Trinitroglycerine-loaded chitosan nanoparticles attenuate renal ischemia-reperfusion injury by modulating oxidative stress
Abstract Renal ischemia-reperfusion (I/R) injury is a common clinical factor for acute kidney injury (AKI). A current study investigated the renoprotective effects of the trinitroglycerine (TNG) combination with chitosan nanoparticles (CNPs) on renal I/R-induced AKI. Rats were randomly assigned to f...
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Nature Portfolio
2024-12-01
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| author | Zeinab Karimi Khatereh Asadi Pooran Ghahramani Ahmad Gholami |
| author_facet | Zeinab Karimi Khatereh Asadi Pooran Ghahramani Ahmad Gholami |
| author_sort | Zeinab Karimi |
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| description | Abstract Renal ischemia-reperfusion (I/R) injury is a common clinical factor for acute kidney injury (AKI). A current study investigated the renoprotective effects of the trinitroglycerine (TNG) combination with chitosan nanoparticles (CNPs) on renal I/R-induced AKI. Rats were randomly assigned to five groups (n = 8/group): Sham, I/R, TNG (50 mg/kg) + I/R, CNPs (60 mg/kg) + I/R, and TNG-CNPs + I/R. Bilateral renal pedicles were occluded for 60 min to induce ischemia. TNG, CNPs, or TNG-CNPs were administered intraperitoneally 30 min before renal ischemia. After 24 h of reperfusion, blood samples were collected, and both kidneys were removed. The left kidney was used for oxidative stress analysis. The right kidney was preserved in 10% formalin for histopathological examination via H&E staining. After renal ischemia-reperfusion injury, there was an observed increase in plasma creatinine (Cr) and blood urea nitrogen (BUN), accompanied by a decrease in glomerular filtration rate (GFR) in rats. Total oxidative stress (TOS) levels were also significantly higher in the I/R group, whereas total antioxidative capacity (TAC) was reduced. Histopathological examination revealed damage in the kidneys of rats in the I/R group. Pretreatment with the TNG-CNP formulation before I/R increased plasma and tissue TAC levels in rats. It also corrected the renal histopathological changes and functional disorders induced by I/R injury, as evidenced by reduced Cr and BUN, increased GFR, and attenuated oxidative stress. The results suggest that the TNG-CNP combination provides renoprotective effects against I/R-induced AKI by improving antioxidant status and minimizing renal injury. |
| format | Article |
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| institution | Kabale University |
| issn | 2045-2322 |
| language | English |
| publishDate | 2024-12-01 |
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| spelling | doaj-art-e47016bf6c764dc29bcb1d9a19235eb32025-01-05T12:30:41ZengNature PortfolioScientific Reports2045-23222024-12-0114111010.1038/s41598-024-83886-3Trinitroglycerine-loaded chitosan nanoparticles attenuate renal ischemia-reperfusion injury by modulating oxidative stressZeinab Karimi0Khatereh Asadi1Pooran Ghahramani2Ahmad Gholami3Shiraz Nephro-Urology Research Center, Shiraz University of Medical SciencesBiotechnology Research Center, Shiraz University of Medical SciencesDepartment of Biology Faculty of Sciences, Shiraz UniversityBiotechnology Research Center, Shiraz University of Medical SciencesAbstract Renal ischemia-reperfusion (I/R) injury is a common clinical factor for acute kidney injury (AKI). A current study investigated the renoprotective effects of the trinitroglycerine (TNG) combination with chitosan nanoparticles (CNPs) on renal I/R-induced AKI. Rats were randomly assigned to five groups (n = 8/group): Sham, I/R, TNG (50 mg/kg) + I/R, CNPs (60 mg/kg) + I/R, and TNG-CNPs + I/R. Bilateral renal pedicles were occluded for 60 min to induce ischemia. TNG, CNPs, or TNG-CNPs were administered intraperitoneally 30 min before renal ischemia. After 24 h of reperfusion, blood samples were collected, and both kidneys were removed. The left kidney was used for oxidative stress analysis. The right kidney was preserved in 10% formalin for histopathological examination via H&E staining. After renal ischemia-reperfusion injury, there was an observed increase in plasma creatinine (Cr) and blood urea nitrogen (BUN), accompanied by a decrease in glomerular filtration rate (GFR) in rats. Total oxidative stress (TOS) levels were also significantly higher in the I/R group, whereas total antioxidative capacity (TAC) was reduced. Histopathological examination revealed damage in the kidneys of rats in the I/R group. Pretreatment with the TNG-CNP formulation before I/R increased plasma and tissue TAC levels in rats. It also corrected the renal histopathological changes and functional disorders induced by I/R injury, as evidenced by reduced Cr and BUN, increased GFR, and attenuated oxidative stress. The results suggest that the TNG-CNP combination provides renoprotective effects against I/R-induced AKI by improving antioxidant status and minimizing renal injury.https://doi.org/10.1038/s41598-024-83886-3NanoparticleChitosanTrinitroglycerineRenal ischemia-reperfusionOxidative stressRenoprotective |
| spellingShingle | Zeinab Karimi Khatereh Asadi Pooran Ghahramani Ahmad Gholami Trinitroglycerine-loaded chitosan nanoparticles attenuate renal ischemia-reperfusion injury by modulating oxidative stress Scientific Reports Nanoparticle Chitosan Trinitroglycerine Renal ischemia-reperfusion Oxidative stress Renoprotective |
| title | Trinitroglycerine-loaded chitosan nanoparticles attenuate renal ischemia-reperfusion injury by modulating oxidative stress |
| title_full | Trinitroglycerine-loaded chitosan nanoparticles attenuate renal ischemia-reperfusion injury by modulating oxidative stress |
| title_fullStr | Trinitroglycerine-loaded chitosan nanoparticles attenuate renal ischemia-reperfusion injury by modulating oxidative stress |
| title_full_unstemmed | Trinitroglycerine-loaded chitosan nanoparticles attenuate renal ischemia-reperfusion injury by modulating oxidative stress |
| title_short | Trinitroglycerine-loaded chitosan nanoparticles attenuate renal ischemia-reperfusion injury by modulating oxidative stress |
| title_sort | trinitroglycerine loaded chitosan nanoparticles attenuate renal ischemia reperfusion injury by modulating oxidative stress |
| topic | Nanoparticle Chitosan Trinitroglycerine Renal ischemia-reperfusion Oxidative stress Renoprotective |
| url | https://doi.org/10.1038/s41598-024-83886-3 |
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