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논문분류	춘계학술대회 초록집
제목	Alpha-1 Antitrypsin Protects Against Cisplatin-Induced Acute Kidney Injury by Restoring Redox and Mitochondrial Homeostasis
저자	Mina Kim
출판정보	2026; 2026(1):
키워드	cisplatin-induced acute kidney injury, Alpha-1 antitrypsin, Oxidative oxidative stress, NADPH oxidase, renal tubular injury
초록	Objectives: Cisplatin is an effective chemotherapeutic agent, but yet its clinical utility is limited by dose-dependent nephrotoxicity. Alpha-1 antitrypsin (AAT) has cytoprotective, anti-inflammatory, and anti-apoptotic properties, but its therapeutic potential in cisplatin-induced acute kidney injury (AKI) remains unclear. Methods: A murine cisplatin–AKI model was used to evaluate whether AAT (80 mg/kg) ameliorates renal injury. Renal function, oxidative stress, NADPH oxidase (NOX) isoforms, mitochondrial metabolism, inflammatory mediators, apoptosis, and fibrosis-related markers were assessed using biochemical, histological, immunohistochemical, and Western blot analyses Results: Cisplatin markedly impaired renal function,Cisplatin markedly impaired renal function and inducedinduced tubular injury , and increased NGAL expression; meanwhile, whereas AAT significantly reversed these changes. Cisplatin also induced severe oxidative stress and disrupted NOXthe isoformbalance balanceof NOX isoforms, whereas; AAT restored redox homeostasis. Cisplatin induced maladaptive mitochondrial changes, with upregulated CPT1A/PDK4 upregulation and suppressed CPT2, UCP3, PGC1α, and DRP1, inducing maladaptive mitochondrial changes suppression, indicating impaired β-oxidation and defective mitochondrial dynamics. ; AAT reversed these alterations, and restoring normalized mitochondrial metabolismc pathways. IL-1β, IL-6R, OPN, and F4/80 expression, recovery of the Bax/Bcl-2 ratio, and MAPK activation were reduced, indicating decreased Inflammation inflammation and apoptosis were reduced, as indicated by lower expression of IL-1β, IL-6R, OPN, and F4/80, recovery of the Bax/Bcl-2 ratio, and decreased MAPK activation. P; profibrotic markers were also reduced. Conclusion: AAT confers multifaceted protection against cisplatin-induced AKI by restoring redox balance, mitochondrial homeostasis, and inflammatory and apoptotic signaling. These findings support AAT as a promising therapeutic strategy agent for preventing cisplatin nephrotoxicity.
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