The protective impacts of <i>Spirulina platensis</i> against cisplatin-induced renal injury through the regulation of oxidative stress, pro-inflammatory cytokines and Bax/Bcl2

Abstract

One of the main antineoplastic chemotherapy medications is <i>cisplatin</i>, of which nephropathy is a major side effect. In this current study, we aim to investigate the molecular protective effect of <i>Spirulina platensis</i> (<i>SP</i>) on <i>cisplatin</i>-induced nephrotoxicity. In total, 48 healthy male albino rats were allocated into 4 groups. Group 1 received saline intraperitoneally (IP) twice per week (normal rats). Group 2 received <i>SP</i> (100 mg/kg BW orally). Group 3 were injected with cisplatin (1.5 mg/kg IP) twice per week. Group 4 received <i>SP</i> and on the 4th day received cisplatin (1.5 mg/kg IP) for 21 days. After 3 weeks of experiment, blood and renal tissues were taken for serum analysis, gene expression using qRT-polymerase chain reaction, and renal histopathology. As per our findings, it was found that <i>SP</i> significantly ameliorated the alterations in body weight, relative kidney weight, and the disturbance in examined renal markers. Furthermore, SP recovered and restored cisplatin-induced oxidative stress biomarkers (MDA and NO) and antioxidant activity (SOD and GSH) and cisplatin-induced upregulation in the gene expression of TNF-α, inducible nitric oxide synthase, TGF1-β, IL-1β, and IL-6. Interestingly, these gene expressions were ameliorated by the SP pre-administration. Furthermore, <i>cisplatin</i> upregulated pro-apoptotic gene <i>Bax</i>, whereas it downregulated anti-apoptotic gene <i>Bcl2</i>. Interestingly, <i>SP</i> mitigated this alteration in apoptosis and anti-apoptotic associated genes. Renal histopathology revealed the protective impacts of <i>SP</i> against <i>cisplatin</i>-induced severe glomerular congestion, hemorrhage, inflammatory cell infiltration, degeneration, and severe necrosis in renal glomeruli and tubules. In conclusion, <i>SP</i> has a protective effect against cisplatin-induced renal damage through modulating oxidative stress and anti-inflammatory, anti-necrotic, and anti-apoptotic-associated genes.