Aspirin eugenol ester ameliorates paraquat-induced oxidative damage through ROS/p38-MAPK-mediated mitochondrial apoptosis pathway

Zhang, Zhendong; Yang, Yajun; Liu, Xi-Wang; Qin, Zhe; Li, Shihong; Li, Jianyong

doi:10.1016/j.tox.2021.152721

Cited by 40 publications

(26 citation statements)

References 43 publications

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“…DNA repair enzymes are essential to break this vicious cycle ( Figure 4 ). For the elimination of ROS shown in Figure 5 , antioxidant enzymes and GSH/GSSH conversion play an essential role in mitochondria ( Zhang et al, 2021 ). The endogenous hormone melatonin maintains these antioxidant processes by protecting mitochondrial function ( Yang et al, 2021b ).…”

Section: Discussionmentioning

confidence: 99%

Three Classes of Antioxidant Defense Systems and the Development of Postmenopausal Osteoporosis

et al. 2022

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Osteoporosis is a common bone imbalance disease that threatens the health of postmenopausal women. Estrogen deficiency accelerates the aging of women. Oxidative stress damage is regarded as the main pathogenesis of postmenopausal osteoporosis. The accumulation of reactive oxygen species in the bone microenvironment plays a role in osteoblast and osteoclast apoptosis. Improving the oxidative state is essential for the prevention and treatment of postmenopausal osteoporosis. There are three classes of antioxidant defense systems in the body to eliminate free radicals and peroxides including antioxidant substances, antioxidant enzymes, and repair enzymes. In our review, we demonstrated the mechanism of antioxidants and their effect on bone metabolism in detail. We concluded that glutathione/oxidized glutathione (GSH/GSSG) conversion involved the PI3K/Akt-Nrf2/HO-1 signaling pathway and that the antioxidant enzyme-mediated mitochondrial apoptosis pathway of osteoblasts was necessary for the development of postmenopausal osteoporosis. Since the current therapeutic effects of targeting bone cells are not significant, improving the systemic peroxidation state and then regulating bone homeostasis will be a new method for the treatment of postmenopausal osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Three Classes of Antioxidant Defense Systems and the Development of Postmenopausal Osteoporosis

et al. 2022

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“…Studies have also shown that autophagy can promote cell apoptosis and ROS are considered to be the main molecules associated with cell apoptosis and autophagy ( 34 , 35 ). ROS can regulate cell growth and survival, as well as inhibit the PI3K/Akt signaling pathway ( 36 ) and activate the MAPK signaling pathway ( 37 ). The present study found that SAL alone and in combination with 17-AAG could cause an increase in the ROS content.…”

Section: Discussionmentioning

confidence: 99%

Synergistic inhibition of the growth of MDA‑MB‑231 cells in triple‑negative breast cancer by salinomycin combined with 17‑AAG and its mechanism

et al. 2022

Oncol Lett

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Salinomycin (SAL), a typical ion carrier antibiotic, inhibits tumor growth and metastasis by inducing apoptosis or autophagy in cancer or cancer stem cells and thus overcomes drug resistance. 17-allylamino-17-demethoxygeldanamycin (17-AAG), a heat shock protein Hsp90 competitive inhibitor, also has a role in inhibiting tumor development. However, their combination on the growth of breast cancer cells and its specific mechanism remains to be elucidated. The present study tested the influence of SAL and 17-AAG on cell growth, apoptosis and autophagy by MTT assays, Annexin V-FITC and propidium iodide double staining assay and immunoelectron microscopy. The influence of SAL and 17-AAG on proteomics was investigated by isobaric tag for relative and absolute quantitation. It was found that SAL combined with 17-AAG synergistically inhibited the cell growth and induced the apoptosis in a concentration-dependent manner, with the expression of caspase 3 and Bcl-2 were decreased while the expression of Bax was increased. In addition, SAL combined with 17-AAG inhibited autophagy, with the expression of microtubule-associated protein 1 light chain 3, Beclin1, p62 being decreased. Mechanistically, SAL combined with 17-AAG synergistically inhibited the reactive oxygen species/JNK signaling pathway. In conclusion, SAL combined with 17-AAG had a synergistic inhibitory effect on cell growth of breast cancer via inducing apoptosis and inhibiting autophagy. The present study might provide a new strategy for potential clinical application of SAL as a new anti-tumor drug especially as a drug combination with other molecular targeting therapeutics.

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“…The MAPK pathway activated in response to extracellular stimuli and regulated the synthesis and release of pro-inflammatory mediators. Inhibition of the phosphorylation of the MAPK pathway can obviously attenuate the pro-inflammatory mediator transcript and release ( Zhang et al, 2021 ). The phosphorylated MAPK cascade would further lead to IκB-α activation, which induces the NF-κB activity ( Ko et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Fluorofenidone Against Acute Lung Injury Through Suppressing the MAPK/NF-κB Pathway

Lv¹,

Yao²,

He³

et al. 2021

Front. Pharmacol.

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Acute lung injury (ALI) is a severe disease that presents serious damage and excessive inflammation in lungs with high mortality without effective pharmacological therapy. Fluorofenidone (AKFPD) is a novel pyridone agent that has anti-fibrosis, anti-inflammation, and other pharmacological activities, while the effect of fluorofenidone on ALI is unclarified. Here, we elucidated the protective effects and underlying mechanism of fluorofenidone on lipopolysaccharide (LPS)-induced ALI. In this study, fluorofenidone alleviated lung tissue structure injury and reduced mortality, decreased the pulmonary inflammatory cell accumulation and level of inflammatory cytokines IL-1β, IL-6, and TNF-α in the bronchoalveolar lavage fluid, and attenuated pulmonary apoptosis in LPS-induced ALI mice. Moreover, fluorofenidone could block LPS-activated phosphorylation of ERK, JNK, and P38 and further inhibited the phosphorylation of IκB and P65. These results suggested that fluorofenidone can significantly contrast LPS-induced ALI through suppressing the activation of the MAPK/NF-κB signaling pathway, which indicates that fluorofenidone could be considered as a novel therapeutic candidate for ALI.

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Aspirin eugenol ester ameliorates paraquat-induced oxidative damage through ROS/p38-MAPK-mediated mitochondrial apoptosis pathway

Cited by 40 publications

References 43 publications

Three Classes of Antioxidant Defense Systems and the Development of Postmenopausal Osteoporosis

Three Classes of Antioxidant Defense Systems and the Development of Postmenopausal Osteoporosis

Synergistic inhibition of the growth of MDA‑MB‑231 cells in triple‑negative breast cancer by salinomycin combined with 17‑AAG and its mechanism

Protective Effect of Fluorofenidone Against Acute Lung Injury Through Suppressing the MAPK/NF-κB Pathway

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