Extract of Oenothera biennis L. stem inhibits LPS-induced inflammation by regulating MAPK and NF-κB signaling pathways

Pak J Pharm Sci. 2020 Jul;33(4):1473-1481.

Abstract

Oenothera biennis L. is a perennial herb distributed across America, Asia, and Europe. The pharmacological effect of Oenothera biennis L. stem is poorly understood. We demonstrated that lipopolysaccharide (LPS)-induced the high production of inflammatory mediators nitric oxide (NO) and prostaglandin E2 (PGE2) and the pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β in peritoneal macrophages (PMs) were significantly inhibited by the crude extract The inflammation related signaling extra cellular signal-regulated ERK, P38 of MAPK and NF-kappaB (NF-κB) activated by LPS dramatically inhibited. In conclusion, our results suggested that the stems of Oenothera biennis L. possess a high anti-inflammatory property, thus, can be used in the industrial production of medicinal products as the raw material in the future.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Cyclooxygenase 2 / metabolism
  • Cytokines / metabolism
  • Dinoprostone / metabolism
  • Inflammation / chemically induced
  • Inflammation / drug therapy*
  • Inflammation Mediators / metabolism
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Lipopolysaccharides / pharmacology
  • Macrophages, Peritoneal / drug effects
  • Macrophages, Peritoneal / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mitogen-Activated Protein Kinases / metabolism*
  • NF-kappa B / metabolism*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Oenothera biennis / chemistry*
  • Plant Extracts / pharmacology*
  • Plant Stems / chemistry*
  • Signal Transduction / drug effects*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • Inflammation Mediators
  • Interleukin-1beta
  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • Plant Extracts
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • Cyclooxygenase 2
  • Mitogen-Activated Protein Kinases
  • Dinoprostone