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Emodin protected against retinal ischemia insulted neurons through the downregulation of protein overexpression of ?-catenin and vascular endothelium factor.

ABSTRACT: BACKGROUND:Emodin has been proved to have an anti-ischemic effect on the brain, however little research has been done on its effect on vision-threatening retinal ischemia. Thus, an investigation was carried out into the hypothetical efficacy of emodin against retinal ischemia and the role of ?-catenin/VEGF in its therapeutic mechanism. METHODS:Retinal ischemia, followed by reperfusion (IR), was inducted by raising the intraocular pressure of a Wistar rat's eye to 120?mmHg for 60?min. Additionally, pre-ischemic/post-ischemic intravitreous injections of emodin (4, 10 and 20??M) or vehicle were carried out on the eye with retinal ischemia. MTT assay, electroretinograms, cresyl violet staining retinal thickness measurements, and fluorogold retrograde labelling of retinal ganglion cells (RGCs) as well as Western blotting were carried out. RESULTS:Cultured RGC-5 cells subjected to oxygen glucose deprivation (OGD) were used to confirm the effective concentrations of emodin (administered 1?h pre-OGD, pre-OGD emodin). The most effective and significant (P?=?0.04) dose of pre-OGD emodin was observed at 0.5??M (cell viability: 47.52?±?3.99%) as compared to pre-OGD vehicle treatment group (38.30?±?2.51%). Furthermore, pre-ischemic intravitreous injection of 20??M emodin (Emo20?+?IR?=?0.99?±?0.18, P?

SUBMITTER: Chao HW

PROVIDER: S-EPMC7654144 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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Emodin protected against retinal ischemia insulted neurons through the downregulation of protein overexpression of β-catenin and vascular endothelium factor.

Chao Howard Wen-Haur HW Chen Yu-Kuang YK Liu Jorn-Hon JH Pan Hwai-Tzong HT Lin Hsin-May HM Chao Hsiao-Ming HM

BMC complementary medicine and therapies 20201110 1

<h4>Background</h4>Emodin has been proved to have an anti-ischemic effect on the brain, however little research has been done on its effect on vision-threatening retinal ischemia. Thus, an investigation was carried out into the hypothetical efficacy of emodin against retinal ischemia and the role of β-catenin/VEGF in its therapeutic mechanism.<h4>Methods</h4>Retinal ischemia, followed by reperfusion (IR), was inducted by raising the intraocular pressure of a Wistar rat's eye to 120 mmHg for 60 m ...[more]

PMID: 33167932

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Project description:Ischemia-induced cell death is a major cause of disability or death after stroke. Identifying the key intrinsic protective mechanisms induced by ischemia is critical for the development of effective stroke treatment. Here, we reported that 14-3-3γ was a selective ischemia-inducible survival factor in cerebral cortical neurons reducing cell death by downregulating Bax depend direct 14-3-3γ/p-β-catenin Ser37 interactions in the nucleus. 14-3-3γ, but not other 14-3-3 isoforms, was upregulated in primary cerebral cortical neurons upon oxygen-glucose deprivation (OGD) as measured by quantitative PCR, western blot and fluorescent immunostaining. The selective induction of 14-3-3γ in cortical neurons by OGD was verified by the in vivo ischemic stroke model. Knocking down 14-3-3γ alone or inhibiting 14-3-3/client interactions was sufficient to induce cell death in normal cultured neurons and exacerbate OGD-induced neuronal death. Ectopic overexpression of 14-3-3γ significantly reduced OGD-induced cell death in cultured neurons. Co-immunoprecipitation and fluorescence resonance energy transfer demonstrated that endogenous 14-3-3γ bound directly to more p-β-catenin Ser37 but not p-Bad, p-Ask-1, p-p53 and Bax. During OGD, p-β-catenin Ser37 but not p-β-catenin Ser45 was increased prominently, which correlated with Bax elevation in cortical neurons. OGD promoted the entry of 14-3-3γ into the nuclei, in correlation with the increase of nuclear p-β-catenin Ser37 in neurons. Overexpression of 14-3-3γ significantly reduced Bax expression, whereas knockdown of 14-3-3γ increased Bax in cortical neurons. Abolishing β-catenin phosphorylation at Ser37 (S37A) significantly reduced Bax and cell death in neurons upon OGD. Finally, 14-3-3γ overexpression completely suppressed β-catenin-enhanced Bax and cell death in neurons upon OGD. Based on these data, we propose that the 14-3-3γ/p-β-catenin Ser37/Bax axis determines cell survival or death of neurons during ischemia, providing novel therapeutic targets for ischemic stroke as well as other related neurological diseases.

Dataset Information

Emodin protected against retinal ischemia insulted neurons through the downregulation of protein overexpression of ?-catenin and vascular endothelium factor.

Publications

Emodin protected against retinal ischemia insulted neurons through the downregulation of protein overexpression of β-catenin and vascular endothelium factor.

Similar Datasets

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