Resveratrol attenuates moxifloxacin-induced oxidative damage in the liver, kidneys, brain, and serum of Wistar rats
- 1Department of Chest Disease, Private Medicana Hospital, Türkiye
- 2Department of Physiology, Faculty of Medicine, Uludağ University, Türkiye
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.
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BibTeX
@article{yıldırım2026resveratrol,
title = {{Resveratrol attenuates moxifloxacin-induced oxidative damage in the liver, kidneys, brain, and serum of Wistar rats}},
author = {Gülfem Yıldırım and Ayşen Çakır},
journal = {The Journal of International Medical Research},
year = {2026},
month = sep,
doi = {10.1177/03000605261488102},
url = {https://doi.org/10.1177/03000605261488102},
note = {CC BY-NC 4.0},
}
RIS
TY - JOUR
TI - Resveratrol attenuates moxifloxacin-induced oxidative damage in the liver, kidneys, brain, and serum of Wistar rats
AU - Gülfem Yıldırım
AU - Ayşen Çakır
PY - 2026
DA - 2026/09/16
JO - The Journal of International Medical Research
DO - 10.1177/03000605261488102
UR - https://doi.org/10.1177/03000605261488102
AB - 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.
SN - 0300-0605
SN - 1473-2300
ER -