Dexmedetomidine as a Protective Agent Against X-Ray Ionizing Radiation-Induced Small Intestinal Injury

This study was conducted to evaluate the potential radioprotective and therapeutic effects of dexmedetomidine (DEX), a selective α2-adrenergic receptor (α2AR) agonist, against ionizing X-ray-induced small intestinal injury in a dose-dependent manner.

Male Sprague Dawley rats were randomly categorized into four groups. These groups were the Control, Ionizing Radiation (IR, 8 Gy X-ray), IR+DEX 100 µg/kg, and IR+DEX 200 µg/kg. DEX was administered intraperitoneally to the treatment groups 30 min before radiation exposure. All groups were sacrificed 24 h following irradiation. Firstly, the small intestinal tissues were evaluated histopathologically (H&E staining). Subsequently, levels of malondialdehyde (MDA) and glutathione (GSH), as markers of oxidative stress, were measured, and immunohistochemical expression of Caspase-3 and 8-hydroxy-2'-deoxyguanosine (8-OHdG) was analyzed.

In the IR group, significant histopathological alterations were observed, including villus atrophy and villus loss due to fusion, crypt loss, and mucosal degeneration. Additionally, there was an increase in MDA levels, a decrease in GSH levels, and a marked elevation in the expression of Caspase-3 and 8-OHdG. In the DEX-treated groups, particularly at the 200 µg/kg dose, significant improvements were noted in these parameters. It was determined that the histological architecture was largely preserved, oxidative stress was reduced, and apoptosis was suppressed.

The findings suggest that DEX may effectively reduce X-ray-induced small intestinal injury in a dose-dependent manner, and that this effect is mediated through antioxidant and anti-apoptotic mechanisms. DEX holds potential for the prevention or treatment of radiation-induced gastrointestinal toxicities.