[Study on inflammatory effect of toxic raphides from Pinellia ternate and its correlation with macrophages]

Zhongguo Zhong Yao Za Zhi. 2013 Apr;38(7):1041-5.
[Article in Chinese]

Abstract

Objective: To study the toxic mechanism of toxic raphides from Pinellia ternata.

Method: Mouse peritoneal macrophage in vitro culture model was adopted to study dose-dependent and time-dependent curves of toxic raphides, with TNF-alpha, IL-1beta and IL-6 in supernatant as indexes. Scanning electron microscopy was used to observe the changes in surface morphology of raphides-treated macrophages. Macrophages-neutrophils co-cultured the transport model to study the effect of toxic raphides' stimulation of macrophages on neutrophils migration.

Result: Toxic raphides' stimulation of macrophages could cause the increase in the levels of TNF-alpha, IL-1beta and IL-6 released, and showed dose dependence and time dependence. Scanning electron microscopy showed that toxic raphides were swallowed by macrophages, with notable cell membrane creases, increase in the number of pseudopods and decrease in integrity of cell membranes, and could significantly induce migration of neutrophils.

Conclusion: The inflammatory process induced by toxic raphides is mainly mediated by macrophages. The toxic mechanism of toxic raphides from P. ternata is that toxic raphides penetrate into tissues to activate resident macrophages, release phagocytic and inflammatory cytokines, and cause migration of neutrophils, which finally results in acute inflammatory response.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Drugs, Chinese Herbal / toxicity*
  • Inflammation Mediators / toxicity*
  • Interleukin-1beta / immunology
  • Interleukin-6 / immunology
  • Macrophages, Peritoneal / drug effects*
  • Macrophages, Peritoneal / immunology*
  • Male
  • Mice
  • Mice, Inbred ICR
  • Pinellia / chemistry*
  • Tumor Necrosis Factor-alpha / immunology

Substances

  • Drugs, Chinese Herbal
  • Inflammation Mediators
  • Interleukin-1beta
  • Interleukin-6
  • Tumor Necrosis Factor-alpha