Antagonistic effect of gingerols against TNF-α release, ROS overproduction and RIP3 expression increase induced by lectin from Pinellia ternata.
- Author:
Hong-li YU
;
Shan-hu MAO
;
Teng-fei ZHAO
;
Hao WU
;
Yao-zong PAN
;
Chen-yan SHU
- Publication Type:Journal Article
- MeSH:
Animals;
Catechols;
pharmacology;
Cells, Cultured;
Drug Antagonism;
Fatty Alcohols;
pharmacology;
Ginger;
chemistry;
Lectins;
toxicity;
Macrophages;
drug effects;
metabolism;
Male;
Mice;
Mice, Inbred ICR;
Pinellia;
chemistry;
toxicity;
Reactive Oxygen Species;
metabolism;
Receptor-Interacting Protein Serine-Threonine Kinases;
genetics;
metabolism;
Tumor Necrosis Factor-alpha;
genetics;
metabolism
- From:
China Journal of Chinese Materia Medica
2015;40(18):3630-3635
- CountryChina
- Language:Chinese
-
Abstract:
To explore the antagonistic effect of gingerols against the inflammation induced by lectin from Pinellia ternata. In this study, ELISA method was used to determine the effect of different extracts from gingerols on the release of inflammatory factor TNF-α from macrophages induced by lectin from P. ternata. The fluorescence probe was used to determine the effect of gingerols on the changes in ROS of macrophages induced by lectin from P. ternata. The western-blot method was applied to study the effect of gingerols on the increase in expression of cell receptor interacting protein RIP3 in macrophages induced by lectin from P. ternata. The scanning electron microscope (SEM) was used to study the effect of gingerols on morphological changes in macrophages induced by lectin from P. ternata. According to the results, gingerols can significantly inhibit the release of inflammatory factor from macrophages induced by lectin from P. ternata, ROS overproduction and increase in RIP3 expression. SEM results showed that gingerols can inhibit the cytomorphosis and necrocytosis induced by lectin from P. ternata. Fresh ginger's detoxication may be related to gingerols' effects in inhibiing release of inflammatory factor, ROS overproduction and increase in RIP3 expression caused by macrophages induced by lectin from P. ternata, which are mainly inflammatory development.
