Sulphur dioxide ameliorates colitis related pathophysiology and inflammation

Area of Science:

• Gastroenterology and Hepatology
• Biochemistry
• Pharmacology

Background:

• Colitis, an inflammatory bowel disease (IBD), involves inflammation, oxidative stress, and cell death.
• Current IBD treatments have significant side effects.
• Sulphur dioxide (SO2), an endogenous gas transmitter, is explored for therapeutic potential in colitis.

Purpose of the Study:

• To investigate the therapeutic role of SO2 in TNBS-induced colitis.
• To elucidate the mechanisms underlying SO2's protective effects in colitis.

Main Methods:

• Colitis was induced in male Wistar rats using intrarectal TNBS administration.
• Rats received oral administration of SO2 precursors (Na2SO3 and NaHSO3).
• Key molecular markers of inflammation, oxidative stress, ER stress, autophagy, and apoptosis were assessed.

Main Results:

• TNBS-induced colitis led to increased oxidative stress, NF-κB and inflammasome activation, ER stress, autophagy, p53 activation, and apoptosis.
• SO2 administration reversed these TNBS-induced pathological changes, ameliorating colitis.
• Inhibition of endogenous SO2 production exacerbated colitis, highlighting SO2's protective role.

Conclusions:

• SO2 exhibits significant anti-inflammatory and antioxidant properties, offering a protective role in colitis.
• Down-regulation of the SO2/glutamate oxaloacetate transaminase pathway is implicated in IBD pathogenesis.
• SO2 holds promise as a potential therapeutic agent for IBD, possibly in conjunction with existing drugs.