Vitamin C reduces vancomycin-related nephrotoxicity through the inhibition of oxidative stress, apoptosis, and inflammation in mice
Juan He, Wenyun Xu, Xiaoxiao Zheng, Bing Zhao, Tongtian Ni, Ping Yu, Siyu Deng, Xiaoxia Pan, Erzhen Chen, Enqiang Mao, Xiaolan Bian
Abstract
BACKGROUND: Vancomycin (VCM) is an antibiotic widely used to treat a range of serious bacterial infections; however, it is associated with nephrotoxicity. Vitamin C (VC) is a classical antioxidant that can alleviate various organ injuries and inflammatory responses by reducing inflammation and oxidative stress. This study aimed to examine the effect of VC on VCM-related nephrotoxicity in mice. METHODS: Mice were randomized into four groups: control, VCM (400 mg/kg/day), VCM (400 mg/kg/day) + VC (200 mg/kg/day), and VC (200 mg/kg/day) groups. Both VCM and VC were administered via intraperitoneal injection for 7 d, after which kidney and blood samples were collected and evaluated. Creatinine (Cr), blood urea nitrogen (BUN), superoxide dismutase (SOD), malondialdehyde (MDA), interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and nuclear factor-κB (NF-κB) were measured. RESULTS: In the VCM group, kidney index, renal injury score, cell apoptosis, serum Cr and BUN, and kidney Cr, BUN, MDA, IL-1β, IL-6, TNF-α, and NF-κB were higher compared to the control group (all P<0.05), while body weight and kidney SOD activity were lower (both P<0.05). By contrast, no differences were observed between the control and VC groups (VC and VCM + VC groups) for all these indicators. CONCLUSIONS: The antioxidant VC reduces VCM-related renal injury by reducing oxidative stress, cell apoptosis, and inflammation.