<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9(16)</volume><submitter>He J</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>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.&lt;h4>Methods&lt;/h4>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.&lt;h4>Results&lt;/h4>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&lt;0.05), while body weight and kidney SOD activity were lower (both P&lt;0.05). By contrast, no differences were observed between the control and VC groups (VC and VCM + VC groups) for all these indicators.&lt;h4>Conclusions&lt;/h4>The antioxidant VC reduces VCM-related renal injury by reducing oxidative stress, cell apoptosis, and inflammation.</pubmed_abstract><journal>Annals of translational medicine</journal><pagination>1319</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8422136</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Vitamin C reduces vancomycin-related nephrotoxicity through the inhibition of oxidative stress, apoptosis, and inflammation in mice.</pubmed_title><pmcid>PMC8422136</pmcid><pubmed_authors>Pan X</pubmed_authors><pubmed_authors>Deng S</pubmed_authors><pubmed_authors>Zheng X</pubmed_authors><pubmed_authors>He J</pubmed_authors><pubmed_authors>Zhao B</pubmed_authors><pubmed_authors>Yu P</pubmed_authors><pubmed_authors>Bian X</pubmed_authors><pubmed_authors>Ni T</pubmed_authors><pubmed_authors>Mao E</pubmed_authors><pubmed_authors>Xu W</pubmed_authors><pubmed_authors>Chen E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Vitamin C reduces vancomycin-related nephrotoxicity through the inhibition of oxidative stress, apoptosis, and inflammation in mice.</name><description>&lt;h4>Background&lt;/h4>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.&lt;h4>Methods&lt;/h4>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.&lt;h4>Results&lt;/h4>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&lt;0.05), while body weight and kidney SOD activity were lower (both P&lt;0.05). By contrast, no differences were observed between the control and VC groups (VC and VCM + VC groups) for all these indicators.&lt;h4>Conclusions&lt;/h4>The antioxidant VC reduces VCM-related renal injury by reducing oxidative stress, cell apoptosis, and inflammation.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2025-04-04T09:37:11.185Z</modification><creation>2025-04-04T09:37:11.185Z</creation></dates><accession>S-EPMC8422136</accession><cross_references><pubmed>34532456</pubmed><doi>10.21037/atm-21-3294</doi></cross_references></HashMap>