Methotrexate hepatotoxicity is associated with oxidative stress, and down-regulation of PPARγ and Nrf2: Protective effect of 18β-Glycyrrhetinic acid.

@article{Mahmoud2017MethotrexateHI,
  title={Methotrexate hepatotoxicity is associated with oxidative stress, and down-regulation of PPAR$\gamma$ and Nrf2: Protective effect of 18$\beta$-Glycyrrhetinic acid.},
  author={Ayman Moawad Mahmoud and Omnia E. Hussein and Walaa G. Hozayen and Sanaa M. Abd El-Twab},
  journal={Chemico-biological interactions},
  year={2017},
  volume={270},
  pages={
          59-72
        }
}

Chicoric acid prevents methotrexate hepatotoxicity via attenuation of oxidative stress and inflammation and up-regulation of PPARγ and Nrf2/HO-1 signaling

CA prevented oxidative stress, inflammation, and liver injury induced by MTX by activating Nrf2 /HO-1 signaling and PPARγ and inhibited apoptosis in MTX-administered rats.

Ferulic acid prevents oxidative stress, inflammation, and liver injury via upregulation of Nrf2/HO-1 signaling in methotrexate-induced rats

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Human placental extract ameliorates methotrexate-induced hepatotoxicity in rats via regulating antioxidative and anti-inflammatory responses

HPE has the ability to ameliorate methotrexate-induced liver injury in rats by mechanisms that include boosting antioxidative responses and down-regulating MDA and pro-inflammatory cytokine production.

Galangin mitigates oxidative stress, inflammation, and apoptosis in a rat model of methotrexate hepatotoxicity

Gal possesses a hepatoprotective effect mediated by attenuating oxidative damage, inflammation, and apoptosis in rats, which relieved liver injury, ameliorated liver function, oxidative stress, and inflammation markers, and increased antioxidants in MTX-treated rats.

Ellagic acid reduces methotrexate-induced apoptosis and mitochondrial dysfunction via up-regulating Nrf2 expression and inhibiting the IĸBα/NFĸB in rats

The clinical application of methotrexate (MTX), an efficacious cytotoxic drug, is restricted due to its associated liver toxicity. Ellagic acid (EA), a natural polyphenol, possesses hepatoprotective,

Activation of pCREB/Nrf-2 signaling mediates re-positioning of liraglutide as hepato-protective for methotrexate -induced liver injury (MILI).

Punicalagin Protects against the Development of Methotrexate-Induced Hepatotoxicity in Mice via Activating Nrf2 Signaling and Decreasing Oxidative Stress, Inflammation, and Cell Death

PU inhibits oxidative damage, inflammation, and apoptosis and upregulates Nrf2 in the liver of MTX-induced mice, suggesting that PU may have great therapeutic potential for the prevention of methotrexate-induced hepatotoxicity.
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18β-Glycyrrhetinic acid protects against methotrexate-induced kidney injury by up-regulating the Nrf2/ARE/HO-1 pathway and endogenous antioxidants

Findings make 18β-GA candidate as a potent agent in preventing MTX-induced kidney injury with possible mechanisms of attenuating oxidative stress and inflammation through up-regulating the Nrf2/ARE signaling.

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