Therapeutic effects of vitamin D on acetic acid-induced colitis in rats

Therapeutic Effect of Amygdalin on Acetic Acid-induced Colitis in Rats: Histopathological and Immunohistochemical Study

“…However, the lamina propria still show congested blood vessels and extravasated RBCs. Similar findings were ascribed by Bademci et al (2020) who reported histological improvement of the colonic inflammation induced by acetic acid in rats after treatment with vitamin D. They attributed this improvement to the effective anti-inflammatory and antioxidant properties of vitamin D. Moreover, Wang et al (2019) reported that methane-rich saline could alleviate tissue damage, control inflammation, inhibit oxidative stress and reduce apoptosis in acetic acid-induced UC. They claimed that methane-rich saline prevented acetic acid-induced colitis by blocking the TLR-4/NF-κB/MAPKs signaling pathway and improved the anti-inflammatory response by promoting the IL-10/JAK1/STAT3 signaling pathway.…”

“…Sen et al (2017) demonstrated severe epithelial damage, loss of crypts, and inflammatory cell infiltration in the colon of acetic acid-treated rats. Also, Bademci et al (2020) demonstrated hyperemia, hemorrhage, and necrotic areas in the colonic mucosa of acetic acid-treated rats. Moreover, Abdel Mohsen & Ahmed (2019) and Xue et al (2020), andXue et al (2020) reported similar findings in addition to the loss of the goblet cell.…”

Campsiandra laurifolia Reduces Oxidative Stress and Inflammation in Rats with Ulcerative Colitis

“…Several mechanisms may be involved in the etiology of UC, such as genetic, environmental, dietary factors, inflammatory mediators, and oxidative stress (OS). [1][2][3][4][5][6] The induction of experimental colitis in rats by AA instillation by enema is a reproducible model that allows the observation of many similarities with UC in humans, including histological, metabolic, and inflammatory infiltrate by macrophages and neutrophils in the colon mucosa, in addition to increased production of inflammatory mediators and reactive oxygen species (ROS). 5,[7][8][9][10] The OS process is established from an imbalance between the number of oxidizing substances and the antioxidant capacity, and this imbalance can be caused by the high production of ROS or by the reduction of antioxidant defenses.…”

“…Several mechanisms may be involved in the etiology of UC, such as genetic, environmental, dietary factors, inflammatory mediators, and oxidative stress (OS). 1 2 3 4 5 6…”