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Octreotide mitigates cisplatin-induced nephrotoxicity through coordinated modulation of the miR-34a/SIRT1 axis and
Mai El-Sayed Ghoneim1, Yousra Y El Banna2, Mohamed H Noureldin3
1Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Sadat City (USC), 32897, Sadat City, Egypt.
Aims:
Cisplatin (CIS) is a widely used chemotherapeutic agent, but its clinical utility is limited by dose-dependent nephrotoxicity. Octreotide (OCT), a somatostatin analog, exhibits anti-inflammatory, antioxidant, and anti-apoptotic properties in several experimental models, yet its therapeutic potential against cisplatin-induced nephrotoxicity remains largely unexplored. This study, therefore, investigated the nephroprotective potential and the underlying molecular mechanisms of octreotide against cisplatin-induced nephrotoxicity, and asked whether protection depends on the timing of administration.
Material And Methods:
Rats were allocated into five groups: Normal control (NC); OCT control (82.5 μg/kg, intramuscularly); CIS (a single intraperitoneal injection of 7 mg/kg); peri-treatment OCT was administered 7 days before and continued 14 days following cisplatin administration; and post-treatment OCT was initiated after cisplatin administration and continued for 14 days.
Key Findings:
Octreotide significantly improved renal function, attenuated tubular injury, and preserved renal histoarchitecture following cisplatin administration. These protective effects were associated with preservation of renal SSTR2 expression, suppression of cisplatin-induced miR-34a upregulation, and restoration of SIRT1 expression. This molecular response coincided with attenuation of p53-mediated apoptosis, enhancement of Nrf2/HO-1-dependent antioxidant defenses, inhibition of NF-κB-induced inflammation, restoration of IL-6-associated reparative responses, and suppression of TGF-β1/α-SMA-mediated profibrotic signaling, with the peri-treatment protocol consistently outperforming post-treatment.
Significance:
Octreotide, particularly the peri-treatment protocol, confers significant protection against cisplatin-induced nephrotoxicity and is associated with coordinated modulation of the SSTR2/miR-34a/SIRT1 signaling axis and its downstream cytoprotective pathways, supporting its potential repurposing as a nephroprotective adjunct to cisplatin-based chemotherapy.
