Please use this identifier to cite or link to this item: http://nopr.niscair.res.in/handle/123456789/56146
Title: Suppression of pro-inflammatory cytokines and mediators production by ginger (Zingiber officinale Roscoe) ethanolic extract and gingerol in lipopolysaccharide-induced RAW 264.7 murine macrophage cells
Authors: Saanin, Sri Nadya
Wahyudianingsih, Roro
Afni, Merry
Afifah, Ervi
Maesaroh, Maesaroh
Widowati, Wahyu
Keywords: Cytokines;Gingerol;Inflammation;Macrophage;Zingiber officinale
Issue Date: Dec-2020
Publisher: NISCAIR-CSIR, India
IPC Code: Int. cl. (2015.01)- A61K 36/00, A61K 36/906, A61K 125/00, A61P 29/00
Abstract: Chronic inflammation could lead to several life-threatening diseases such as cancer and cardiovascular diseases. Ginger (Zingiber officinale Roscoe) has been used for many years to treat various diseases and health problems, including inflammation. This study was conducted to assess ginger ethanolic extract (GEE) and its compound gingerol’s potential as an anti-inflammatory agent by evaluating the concentration of pro-inflammatory cytokines and mediators such as TNF-α, IL-1β, IL-6, COX-2, and NO in LPS-induced RAW 264.7 cells. The safe concentration of GEE and gingerol for the RAW 264.7 cells were evaluated using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. The quantification of TNF-α, IL-1β, IL-6, COX-2, was conducted based on the ELISA method, while the quantification of NO was conducted by the nitrate/nitrite colourimetric method. The results showed that GEE and gingerol were able to inhibit TNF-α, IL-1β, IL-6, COX-2, and NO production in LPS-induced RAW 264.7 cells. GEE has better anti-inflammatory activity than gingerol. GEE in the concentration of 50 µg/mL has the highest inhibition activity over positive control or inflammatory cells model. GEE exhibited good anti-inflammatory properties through reduction of pro-inflammatory mediators such as TNF-α, IL-1β, IL-6, COX-2 and NO. Thus, ginger ethanolic extract has a high potential in the treatment of inflammation-related diseases.
Page(s): 260-266
URI: http://nopr.niscair.res.in/handle/123456789/56146
ISSN: 0976-0512 (Online); 0976-0504 (Print)
Appears in Collections:IJNPR Vol.11(4) [December 2020]

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