Effects of ghrelin on pulmonary NOD2 mRNA expression and NF-κB activation when protects against acute lung injury in rats challenged with cecal ligation and puncture

Ghrelin Gene Products in Acute and Chronic Inflammation

“…In healthy human subjects, LPS administration induced a biphasic change in circulating ghrelin levels, with a rapid increase reaching the maximum after the pick of TNF-a and a subsequent decrease with the nadir 5 h after LPS administration (Vila et al 2007). In rodent models of sepsis, induced either by LPS injection or caecal ligation and perforation, ghrelin treatment reduced the level of pro-inflammatory cytokines both in circulation and in tissues impacted by sepsis, such as lung and kidney (Peng et al 2012;Wang et al 2009;Wu et al 2007b). It has been shown that ghrelin protective effects are mediated by the activation of the vagal nerve (Wu et al 2007a), inhibition of sympathetic nervous system, seen as reduced gut-derived norepinephrine release (Jacob et al 2010;Wu et al 2007c), and inhibition of NF-jB pathway (Peng et al 2012;Wu et al 2007b).…”

“…The effect of ghrelin on pro-inflammatory cytokines induction and release has been related, in several studies, to a suppression of the expression and/or activity of the transcription factor NF-jB (Barazzoni et al 2014;Hou et al 2009;Konturek et al 2006;Li et al 2004;Liu et al 2010;Peng et al 2012;Slomiany and Slomiany 2013;Wang et al 2012;Waseem et al 2008;Wu et al 2005;Yuan et al 2009;Zhou and Xue 2009). However, it has been proposed that in some circumstances and with some cell types, ghrelin may act as a pro-inflammatory peptide inducing, rather than reducing, NF-jB expression and proinflammatory IL-8 secretion (Kwan et al 2010;Rezaeian et al 2012;Sung et al 2011;Zhao et al 2006).…”

“…In rodent models of sepsis, induced either by LPS injection or caecal ligation and perforation, ghrelin treatment reduced the level of pro-inflammatory cytokines both in circulation and in tissues impacted by sepsis, such as lung and kidney (Peng et al 2012;Wang et al 2009;Wu et al 2007b). It has been shown that ghrelin protective effects are mediated by the activation of the vagal nerve (Wu et al 2007a), inhibition of sympathetic nervous system, seen as reduced gut-derived norepinephrine release (Jacob et al 2010;Wu et al 2007c), and inhibition of NF-jB pathway (Peng et al 2012;Wu et al 2007b). In addition, ghrelin exerts its protective action through inhibition of high-mobility group box release (Chorny et al 2008;Wu et al 2009) and through an antimicrobial activity (Chorny et al 2008).…”

“…Many others are registered on clinicalTrials.gov and are ongoing. The anti-inflammatory activity of ghrelin was demonstrated in vivo in several animal disease models, including colitis (Gonzalez- Rey et al 2006), sepsis and sepsis-related organ dysfunctions (Chang et al 2003a(Chang et al , 2003bChorny et al 2008;Jacob et al 2010;Peng et al 2012;Wang et al 2009;Wu et al 2005Wu et al , 2007aWu et al , b, c, 2009Wu et al , 2012, and encephalomyelitis (Souza-Moreira et al 2013;Theil et al 2009). …”

Metabolism-mediated drug interaction potential of HS-23, a new herbal drug for the treatment of sepsis in human hepatocytes and liver microsomes

“…Many endogenous molecules [e.g., anti-thrombin III (Hagiwara et al 2008b), fetuin A , ghrelin (Peng et al 2012;Cheyuo et al 2012;Wu et al 2012), and intravenous immunoglobulin (Hagiwara et al 2008a)], herbal extracts [e.g., Danngui (Zhu et al 2008), mung bean , and Prunella vulgaris (Jun et al 2012)], and herbal components [e.g., epigallocatechin 3-gallate (Li et al 2007a), persicarin , tanshinone IIA sulfonate (Li et al 2007b), carbenoxolone (Li et al 2013), acteoside (Lee et al 2005;Seo et al 2013), and emodin-6-O-b-D-glucoside (Lee et al 2013a, b)] have been proven to effectively inhibit HMGB1 release and prolong survival in experimental animal models of sepsis (Wang et al 2014).…”