Antagonism mechanism of gingerols against inflammatory effect of toxic raphides from Pinella pedatisecta.
- Author:
Yang-Ping JIN
1
;
Hao WU
1
;
Hong-Li YU
1
;
Yao-Zong PAN
1
;
Ye-Qing CHEN
1
;
Kui-Long WANG
1
;
Cheng-Chao ZHANG
1
;
Wei WANG
1
Author Information
- Publication Type:Journal Article
- Keywords: gingerols; inflammatory factor; macrophages; neutrophil; rapides of Pinellia pedatisecta; scanning electron microscope
- From: China Journal of Chinese Materia Medica 2016;41(6):1087-1092
- CountryChina
- Language:Chinese
- Abstract: This study was to investigate the mechanism of gingerols antagonizing the inflammatory effect of toxic raphides from Pinella pedatisecta. Mice peritonitis models induced by toxic raphides from P. pedatisecta were applied to observe the effect of gingerols on inflammatory mediators PGE2 in the exudates of abdominal inflammation in mice; rats peritoneal macrophage in vitro culture models were adopted to study the anti-inflammatory effects of gingerol against toxic raphides, with TNF-α and IL-1β in supernatant as indexes. Scanning electron microscopy was used to observe the changes in surface morphology of macrophages treated by raphides and gingerols. Macrophages-neutrophils co-cultured models were used to study the antagonism of gingerols against the effect of toxic raphides' stimulation on neutrophils migration. Results showed that gingerols could significantly inhibit the production of PGE2 in the exudates of abdominal inflammation induced by toxic raphides from P. pedatisecta in mice. Gingerols could significantly inhibit the toxic raphides from P. pedatisecta to induce the release of inflammatory factors, with certain dose dependence. Scanning electron microscopy showed that gingerols could significantly inhibit phagocytosis of macrophages, cytomembrane injury, and neutrophils migration induced by toxic raphides from P. pedatisecta. The results showed that the antagonism mechanism of gingerols against the toxic raphides from P. pedatisecta may be associated with inhibiting the pro-inflammatory toxicity including macrophage activation, inflammatory factors release, and neutrophils migration.
