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https://biore.bio.bg.ac.rs/handle/123456789/7750| Title: | Protective Effects of Rosa canina Fruit Extract against Kidney Damage Induced by CCl4 | Authors: | Gazwi, Hanaa S S Ragab, Amany E Soltan, Osama I A Abdein, Mohamed A Shakoor, Bushra Shafiq, Nusrat Refaat, Inas Hussein Al-Rejaie, Salim S Đurašević, Siniša Mohany, Mohamed Zaki, Asmaa H |
Keywords: | CCl(4);Nrf2/HO-1 pathway;Rosa canina;UPLC-ESI-MS/MS;nephrotoxicity | Issue Date: | 18-Jul-2025 | Rank: | M21a+ | Publisher: | Elsevier | Journal: | Regulatory toxicology and pharmacology : RTP | Start page: | 105913 | Abstract: | The study explored the nephroprotective potential of Rosa canina (dog rose) ethanolic fruit extract against carbon tetrachloride (CCl4)-induced nephrotoxicity in rats, while also analyzing its phytochemical composition using UPLC-ESI-MS/MS. Male Wistar rats were allocated into five groups: control, R. canina extract alone, CCl4-induced nephrotoxicity, CCl4 with R. canina extract and CCl4 with silymarin. UPLC-ESI-MS/MS revealed 15 compounds in R. canina extract, predominantly anthocyanins, flavonoids, and lycopene. Treatment with R. canina extract significantly ameliorated CCl4-induced kidney dysfunction, abating oxidative stress and inflammation. Enhanced expression of HO-1 (heme oxygenase-1) and Nrf2 (nuclear factor erythroid 2-related factor 2) mRNA in the kidney suggested their involvement in protective mechanisms. Inhibition of HO-1 attenuated R. canina's protective effect against CCl4-induced kidney injury, underscoring the significance of the Nrf2/HO-1 pathway. For further validation, high throughput molecular docking analysis were performed. The docking analysis revealed the interaction between HO-1 and Nrf2 against Pelarginidin, Malvidin and Petunidin. Among all the three compounds, pelargonidin showed the highest binding score of -9.3kcal/mol and -7.7kcal/mol against Nrf2 and HO-1 respectively. In conclusion, R. canina extract, rich in phenolics, exhibited nephroprotective effects via inflammation and oxidative stress attenuation, potentially mediated through Nrf2/HO-1 pathway modulation against CCl4-induced nephrotoxicity. |
URI: | https://biore.bio.bg.ac.rs/handle/123456789/7750 | ISSN: | 02732300 | DOI: | 10.1016/j.yrtph.2025.105913 |
| Appears in Collections: | Journal Article |
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