| Titre : | Experimental evaluation of the nephroprotective activityandacutetoxicity of a silymarin-based veterinary solution against cisplatininduced nephrotoxicity in Wistar rats : Biochemical andhistopathological study |
| Auteurs : | Omar Badi, Auteur ; Mohamed Zaouani, Directeur de thèse |
| Type de document : | texte imprimé |
| Editeur : | Alger : École Nationale Supérieure Vétérinaire, 2026 |
| Format : | 70 f. / ill. / 30 cm |
| Accompagnement : | CD-Rom |
| Note générale : |
Mémoire de Master: Sciences Vétérinaire: Alger, École Nationale Supérieure Vétérinaire: 2026
Bibliogr., f. 71-75 |
| Langues : | Anglais |
| Mots-clés : | Silymarin ; Cisplatin ; Renoprotection ; Nephrotoxicity ; Wistar rat ; Acute Kidney Injury ; Proximal tubule ; Histopathology |
| Résumé : |
Background: Nephropathies induced by therapeutic agents or environmental
xenobiotics represent a major clinical issue in veterinary medicine, with oxidative stress acting as a primary driver of renal injury. This study investigated the acute toxicity and the preventive renoprotective efficacy of an innovative silymarin-basedveterinary solution against cisplatin-induced acute kidney injury (AKI). Materials and Methods: Systemic safety was evaluated in adult male Wistar rats usingan OECD Guideline 425 oral limit test at a single dose of 2,000 mg/kg. For the nephroprotective arm, rats (n = 5–6/group) were allocated into four groups: NegativeControl, Positive Toxic Control (cisplatin-only), Silymarin treatment (400 mg/kg/dayorally for 10 days + cisplatin on Day 10), and Ascorbic Acid reference (200 mg/kg/day orally for 10 days + cisplatin on Day 10). AKI was induced on Day 10bya single intraperitoneal injection of cisplatin (50 mg/kg). Glomerular and tubular functional endpoints (plasma urea, creatinine, and electrolytes) were quantified onDay 13, alongside qualitative renal histopathological scoring at 400× magnification. Results: The single oral limit dose of 2,000 mg/kg resulted in zero mortality, establishing an oral LD₅₀ > 2,000 mg/kg (GHS Category 5) and demonstrating excellent systemic safety. Cisplatin challenge in the positive control group triggeredasevere uremic crisis, characterized by a 4.7-fold increase in plasma urea and a 4.5-foldsurge in plasma creatinine, which correlated microscopically with severe acute tubular necrosis (ATN), intense proximal tubular degeneration, Bowman's space enlargement, and interstitial leukocyte infiltration. Ten days of oral pretreatment with the silymarinsolution significantly attenuated renal failure, inducing a 34.5% reduction in plasma urea (20.16 ± 4.43 mmol/L) and a 40.0% reduction in plasma creatinine (112.5 ±58.8µmol/L). Plasma electrolytes (Na⁺, K⁺, Cl⁻, and Ca²⁺) were effectively maintainedwithin physiological baseline values. Histopathological assessment confirmed superior preservation of the renal cortical architecture, with maintained cellular boundaries and complete eradication of sloughed intratubular necrotic debris or secondary inflammatory cascades, outperforming the ascorbic acid reference group. Conclusion: The experimental silymarin-based veterinary solution is highly toleratedand exerts robust, multi-targeted nephroprotection against chemotherapeutic-inducedAKI. These findings provide a solid pharmacological foundation supporting its clinical development as a powerful cytoprotective agent in veterinary medicine. |
Exemplaires (2)
| Code-barres | Cote | Support | Localisation | Section | Disponibilité |
|---|---|---|---|---|---|
| Ma4.20044.00/1 | Ma4.20044.00 | Mémoire de Master | B. Magasin des Thèses et PFE | C.Memoires de Master | Consultation sur place Exclu du prêt |
| Ma4.20044.00/2 | Ma4.20044.00 | Mémoire de Master | B. Magasin des Thèses et PFE | C.Memoires de Master | Document en bon état Disponible |
