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

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

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.

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.

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.