Resveratrol attenuates moxifloxacin-induced oxidative damage in the liver, kidneys, brain, and serum of Wistar rats
TL;DR
Resveratrol co-administration attenuated several moxifloxacin-associated oxidative and apoptotic alterations, particularly in the kidney and liver tissues, but the absence of a resveratrol-only group and the preconditioning design limit the interpretation of its independent effects and clinical applicability.
Abstract
Objective Moxifloxacin, a widely used fluoroquinolone, has been associated with oxidative stress and tissue injury. Resveratrol may attenuate oxidative damage. This study investigated the effects of resveratrol co-administration on oxidative and apoptotic biomarkers in rats exposed to moxifloxacin. Methods Twenty-four male Wistar albino rats were randomly assigned to three groups (n = 8 per group): (a) control; (b) moxifloxacin; and (c) moxifloxacin + resveratrol groups. Moxifloxacin was administered intraperitoneally at 50 mg/kg/day during the final 7 days of a 28-day experimental period, whereas resveratrol was administered at 40 mg/kg/day for 28 days. Levels of superoxide dismutase, malondialdehyde, and caspase-3 as well as total antioxidant status and total oxidant status were assessed in the serum, brain, kidney, and liver tissues. Results Serum total antioxidant status significantly decreased in the moxifloxacin group compared with that in the control group (2.639 ± 0.169 vs. 3.531 ± 0.176 mmol Trolox equivalent/L, p = 0.007). Co-administration of moxifloxacin and resveratrol significantly increased serum total antioxidant status compared with administration of moxifloxacin alone (3.380 ± 0.190 vs. 2.639 ± 0.169 mmol Trolox equivalent/L, p = 0.018), whereas no significant difference was observed in the control group (p = 0.557). Kidney total oxidant status was significantly higher in the moxifloxacin group than in the control (p = 0.008) and moxifloxacin + resveratrol (p = 0.002) groups. Liver superoxide dismutase levels were significantly lower in the moxifloxacin group than in the control (p < 0.001) and moxifloxacin + resveratrol (p = 0.001) groups. Kidney caspase-3 levels were significantly increased in the moxifloxacin group compared with those in the control group (p < 0.001), whereas co-administration of moxifloxacin and resveratrol partially attenuated this alteration. Additionally, moxifloxacin increased the levels of malondialdehyde in the kidney, liver, and brain tissues, with attenuation following resveratrol co-administration. Conclusions Resveratrol co-administration attenuated several moxifloxacin-associated oxidative and apoptotic alterations, particularly in the kidney and liver tissues. However, the absence of a resveratrol-only group and the preconditioning design limit the interpretation of its independent effects and clinical applicability. Further pharmacokinetic, mechanistic, and clinical studies are required.