Inhibitory effect of Houttuynia cordata Thunb on LPS-induced retinal microglial activation

Ying-Hui Zhang1, Le-Meng Ren2, Xiao-Yun Wang1

  • 1The Second Hospital of Shandong University, Shandong University, Jinan 250033, Shandong Province, China.

Abstract

Insights

Houttuynia cordata Thunb (HCT) inhibits lipopolysaccharide (LPS)-induced microglial activation by suppressing p-p38-MAPK. This suggests HCT may treat ocular diseases involving over-activated microglia.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Immunology

Background:

  • Microglial activation by lipopolysaccharide (LPS) is implicated in various ocular diseases.
  • Understanding the molecular mechanisms of microglial activation is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the inhibitory effect of Houttuynia cordata Thunb (HCT) on LPS-induced microglial activation.
  • To elucidate the molecular mechanisms underlying HCT's action, focusing on the p38-MAPK pathway.

Main Methods:

  • Primary rat retinal microglia were cultured and treated with LPS and/or HCT.
  • Cell viability (MTT), proliferation (BrdU), inflammatory factor release (ELISA), migration (Transwell), and p38-MAPK signaling (Western blot) were assessed.

Main Results:

  • HCT significantly inhibited LPS-induced microglial proliferation and migration in a dose-dependent manner.
  • HCT reduced the release of pro-inflammatory factors (TNF-α, iNOS, IL-1β) and suppressed the upregulation of phosphorylated p38-MAPK (p-p38-MAPK).
  • HCT did not affect cell viability or total p38-MAPK levels.

Conclusions:

  • HCT effectively inhibits LPS-induced retinal microglial activation.
  • The mechanism involves the suppression of the p-p38-MAPK signaling pathway.
  • HCT shows potential as a therapeutic agent for ocular diseases characterized by microglial overactivation.

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