Hemin Exerts Multiple Protective Mechanisms and Attenuates Dextran Sulfate Sodium–induced Colitis

Abstract

These results demonstrate that upregulation of HO-1 by hemin ameliorated experimental colitis. Moreover, our study suggests a broader protective mechanism of hemin.

Bilirubin suppresses Th17 immunity in colitis by upregulating CD39

“…Histological examination showed less mononuclear cell infiltration, decreased crypt distortion, and intraparenchymal edema in colonic sections from UCB-treated compared with untreated mice ( Figure 1C Figure 1E), suggesting that UCB favors the acquisition of immunoregulatory features by pathogenic Th17 cells. The mRNA levels of heme oxygenase-1 (HO-1; Hmox1), the enzyme responsible for catalyzing the conversion of heme into biliverdin -the UCB precursor -were higher in spleen and MLN-derived mononuclear cells of mice subjected to DSS colitis when compared with DSS-untreated controls ( Figure 1F), as reported previously and in keeping with the induction of HO-1 by stress (29)(30)(31).…”

Heme Oxygenase-1 Ameliorates Dextran Sulfate Sodium-induced Acute Murine Colitis by Regulating Th17/Treg Cell Balance

“…DSS is a widely used chemical to induce a murine model of IBD, the clinical and pathological manifestations of which are found to resemble human UC (43)(44)(45). Thus, we fed the mice with 4% DSS for 7 days on the basis of pretreatment with or without hemin and SnPP according to our previous study (46) to observe the effect of HO-1 induction on DSS-induced colitis. The results demonstrate that the DSS-induced acute experimental colitis model increased the Th17 cell population and IL-17 production level.…”

Eff ects of hemin, a heme oxygenase-1 inducer in L-arginine-induced acute pancreatitis and associated lung injury in adult male albino rats

“…Th is could be explained by the fact that hemin requires a preconditioning interval of several hours, which is mediated in part by induction of HO-1 to mediate its protective eff ect (Lu et al 2014). In vivo, systemic pre-treatment with hemin was protective in multiple acute injury models, including brain (Zhang et al 2008), heart (Hangaishi et al 2000), kidney (Demirogullari et al 2006), liver (Xue et al 2007), and gut ischemia/reperfusion (Attuwaybi et al 2004) and colitis (Zhong et al 2010), and pancreatitis (Habtezion et al 2011). Since hemin is not…”