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<p>Cypermethrin is a pyrethroid showing nephrotoxicity by generating ROS-impaired oxidative stress and changes in inflammatory and apoptotic markers. The harmful consequences are intended to be mitigated by the imbalance between oxidants and antioxidants. The anti-inflammatory and antioxidant possessions of nanocurcumin (NC) with improved bioavailability ameliorate Cyp toxicity in rat kidneys. In our study, Group I was the control while Group II was treated alone with NC (5&#xa0;mg). Group III was given 50&#xa0;mg/kg of Cyp for two weeks. Groups IV, V, and VI received Cyp as in group III and co-treatment with varying NC doses after 5&#xa0;days of Cyp dosing, respectively. All treatments were given orally for two weeks. After the termination of the study, LPO, 4-HNE, GSH, antioxidant catalase, and SOD were evaluated as markers of inflammation and apoptosis along with ELISA, qRT-PCR, and histopathology were used to assess morphological changes. Our work has shown that Cyp causes nephrotoxicity by altering all parameters. The Cyp-treated group was shown to have higher expression of the oxidative stress marker LPO and inflammatory interleukins as well as Bax, NF-kB, caspase-3, and caspase-9. Although LPO, inflammation, and apoptosis are reduced, antioxidant status is improved by NC.</p>

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Nephrotoxic effect of cypermethrin ameliorated by nanocurcumin through antioxidative mechanism

  • 期刊论文

  • 发表日期：

    2025年1月29日

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  • Saeed Alshahrani,
  • Mohammad Ashafaq,
  • Abdulmajeed M. Jali,
  • Yosif Almoshari,
  • Mohammad Intakhab Alam,
  • Hamad Al Shahi,
  • Ayed A. Alshamrani,
  • Sohail Hussain

摘要

Cypermethrin is a pyrethroid showing nephrotoxicity by generating ROS-impaired oxidative stress and changes in inflammatory and apoptotic markers. The harmful consequences are intended to be mitigated by the imbalance between oxidants and antioxidants. The anti-inflammatory and antioxidant possessions of nanocurcumin (NC) with improved bioavailability ameliorate Cyp toxicity in rat kidneys. In our study, Group I was the control while Group II was treated alone with NC (5 mg). Group III was given 50 mg/kg of Cyp for two weeks. Groups IV, V, and VI received Cyp as in group III and co-treatment with varying NC doses after 5 days of Cyp dosing, respectively. All treatments were given orally for two weeks. After the termination of the study, LPO, 4-HNE, GSH, antioxidant catalase, and SOD were evaluated as markers of inflammation and apoptosis along with ELISA, qRT-PCR, and histopathology were used to assess morphological changes. Our work has shown that Cyp causes nephrotoxicity by altering all parameters. The Cyp-treated group was shown to have higher expression of the oxidative stress marker LPO and inflammatory interleukins as well as Bax, NF-kB, caspase-3, and caspase-9. Although LPO, inflammation, and apoptosis are reduced, antioxidant status is improved by NC.