Table 1.

Pathways participating in the physiopathology of some gastrointestinal diseases and effects of remote ischemic preconditioning

Some mechanisms of ACP-induced hepatotoxicity, RE, IBD and AP	Effects of RIP
Inflammatory cytokine production	Reduced inflammatory cytokines
Increased oxidative stress	Inhibits oxidative stress
Depletion of glutathione	Increased glutathione synthesis
NO expression and release	Modulation of NO function
iNOS expression	Modulation of iNOS
HO-1 and hsp70 production	Promotes HO-1 and hsp70 production
TLR signaling	Modulates TLR signaling
Th1 and Th2 cytokine imbalance	Reduced inflammatory cytokines
STAT and NF-kappaB signaling	Modulation of STAT and NF-KappaB
TGF-β production	Regulation of TGF-β production

Note: Adapted from text. ACP: Acetaminophen; RE: Radiation-induced enteritis; IBD: Inflammatory bowel disease; AP: Acute pancreatitis; RIP: Remote ischemic preconditioning; HO-1: Heme oxygenase-1; hsp70: Heat shock protein-70; TLR: Toll-like receptor; NO: Nitric oxide; iNOS: Inducible nitric oxide synthase; STAT: Signal transduction and activator of transcription; NF-kappaB: Nuclear factor-kappaB; TGF-β: Transforming growth factor-beta.