A novel, highly-water-soluble apigenin derivative provides neuroprotection following ischemia in male rats by regulating the ERK/Nrf2/HO-1 pathway

Zhang, Sen; Xu, Sikai; Duan, Huifang; Zhu, Zhenhua; Zhou, Yang; Cao, Jianan; Zhao, Yuxiang; Huang, Zhiheng; Wu, Qinan; Duan, Jin‐Ao

doi:10.1016/j.ejphar.2019.03.024

Cited by 25 publications

(15 citation statements)

References 41 publications

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“…all mice were euthanized by cervical dislocation after the behavioral tests, and the hippocampus samples were promptly collected and placed on ice. The samples were then placed into radioimmunoprecipitation assay buffer (Beyotime institute of Biotechnology) with an enzyme inhibitor (Beyotime Institute of Biotechnology) at 5˚C and rapidly homogenized for western blotting, as previously reported (21,26). Protein concentration was determined colorimetrically by BCA assay (Pierce; Thermo Fisher Scientific, inc.).…”

Section: Tail Suspension Testmentioning

confidence: 99%

The antidepressant effects of apigenin are associated with the�promotion of autophagy via the mTOR/AMPK/ULK1 pathway

Zhang

Jiang

et al. 2019

Mol Med Report

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The present study aimed to investigate whether apigenin elicits antidepressant effects in depressant-like mice via the regulation of autophagy. The depressant-like behaviors were established in a chronic restraint stress model. Male BalB/c mice were subjected to restraint stress for 6 h/day for a period of 21 days, and deficits in sucrose preference, tail suspension and forced swim tests were confirmed to be improved following oral apigenin. To investigate the underlining mechanisms, the hippocampal levels of p62 and microtubule-associated protein light chain 3-ii/i (lc3-ii/i) were measured using western blot analysis. The expression levels of lc3-ii/i and p62 indicated that the significantly inhibited autophagy level induced by chronic restraint stress can be increased following apigenin treatment. Similar to the level of autophagy, the expression levels of adenosine monophosphate-activated protein kinase (aMPK) and unc-51 like autophagy activating kinase-1 were downregulated after chronic restraint stress stimulation and, subsequently upregulated following treatment with apigenin. conversely, the levels of mammalian target of rapamycin (mTor) were increased in chronic restraint stress mice and inhibited by apigenin. Collectively, the present findings indicated that apigenin potentially promotes autophagy via the aMPK/mTor pathway and induces antidepressive effects in chronic restraint stress mice.

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Section: Tail Suspension Testmentioning

confidence: 99%

The antidepressant effects of apigenin are associated with the�promotion of autophagy via the mTOR/AMPK/ULK1 pathway

Zhang

Jiang

et al. 2019

Mol Med Report

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“…Upon the deficiency of miR-24, the increased expression of KEAP1 is found together with a decreased expression of NRF2 and heme oxygenase-2 (HO-2) in both HG-VSMCs in diabetic rats. In the same study, the upregulation of miR-24 improved the reendothelialization in balloon-injured diabetic rats, which was due to decreased oxidative stress via the NRF2/HO-1 signaling pathway that restored the activity of antioxidant enzymes SOD and glutathione peroxidize (GPx) in balloon-injured diabetic rats [ 26 ].…”

Section: Nrf2 Signaling In Oxidative Stress-mediated Diseasesmentioning

confidence: 99%

Bioactive Compounds in Oxidative Stress-Mediated Diseases: Targeting the NRF2/ARE Signaling Pathway and Epigenetic Regulation

Venkidasamy²,

et al. 2021

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Oxidative stress is a pathological condition occurring due to an imbalance between the oxidants and antioxidant defense systems in the body. Nuclear factor E2-related factor 2 (NRF2), encoded by the gene NFE2L2, is the master regulator of phase II antioxidant enzymes that protect against oxidative stress and inflammation. NRF2/ARE signaling has been considered as a promising target against oxidative stress-mediated diseases like diabetes, fibrosis, neurotoxicity, and cancer. The consumption of dietary phytochemicals acts as an effective modulator of NRF2/ARE in various acute and chronic diseases. In the present review, we discussed the role of NRF2 in diabetes, Alzheimer’s disease (AD), Parkinson’s disease (PD), cancer, and atherosclerosis. Additionally, we discussed the phytochemicals like curcumin, quercetin, resveratrol, epigallocatechin gallate, apigenin, sulforaphane, and ursolic acid that have effectively modified NRF2 signaling and prevented various diseases in both in vitro and in vivo models. Based on the literature, it is clear that dietary phytochemicals can prevent diseases by (1) blocking oxidative stress-inhibiting inflammatory mediators through inhibiting Keap1 or activating Nrf2 expression and its downstream targets in the nucleus, including HO-1, SOD, and CAT; (2) regulating NRF2 signaling by various kinases like GSK3beta, PI3/AKT, and MAPK; and (3) modifying epigenetic modulation, such as methylation, at the NRF2 promoter region; however, further investigation into other upstream signaling molecules like NRF2 and the effect of phytochemicals on them still need to be investigated in the near future.

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“…API not only scavenges free radicals directly but also enhances the antioxidant ability of cells by regulating heme oxygenase (HO-1), glutamate-cysteine ligase, catalytic subunit (GCLC) and glutamate-cysteine ligase, modifier subunit (GCLM) gene transcription via the extracellular regulated protein kinases 2 (ERK2)/nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathways (Hassanpour and Niknam, 2020;Huang et al, 2013). Many studies have found that API helps in preventing oxidative stress injury by increasing the expression of antioxidant enzymes both at the mRNA and protein levels in several cells (Ogura et al, 2020;Zhang et al, 2019;Xu et al, 2016). However, to the best of our knowledge, there is no published study focusing on the direct antioxidant effects of API on myocytes.…”

Section: Antioxidant Functionmentioning

confidence: 99%

Apigenin as a promising myocyte protectant against damage and degradation

Huang¹,

Zhang²,

Ning³

et al. 2022

Biocell

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Myocytes power the movement of all organs in the body. Damage to and degradation of myocytes causes hypokinesia and muscle-related degenerative diseases. Apigenin, a kind of flavone, is being used to treat many disorders. It exerts a host of different pharmacological activities, such as anti-inflammatory, anti-mutagenic, cardioprotective, and antioxidant effects. Accordingly, apigenin is considered a promising candidate for myocyte protection. In this review, we introduced the characteristics of apigenin. The means of apigenin protection of myocytes as well as the mechanism were summarized and discussed. The protective effects can be classified into proliferation-promoting, anti-inflammatory, atrophy-preventing, metabolism-increasing, and antioxidative effects.Additionally, we provided some outlook on the valuable applications of apigenin in sports medicine, which eagerly require further fundamental research.

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A novel, highly-water-soluble apigenin derivative provides neuroprotection following ischemia in male rats by regulating the ERK/Nrf2/HO-1 pathway

Cited by 25 publications

References 41 publications

The antidepressant effects of apigenin are associated with the�promotion of autophagy via the mTOR/AMPK/ULK1 pathway

The antidepressant effects of apigenin are associated with the�promotion of autophagy via the mTOR/AMPK/ULK1 pathway

Bioactive Compounds in Oxidative Stress-Mediated Diseases: Targeting the NRF2/ARE Signaling Pathway and Epigenetic Regulation

Apigenin as a promising myocyte protectant against damage and degradation

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