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This study investigates the protective effect of opuntiol, a naturally occurring flavonoid, against lipopolysaccharide (LPS)-induced acute kidney injury in mice. Acute kidney injury (AKI) is a serious clinical complication characterized by inflammation, oxidative stress, and apoptosis, often resulting in high morbidity and mortality. Male mice were divided into six groups and administered opuntiol (25, 50 and 100 mg/kg b. wt.) intraperitoneally prior to LPS (10 mg/kg b. wt.) administration. The most effective dose was 50 mg/kg b. wt., as indicated in the dose-finding study. Kidney function markers (urea, creatinine, blood urea nitrogen (BUN), uric acid), antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), cyclooxygenase-2 (COX-2), and gene expression levels (pro-inflammatory, apoptotic, and antioxidant genes) were analyzed using biochemical assays and qRT-PCR. Opuntiol significantly reduced elevated levels of serum urea, creatinine, BUN, and uric acid compared to the LPS group. Further, opuntiol restored antioxidant enzyme activities and MDA levels were significantly decreased. Opuntiol also downregulated inflammatory markers and gene expressions (TNF-α, NF-κB, TLR4, Bax, Caspase-3, etc.) while upregulating anti-apoptotic (Bcl-2) and antioxidant (Nrf-2) genes. Opuntiol offers significant protection against LPS-induced AKI by mitigating oxidative damage, inflammation, and apoptotic signaling. It enhances renal function and promotes antioxidant defense. These findings support the therapeutic potential of opuntiol as a novel nephroprotective agent in managing sepsis-associated kidney injury and encourage further preclinical and clinical investigations.
Li et al. (Tue,) studied this question.