Comparison of the healing effects of mesazaline and Ganoderma lucidum in acetic acid-induced colitis in rats

Abstract

Purpose The etiology and pathogenesis of distal colitis (DC) are poorly understood. Activation of intestinal inflammatory response may lead to intestinal tissue necrosis. Antioxidant and anti-inflammatory agents are among the treatment options. Our study aimed to compare the protective effects of mesalazine and Ganoderma lucidum in acetic acid (AA)-induced colitis in rats. Methods Twenty-four rats were randomly grouped as colitis, mesalazine, G. lucidum , and combined ( G. lucidum + mesalazine) groups. DC was induced by intrarectal administration of AA. Statistical comparisons were done by using parameters including colonic tissue IL-1, IL-6, TNF-α, and CRP levels. Histopathologic changes of the samples of colonic tissue were scored as mucosal damage score and inflammatory score. A P-value of <0.05 was considered significant. Results Intrarectal administration of AA leads to increased interleukin and CRP levels. High mucosal damage and inflammatory scores were noted in colitis group animals. Single mesalazine or G. lucidum treatment produced considerably decreased tissue interleukin and CRP levels. The lowest tissue interleukin and CRP levels were noted in the combined treatment group of animals. Mucosal damage and inflammatory scores were found to be significantly low in this group of animals. Conclusion The intrarectal administration of AA results in an activation of intestinal inflammation and severe mucosal damage in colonic tissue. Single use of mesalazine and G. lucidum treatment decreases the severity of intestinal inflammatory response and mucosal damage. The healing effects of the combined treatment of mesalazine and G. lucidum seem to be more effective than that of separate use in the treatment of DC.

The healing effect of resveratrol and platelet rich plasma in corrosive esophagitis model in rats

“…For the evaluation of oxidation and biochemical evaluation was performed as Özden et al 8 Table 1 shows the evaluation of tissue biochemical and histopathologic results in detail. The highest tissue IL-1, IL-6 and TNF-α levels were observed in esophagitis group animals.…”

Protective effects of sigma 1 receptor agonist PRE084 on 2,4,6-trinitrobenzene sulfonic acid–induced experimental colitis in mice

“…Cytokines are produced by gut-associated immune cells and regulate acute and chronic inflammatory responses at both local and systemic levels as well as the intestinal mucosal barrier. In a previous study using TNBS-induced UC, activated macrophages accumulated in the colonic mucosa, promoting the overproduction of many proinflammatory cytokines such as TNF-α, IL-1β, and IL-6, and inhibiting the production of the anti-inflammatory cytokine IL-10, leading to mucosal damage and ulceration [ 9 10 ]. The severity of colitis is positively correlated with the levels of cytokines in patients with UC [ 27 ].…”

“…Multiple factors, including cytokines, reactive oxygen species (ROS) overproduction, and massive neutrophil infiltration, can cause UC by damaging the intestinal mucosa [ 10 11 12 13 ]. Mucosal inflammation and ulceration in UC are caused by activated cells of the immune system.…”