF-kappa B* / genetics
  • NF-kappa B* / metabolism
  • Rats

Substances

  • NF-kappa B
  • resolvin D1
  • Docosahexaenoic Acids
  • Chlorogenic Acid