Emodin protects mice against radiation-induced mortality and intestinal injury via inhibition of apoptosis and modulation of p53

Wang, Jing; Zhang, Yue; Zhu, Qiuzhen; Liu, Yulan; Cheng, Hao; Zhang, Yuefan; Li, Tiejun

doi:10.1016/j.etap.2016.08.005

Cited by 16 publications

(11 citation statements)

References 24 publications

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“…2 ) ( Yong et al, 2017 , Guclu et al, 2016 , Wang et al, 2018a ). Bax is located in the mitochondrial membranes and exerts pro-apoptosis effect through the mitochondrial pathway, promoting cytochrome C activation ( Mac Nair et al, 2016 ); p53 and Caspase-3 are executive molecules of apoptosis by blocking cell cycle ( Wang et al, 2016 ). Enzymes such as SOD, CAT, and GSH-Px, can regulate p53, Bax and Bcl-2 (BCL2 Apoptosis Regulator) ( Fig.…”

Section: Focus On the Biological Activities Of The Ozone (O mentioning

confidence: 99%

Ozone: a natural bioactive molecule with antioxidant property as potential new strategy in aging and in neurodegenerative disorders

Scassellati

Galoforo

Bonvicini

et al. 2020

Ageing Research Reviews

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Highlights Aging and neurodegenerative diseases are characterized by complex and multifactorial aetiology and challenges regarding treatments efficacy and costs persist. Oxygen-ozone (O 2 -O 3 ) therapy is a non-invasive, non-pharmacological, low cost and no-side effect procedure based on antioxidant capacity of O 3 . A plethora of scientific evidence supports other crucial properties of O 3 in physiopathological processes. Nrf2 is one of the principal molecular signalling on which O 3 exercises its antioxidant/anti-apoptotic/pro-autophagy effects, involved in aging and in neurodegenerative disorders. This review provides a consistent rationale to implement future clinical studies to apply the O 2 -O 3 treatment along with other antioxidants (polyphenols, mushrooms) in aging and in neurodegeneration.

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Section: Focus On the Biological Activities Of The Ozone (O mentioning

confidence: 99%

Ozone: a natural bioactive molecule with antioxidant property as potential new strategy in aging and in neurodegenerative disorders

Scassellati

Galoforo

Bonvicini

et al. 2020

Ageing Research Reviews

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“…Emodin is one of the bioactive components extracted from Rheum palmatum L ., which has been used as a traditional Chinese herbal medicine for decades in Eastern Asia [ 28 ]. Emodin was reported in previous studies to exert endothelial protective effects in various diseases involving vascular endothelium injuries brought by hyperglycemia, irradiation, and cytotoxic drugs [ 29 , 30 ]. Emodin has also been considered to be an anti-inflammatory agent in infectious diseases, autoimmune diseases and allotransplantation [ 31 , 32 ].…”

Section: Discussionmentioning

confidence: 99%

Emodin, A Chinese Herbal Medicine, Inhibits Reoxygenation-Induced Injury in Cultured Human Aortic Endothelial Cells by Regulating the Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) and Endothelial Nitric Oxide Synthase (eNOS) Signaling Pathway

et al. 2018

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BackgroundIschemia-reperfusion injury is associated with vascular dysfunction. The aim of this study was to investigate the role of emodin, a Chinese herbal medicine, in hypoxia-reoxygenation injury in cultured human aortic endothelial cells (HAECs) and its effects on the expression of the peroxisome proliferator-activated receptor-γ (PPAR-γ) and endothelial nitric oxide synthase (eNOS) signaling pathway.Material/MethodsAn in vitro hypoxia-reoxygenation model used cultured human aortic endothelial cells (HAECs). A colorimetric method evaluated the activity of peroxisome proliferator-activated receptor-γ (PPAR-γ). Phosphorylation of PPAR-γ and endothelial nitric oxide synthase (eNOS) were measured by Western blotting. Expression of inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 were evaluated by enzyme-linked immunosorbent assay (ELISA) and Western blotting. Nitric oxide (NO) production was detected by diaminofluorescein-FM diacetate (DAF-FM DA) fluorescence. Immunoprecipitation was used to evaluate the molecular coupling of heat shock protein (HSP)90 and eNOS.ResultsHypoxia-reoxygenation injury of HAECs reduced the activity and phosphorylation of PPAR-γ, and eNOS, NO production, and HSP90/eNOS molecular coupling in a time-dependent manner. Hypoxia-reoxygenation increased the levels of inflammatory cytokines TNF-α, IL-6, and IL-8 in a time-dependent manner. Emodin treatment recovered PPAR-γ activity and phosphorylation, eNOS phosphorylation, and HSP90/eNOS coupling in HAECS in a concentration-dependent manner, which was reversed by the PPAR-γ inhibitor GW9662, and the eNOS inhibitor, L-NAME. The recovery of HSP90/eNOS coupling by emodin was impaired by GW9662 treatment.ConclusionsAn in vitro hypoxia-reoxygenation (ischemia-reperfusion injury) model of induction of endothelial cell inflammatory mediators showed that emodin recovered the PPAR-γ and eNOS pathway activity.

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“…Many studies have revealed that emodin plays a neuroprotective role after cerebral, cardiac, intestinal and renal ischaemia‐reperfusion injury. The protective response of emodin to ischaemic insults depends on the regulation of various signalling pathways within the injured areas to diminish brain damage . The inactivation of protein kinase 2 pathways via NF‐kB and MAPKs is involved in emodin‐induced protection against renal ischaemia/reperfusion injury .…”

Section: Discussionmentioning

confidence: 99%

Nrf2-mediated neuroprotection against oxygen-glucose deprivation/reperfusion injury by emodin via AMPK-dependent inhibition of GSK-3β

Park

Choi

Park

2018

Journal of Pharmacy and Pharmacology

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Emodin protects mice against radiation-induced mortality and intestinal injury via inhibition of apoptosis and modulation of p53

Cited by 16 publications

References 24 publications

Ozone: a natural bioactive molecule with antioxidant property as potential new strategy in aging and in neurodegenerative disorders

Ozone: a natural bioactive molecule with antioxidant property as potential new strategy in aging and in neurodegenerative disorders

Emodin, A Chinese Herbal Medicine, Inhibits Reoxygenation-Induced Injury in Cultured Human Aortic Endothelial Cells by Regulating the Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) and Endothelial Nitric Oxide Synthase (eNOS) Signaling Pathway

Nrf2-mediated neuroprotection against oxygen-glucose deprivation/reperfusion injury by emodin via AMPK-dependent inhibition of GSK-3β

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