Retinal cell-targeted liposomal ginsenoside Rg3 attenuates retinal ischemia-reperfusion injury via alleviating oxidative stress and promoting microglia/macrophage M2 polarization

Huang, Yanmei; Lü, Jing; Zhao, Laien; Fu, Xiaoxuan; Peng, Shengjun; Wen, Zhi‐Hong; Wang, Rong; Yuan, Wei; Luo, Rongrui; Wang, Xiaojie; Li, Zelin; Zhang, Zhuhong

doi:10.1016/j.freeradbiomed.2023.06.024

Cited by 3 publications

(3 citation statements)

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“…[ 51 ] Our previous study reported that STAT3 may be associated with the polarization of microglia in RIR injury and that rhein can inhibit the activation of the STAT3 signaling pathway; however, the ability of rhein to regulate the STAT3 signaling pathway in RIR injury has not been reported. [ 9 , 24 , 52 ] Our in vitro and in vivo results show that Rh‐GFFYE can inhibit the phosphorylation of STAT3 protein, which is similar to our previous report on the mechanism of action of ginsenoside Rg3 liposomes in RIR injury. [ 9a ] These results provide a rationale for the regulation of microglia polarization by the natural product rhein.…”

Section: Discussionsupporting

confidence: 89%

“…[ 9 , 24 , 52 ] Our in vitro and in vivo results show that Rh‐GFFYE can inhibit the phosphorylation of STAT3 protein, which is similar to our previous report on the mechanism of action of ginsenoside Rg3 liposomes in RIR injury. [ 9a ] These results provide a rationale for the regulation of microglia polarization by the natural product rhein.…”

Section: Discussionsupporting

confidence: 89%

“…[ 8 ] Recent studies have shown that promoting the transition of microglia/macrophages from the M1 phenotype to the M2 phenotype attenuates RIR injury. [ 9 ] Moreover, the activation of the signal transducer and activator of transcription‐3 (STAT3) signaling pathway has been shown to facilitate M1 microglia/macrophage polarization and enhance the expressions of inflammatory cytokines. [ 10 ] However, current clinical treatments for retinal ischemia‐related diseases focus on a single pathological mechanism.…”

Section: Introductionmentioning

confidence: 99%

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Retinal Microenvironment‐Protected Rhein‐GFFYE Nanofibers Attenuate Retinal Ischemia‐Reperfusion Injury via Inhibiting Oxidative Stress and Regulating Microglial/Macrophage M1/M2 Polarization

Zhang,

Peng,

et al. 2023

Advanced Science

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Retinal ischemia is involved in the occurrence and development of various eye diseases, including glaucoma, diabetic retinopathy, and central retinal artery occlusion. To the best of our knowledge, few studies have reported self‐assembling peptide natural products for the suppression of ocular inflammation and oxidative stress. Herein, a self‐assembling peptide GFFYE is designed and synthesized, which can transform the non‐hydrophilicity of rhein into an amphiphilic sustained‐release therapeutic agent, and rhein‐based therapeutic nanofibers (abbreviated as Rh‐GFFYE) are constructed for the treatment of retinal ischemia‐reperfusion (RIR) injury. Rh‐GFFYE significantly ameliorates oxidative stress and inflammation in an in vitro oxygen‐glucose deprivation (OGD) model of retinal ischemia and a rat model of RIR injury. Rh‐GFFYE also significantly enhances retinal electrophysiological recovery and exhibits good biocompatibility. Importantly, Rh‐GFFYE also promotes the transition of M1‐type macrophages to the M2 type, ultimately altering the pro‐inflammatory microenvironment. Further investigation of the treatment mechanism indicates that Rh‐GFFYE activates the PI3K/AKT/mTOR signaling pathway to reduce oxidative stress and inhibits the NF‐κB and STAT3 signaling pathways to affect inflammation and macrophage polarization. In conclusion, the rhein‐loaded nanoplatform alleviates RIR injury by modulating the retinal microenvironment. The findings are expected to promote the clinical application of hydrophobic natural products in RIR injury‐associated eye diseases.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

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Retinal Microenvironment‐Protected Rhein‐GFFYE Nanofibers Attenuate Retinal Ischemia‐Reperfusion Injury via Inhibiting Oxidative Stress and Regulating Microglial/Macrophage M1/M2 Polarization

Zhang,

Peng,

et al. 2023

Advanced Science

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Multi-layered effects of Panax notoginseng on immune system

Yang,

Qu,

Wang

et al. 2024

Pharmacological Research

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Exploring the Molecular Targets for Type 2 Diabetes-Induced Alzheimer’s Disease Through Bioinformatics Analysis

Gao

Huang

et al. 2023

Epigenomics

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Aim: The purpose of this study was to elucidate the potential mechanisms of Alzheimer’s disease (AD) induced by Type 2 diabetes mellitus (T2DM) through bioinformatics analysis, to provide new treatment targets for this disease. Methods: We used weighted gene coexpression network analysis and differentially expressed genes analysis to identify significantly differentially expressed genes shared by T2DM and AD. Molecular docking was used to predict possible protein targets for T2DM-induced AD. Results: The direct interaction of CD44 and STAT3 may play a significant role in the development of T2DM-induced AD. Conclusion: A new approach to treating T2DM-associated AD may be provided by these hub genes and their predicted molecular targets.

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Retinal cell-targeted liposomal ginsenoside Rg3 attenuates retinal ischemia-reperfusion injury via alleviating oxidative stress and promoting microglia/macrophage M2 polarization

Cited by 3 publications

References 96 publications

Retinal Microenvironment‐Protected Rhein‐GFFYE Nanofibers Attenuate Retinal Ischemia‐Reperfusion Injury via Inhibiting Oxidative Stress and Regulating Microglial/Macrophage M1/M2 Polarization

Retinal Microenvironment‐Protected Rhein‐GFFYE Nanofibers Attenuate Retinal Ischemia‐Reperfusion Injury via Inhibiting Oxidative Stress and Regulating Microglial/Macrophage M1/M2 Polarization

Multi-layered effects of Panax notoginseng on immune system

Exploring the Molecular Targets for Type 2 Diabetes-Induced Alzheimer’s Disease Through Bioinformatics Analysis

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