Nephroprotective effects of Zanthoxylum armatum DC. extract via modulation of oxidative and nitrosative stress in acute kidney injury in rats

花椒提取物通过调节大鼠急性肾损伤中的氧化应激和亚硝化应激发挥肾脏保护作用

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Abstract

BACKGROUND: Zanthoxylum armatum DC. has anti-inflammatory, antibacterial, antioxidant, and antipyretic properties, which are widely recognized. In this study, phytochemical components, antioxidant efficacy, in vivo nephroprotective activity, and immunomodulatory potential of Z. armatum DC. hydroethanolic extract have been investigated in a gentamicin-induced acute kidney injury (AKI) rat model. METHODS: Rats treated with gentamicin (100 mg/kg) for 8 days were administered Zanthoxylum armatum DC. extract. Based on biochemistry, oxidative stress indices, cytokine levels, kidney injury biomarkers, and histopathology, the nephroprotective and immunomodulatory efficacy of Z. armatum DC. extract was evaluated. RESULTS: Catalase, glutathione reductase, superoxide dismutase, and interleukin-10 levels in blood and tissue homogenates decreased due to gentamicin toxicity, whereas serum creatinine, blood urea nitrogen, lipid peroxide, tumor necrosis factor-alpha, cystatin C, kidney injury molecule-1, and gamma-glutamyl transpeptidase levels elevated. Zanthoxylum armatum DC. treatment reduced kidney damage, cytokine imbalance, and oxidative stress; however, results were nearly similar to standard drug. The organoprotective efficacy of Z. armatum DC. was further validated by histopathology of kidney, liver, and heart tissues. CONCLUSION: The present research shows that Z. armatum DC. can ameliorate gentamicin-induced AKI, which may be attributed to its antioxidant properties, phenolic and flavonoid phytoconstituents, and ability to suppress inflammatory cytokines. Further studies may therefore be developed to assess its safety and efficacy for clinical trials. STATEMENT OF NOVELTY: Z. armatum DC. hydroethanolic extract has various properties like antioxidant, organoprotective, anti-inflammatory, and potential to inhibit biochemical parameters involved in renal impairment via blocking p38 mitogen-activated protein kinase/nuclear factor kappa B p65 signaling pathway.

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