Background and Aims Melatonin may be involved in
gastrointestinal tract physiology and could affect inflammation-related gastrointestinal disorders. Rat models of
ulcerative colitis imply melatonin is beneficial. To determine potential pathophysiological mechanisms, we assessed colonic nuclear factor-kappa beta expression and
measured serum levels of pentraxin-3, lipid peroxides, and
total thiols in an acetic acid model of this disease.
Materials and Methods Thirty rats were divided into five
groups: a control group, an acetic acid-induced colitis
group, a group treated with melatonin before colitis
induction, a group treated short-term after colitis induction,
and a group treated long-term after colitis induction. After
four weeks, blood samples were taken for measurement of
pentraxin-3, lipid peroxide, and total thiols. Sections of the
colon were taken for histopathological examination and
immunohistochemical detection of nuclear factor-kappa
beta expression.
Results Melatonin administration reduced nuclear factorkappa beta immunohistochemical expression, reduced
serum levels of lipid peroxide and pentraxin-3, and maintained serum levels of total thiols. However, in long-term
treatment the protective effect of melatonin was not as
marked.
Conclusion Melatonin is effective in prevention and
short-term treatment of the inflammatory process in aceticacid induced colitis whereas the benefit of long-term
treatment is unclear. Benefit may be linked to protection
mechanisms against inflammatory processes by inhibiting
the nuclear factor-kappa beta and conserving endogenous
antioxidant reserves of total thiols, thus reducing the level
of colonic damage possibly caused by lipid peroxides.