Dihydromyricetin Modulates Nrf2 and NF-κB Crosstalk to Alleviate Methotrexate-Induced Lung Toxicity

Matouk, Asmaa I.; Awad, Eman M.; El‐Tahawy, Nashwa Fathy Gamal; El-Sheikh, Azza A. K.; Anter, Aliaa

doi:10.3390/ph16040481

Cited by 8 publications

(2 citation statements)

References 94 publications

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“…In the present study, MTX mediated the inflammatory response in the lung through a significant increase in the levels of lung IL-6, IL-1β, and NF-κB. This corroborates earlier reports (Zaki et al, 2021;Kaymak et al, 2022;Matouk et al, 2023). NO is recognized as an inflammatory response mediator and regulator.…”

Section: Dar Et Al (2021) and Matouk Et Al (2023)supporting

confidence: 93%

Effect of Aminoguanidine on Methotrexate-Induced Lung Toxicity in Male Wistar Rats

Ali

Mohammed

2023

Records of Pharmaceutical and Biomedical Sciences

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The present work was designed to investigate the effect of aminoguanidine (AMG) on methotrexate (MTX)-induced lung toxicity in rats. Forty adult male rats weighing 200-220 gm divided into four groups, 10 each were used in the study. The control group received normal saline. AMG-treated group: rats received 50 mg/kg/day AMG. Whereas the MTX-treated group: rats received 0.5 mg/kg MTX twice weekly, and AMG+MTX-treated group: rats were co-administered AMG and MTX at the same doses as in the previous groups. All groups received their treatment via the IP route. Additionally, the experiment duration was 4 weeks. MTX administration revealed a significant decrease in SOD, CAT, GSH, Nrf2, and Bcl-2 accompanied by a significant increase in MDA, NO, IL-6, IL-1β, NF-κB, caspase-3, and Bax compared to the control group. Moreover, there were histological abnormalities in the lung tissue. However, the AMG+MTX-treated group produced a significant increase in SOD, CAT, GSH, Nrf2, and Bcl-2, and a significant decrease in MDA, NO, IL-6, IL-1β, NF-κB, caspase-3, and Bax compared to the MTX-treated group. Besides, the histological results strongly supported our biochemical findings. The present study demonstrated the protective effect of AMG against MTXinduced lung toxicity in rats through its antioxidant, anti-inflammatory, and anti-apoptotic actions.

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Section: Dar Et Al (2021) and Matouk Et Al (2023)supporting

confidence: 93%

Effect of Aminoguanidine on Methotrexate-Induced Lung Toxicity in Male Wistar Rats

Ali

Mohammed

2023

Records of Pharmaceutical and Biomedical Sciences

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“…For example, DMY can effectively reduce the size of hematoma and cell apoptosis in brain tissue, increase the expression of LCN2, and inhibit ferroptosis caused by SLC3A2 to alleviate cerebral hemorrhage [ 18 ]. In addition, when DMY was used to interfere with fibrotic lung injury induced by methotrexate, it was found through lung histopathological examination that DMY could reduce the levels of NF-κB, IL-1β and TGF-β1 to inhibit lung inflammation and pulmonary fibrosis [ 19 ]. DMY also has a therapeutic effect on kidney lesions.…”

Section: Discussionmentioning

confidence: 99%

Protective effect and pharmacokinetics of dihydromyricetin nanoparticles on oxidative damage of myocardium

Du,

Lu,

Xiao

et al. 2024

PLoS ONE

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Purpose This study aims to investigate the protective mechanism of dihydromyricetin PLGA nanoparticles (DMY-PLGA NPs) against myocardial ischemia-reperfusion injury (MIRI) in vitro and the improvement of oral bioavailability in vivo. Methods DMY-PLGA NPs was prepared and characterized by emulsifying solvent volatilization, and the oxidative stress model of rat H9c2 cardiomyocyte induced by H2O2 was established. After administration, cell survival rate, lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) were detected, and the expressions of PGC1α and PPARα were detected by western blot (WB). At the same time, the pharmacokinetics in rats were studied to explore the improvement of bioavailability. Results DMY-PLGA NPs can significantly increase cell survival rate, decrease LDH and MDA content, increase SOD content and PGC1α、PPARα protein expression. Compared with DMY, the peak time of DMY-PLGA NPs was extended (P<0.1), and the bioavailability was increased by 2.04 times. Conclusion DMY-PLGA NPs has a significant protective effect on H9c2 cardiomyocytes, which promotes the absorption of DMY and effectively improves bioavailability.

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Potential Effect of Etoricoxib in Reducing Inflammation in Methotrexate-Induced Pulmonary Injury in Rats: Role of Oxidative Stress and the TLR4/p38-MAPK/NF-κB Signaling Pathway

Abdelall,

Khames,

Bekhit

et al. 2024

Inflammation

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Numerous chemotherapeutic medications can have hazardous effects on the lungs, which can result in severe lung diseases. Methotrexate (MTX) is prescribed for cancer and inflammation-related disorders; nevertheless, it is exceptionally highly toxic and has multiple kinds of adverse reactions, including pulmonary injury. Our work was designed to demonstrate the ability of etoricoxib (ETO) to mitigate MTX-induced lung injury in experimental animals. Adult male Wistar rats were separated into four groups. The first group consisted of healthy controls that received carboxymethyl cellulose (1 ml/day, p.o.), the second group received a single dose of MTX (20 mg/kg/day, i.p.), the third group received ETO (10 mg/kg/day, p.o.) for three weeks, and the fourth group first received a single MTX (20 mg/kg, i.p.) and then was treated with ETO for three weeks. Concomitant treatment with ETO and MTX improved the histological structure of the lung tissue. It significantly altered the levels of oxidant/antioxidant markers, such as malondialdehyde (MDA), heme oxygenase-1 (HO-1), reduced glutathione (GSH), and nuclear factor erythroid 2-related factor 2 (Nrf-2), in favor of antioxidants. Moreover, ETO can normalize the proinflammatory cascade, which includes tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). At the molecular level, ETO downregulated the protein expression of toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), and p38 mitogen-activated protein kinase (p38 MAPK) in inflamed rat lungs. In conclusion, our findings indicate that oral administration of ETO ameliorates MTX-induced lung injury by inhibiting oxidative stress and suppressing the TLR4/NF-κB and TLR4/p38-MAPK inflammatory signaling pathways.

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Dihydromyricetin Modulates Nrf2 and NF-κB Crosstalk to Alleviate Methotrexate-Induced Lung Toxicity

Cited by 8 publications

References 94 publications

Effect of Aminoguanidine on Methotrexate-Induced Lung Toxicity in Male Wistar Rats

Effect of Aminoguanidine on Methotrexate-Induced Lung Toxicity in Male Wistar Rats

Protective effect and pharmacokinetics of dihydromyricetin nanoparticles on oxidative damage of myocardium

Potential Effect of Etoricoxib in Reducing Inflammation in Methotrexate-Induced Pulmonary Injury in Rats: Role of Oxidative Stress and the TLR4/p38-MAPK/NF-κB Signaling Pathway

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