Attenuation of proinflammatory responses by S -[6]-Gingerol via inhibition of ROS/NF-Kappa B/COX2 activation in HuH7 cells

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Journal Article
Evidenced based Complementary and Alternative Medicine, 2013, 2013 pp. 1 - 8
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Hepatic inflammation underlies the pathogenesis of chronic diseases such as insulin resistance and type 2 diabetes mellitus. S-[6]-Gingerol has been shown to have anti-inflammatory properties. Important inflammatory mediators of interleukins include nuclear factor ?B (NF?B) and cyclooxygenase 2 (COX2). We now explore the mechanism of anti-inflammatory effects of S-[6]-gingerol in liver cells. Methods. HuH7 cells were stimulated with IL1ß to establish an in vitro hepatic inflammatory model. Results. S-[6]-Gingerol attenuated IL1ß-induced inflammation and oxidative stress in HuH7 cells, as evidenced by decreasing mRNA levels of inflammatory factor IL6, IL8, and SAA1, suppression of ROS generation, and increasing mRNA levels of DHCR24. In addition, S-[6]-gingerol reduced IL1ß-induced COX2 upregulation as well as NF?B activity. Similar to the protective effects of S-[6]-gingerol, both NS-398 (a selective COX2 inhibitor) and PDTC (a selective NF?B inhibitor) suppressed mRNA levels of IL6, IL8, and SAA1. Importantly, PDTC attenuated IL1ß-induced overexpression of COX2. Of particular note, the protective effect of S-[6]-gingerol against the IL1ß-induced inflammatory response was similar to that of BHT, an ROS scavenger. Conclusions. The findings of this study demonstrate that S-[6]-gingerol protects HuH7 cells against IL1ß-induced inflammatory insults through inhibition of the ROS/NF?B/COX2 pathway
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