Effect of bevacizumab on acetic acid-induced ulcerative colitis in rats.

Background: The aim of this study was to examine the effect of intraperitoneally administered bevacizumab on colitis induced by acetic acid.

Methods: An experimental model of acetic acid-induced colitis was introduced in rats. After the induction of colitis, bevacizumab was administered intraperitoneally at two different daily doses of low (2.5 mg/kg) or high (5 mg/kg) concentration. Control groups were included for colitis and bevacizumab. After 7 d, the rats were sacrificed, and colonic tissues were harvested for macroscopic and microscopic examination of colonic damage. Tumor necrosis factor alpha, interleukin 1 beta (IL-1β), IL-6, myeloperoxidase, malondialdehyde, glutathione, and superoxidismutase values were measured biochemically.

Results: There was no statistically significant macroscopic improvement in damage to the colon tissues (P > 0.05). The severity of inflammation was significantly reduced (0.98 ± 0.22) in the low-dose bevacizumab-treated rat group compared with the control group (P < 0.001). The decrease in the inflammation score in the high-dose bevacizumab-treated rat group was not statistically significant (1.40 ± 0.33). In addition, although there was no significant change in the myeloperoxidase levels biochemically, IL-6 and malondialdehyde levels decreased in the low-dose treatment group (P = 0.014, P = 0.002, respectively). A significant decrease was found at both treatment doses in IL-1β (P < 0.001, P = 0.010), tumor necrosis factor alpha (P < 0.001, P = 0.015), superoxidismutase (P = 0.046, P = 0.011), and glutathione (P = 0.012 and P < 0.001) levels.

Conclusions: Both treatment doses of bevacizumab were observed to have a protective effect in an experimental colitis model, and the dosage of 2.5 mg/kg bevacizumab was found to have a more prominent effect.