Molecular hydrogen is comparable to sulfasalazine as a treatment for DSS-induced colitis in mice.
Tyler W LeBaronFereshteh AsgharzadehMajid KhazeiBranislav KuraAlex TarnavaJan SlezakPublished in: EXCLI journal (2021)
Colitis is an inflammatory condition of the bowels associated with abdominal pain, diarrhea, fatigue, and fever. Its etiology is multifactorial but related to the overproduction of inflammatory and oxidative mediators. There is currently no cure for this disease, and drugs used to manage it often have deleterious side effects. H2 is recognized as having anti-inflammatory and antioxidant effects, which may qualify it as a novel therapeutic for colitis. We induced an acute model of colitis in mice by administering dextran sulfate sodium (DSS) in drinking water for seven days. Mice were divided into five groups (n=6); normal, colitis, H2-treated colitis, sulfasalazine-treated colitis, and H2 plus sulfasalazine-treated colitis. From days three to ten, mice were given H2, sulfasalazine, or both. H2 was administered via dissolving a hydrogen-generating tablet in water to make hydrogen-rich water (HRW), which was ingested ad libitum and via oral gavage (200 μL). The Disease Activity Index (DAI), histological changes, and markers of inflammation and oxidative stress were assessed. HRW and sulfasalazine significantly improved bodyweight, DAI, mucosal damage, crypt loss, and spleen weight compared to control. Both treatments significantly decreased inflammation (high-sensitive C-reactive protein) and restored redox balance (total thiol, superoxide dismutase, catalase activity). There was a trend for the combination treatment to be more effective than either HRW or sulfasalazine alone. Furthermore, HRW tended to be as effective as, and often more effective than, sulfasalazine. HRW may serve as a therapeutic for ameliorating DSS-induced colitis in mice.
Keyphrases
- oxidative stress
- high fat diet induced
- ulcerative colitis
- drinking water
- disease activity
- diabetic rats
- systemic lupus erythematosus
- rheumatoid arthritis
- dna damage
- rheumatoid arthritis patients
- wild type
- induced apoptosis
- ischemia reperfusion injury
- type diabetes
- insulin resistance
- ankylosing spondylitis
- weight loss
- body mass index
- signaling pathway
- risk assessment
- replacement therapy
- nitric oxide
- respiratory failure
- health risk assessment
- high glucose
- juvenile idiopathic arthritis
- heat shock protein
- heat shock