Table 1.

Roles of H₂S in the pathophysiology of IBD and CRC.

Diseases	Effects of H2S	Possible pathogenesis/Epidemiologic study	References
IBD	Pro-inflammatory effects	Impaired oxidation of n-butyrate	Levitt et al., 2002
		Patients with UC had excessive SRB colonization or H2S in feces	Pitcher et al., 2000; Rowan et al., 2009
	Anti-infammatory effects	Suppression of the activation of NF-kB	Oh et al., 2006
		Promotion of ucler healing in rats	Wallace et al., 2007b
		Downregulation of TNF-α,IFN-γ and iNOS epression	Li et al., 2007; Wallace et al., 2007a
		Contribution to the resolution of experimental colitis	Wallace et al., 2009
		Acting as an antioxidant	Hirata et al., 2011
		Preventation of neutrophil accumulation and viaits anti-oxidant ability	Hirata et al., 2011
	No effects	No difference in SRB between patients with IBD and controls	Fite et al., 2004; Picton et al., 2007
CRC	Carcinogenic factor	Decrease of suifide-detoxifying enzymes	Ramasamy et al., 2006
		Genomic DNA damage	Attene-Ramos et al., 2007
		Stimulation of the growth and migration	Cai et al., 2010; Szabo et al., 2013; Modis et al., 2014
		Inhibition of cell apoptosis	Sen et al., 2012
		Stimulation of tumor angiogenesis and peritumoral vasodilation	Szabo et al., 2013
	Cancer suppressive factor	Reduction of cell viability	Cao et al., 2010
		Inhibition of proliferation and promotion of protective autophagy	Wu et al., 2012