DL-3-n-butylphthalide Protected Retinal Müller Cells Dysfunction from Oxidative Stress

Xing, Xiaoli; Huang, Liangyu; Lv, Yingjuan; Liu, Xun; Su, Ruihong; Li, Xiaorong; Dong, Lijie

doi:10.1080/02713683.2019.1624777

Cited by 19 publications

(14 citation statements)

References 23 publications

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“…L-3-n-Butylphthalide (NBP), also known as levo-apigenin extracted from celery seed, has been used in the treatment of mild to moderate acute ischemic stroke by improving blood circulation and protecting nerve tissue [ 19 – 21 ]. Studies on the MOA have shown that NBP attenuates nerve cell injury via blockage of intracellular ROS production and downregulation of oxidative stress levels [ 22 , 23 ]. Meanwhile, NBP has also been shown to protect against brain injury by modulating the level of intracellular autophagy [ 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Autophagy Facilitates XY03-EA-Mediated Neuroprotection against the Cerebral Ischemia/Reperfusion Injury in Rats

Cui

Hao

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Objective. L-3-n-Butylphthalide (NBP) is used to treat moderate and severe acute ischemia stroke. A previous screening study indicates that XY03-EA, a novel derivative of NBP, is more potent than NBP in the oxyradical scavenging capacity. In this study, in vivo and in vitro ischemia/reperfusion (I/R) models were used to test whether the XY03-EA offered therapeutic benefits in the ischemic stroke and explore the underlying mechanism of action. Methods. For this purpose, behavioral scores, cerebral infarct volume, cerebral blood flow, oxidative stress levels, inflammatory factor expression, energy metabolism levels, and autophagy activation were estimated in the rat middle cerebral artery occlusion and reperfusion (MCAO/R) model. The nonhuman primate MCAO/R model was conducted to validate the therapeutic effect of XY03-EA applied for 3 weeks. The neurological deficit score (NDS) progression rate and the infarct volume were continuously recorded on days 3, 7, 14, and 21. The PC-12 cell OGD/R model was used to assess the cell survival rate, reactive oxygen species (ROS) levels, the expression of autophagy execution molecules, and the activation of autophagy-related signaling pathways. Results. XY03-EA decreased the cerebral injuries and NDS by increasing cerebral blood flow, improving brain energy metabolism, accelerating ROS clearance, suppressing inflammatory responses, and inhibiting autophagy in the MCAO/R model rats. In the nonhuman primate MCAO/R model, the treatment of XY03-EA for 3 weeks could significantly inhibit the NDS progression rate and indicate a positive trend to reduce the infarct volume in a dose-dependent way. Mechanistically, XY03-EA inhibited ROS-dependent autophagy activation and thereby protected the PC-12 cells from the autophagic cell death induced by OGD/R. Conclusions. In this study, we found that XY03-EA alleviated the cerebral I/R injuries in rats and nonhuman primates. Our results demonstrated that XY03-EA exerted neuroprotective effects against the ROS-mediated autophagic neurocyte death and had great potential for the treatment of ischemic stroke.

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Section: Introductionmentioning

confidence: 99%

Inhibition of Autophagy Facilitates XY03-EA-Mediated Neuroprotection against the Cerebral Ischemia/Reperfusion Injury in Rats

Cui

Hao

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…hMCs exhibit the characteristics of fibroblasts, including alterations in cytoskeletal structure and generation of traction force in the retina 23 . The differentiation of fibroblasts into myofibroblasts is closely associated with the progression of retinal fibrosis.…”

Section: Resultsmentioning

confidence: 99%

“…hMCs exhibit the characteristics of fibroblasts, including alterations in cytoskeletal structure and generation of traction force in the retina. 23 The differentiation of fibroblasts into myofibroblasts is closely associated with the progression of retinal fibrosis. As TGF-β1 is a well-known stimulator of myofibroblast activation, 24 we treated hMCs with TGF-β1 and studied its effects on the levels (Figure 2A).…”

Section: Yap Activation Induces MC Differentiation and Ecm Productionmentioning

confidence: 99%

YAP is essential for TGF‐β‐induced retinal fibrosis in diabetic rats via promoting the fibrogenic activity of Müller cells

Zhang

Kong

2020

J Cellular Molecular Medi

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“…In addition, abnormal expression of ECM proteins in the TM is related to the oxidative stress response in the TM 9 . Many ocular diseases and related treatments are associated with oxidation and inflammation 10–15 . Some studies have also reported markedly elevated levels of oxidative stress markers in the AH from patients with POAG, along with altered expression of markers of antioxidant defences and an enhanced inflammatory response 16–18 …”

Section: Introductionmentioning

confidence: 99%

“…9 Many ocular diseases and related treatments are associated with oxidation and inflammation. [10][11][12][13][14][15] Some studies have also reported markedly elevated levels of oxidative stress markers in the AH from patients with POAG, along with altered expression of markers of antioxidant defences and an enhanced inflammatory response. [16][17][18] Quantitative proteomics based on mass spectrometry (MS) is an important methodology for biological and clinical research.…”

Section: Introductionmentioning

confidence: 99%

Low expression of GSTP1 in the aqueous humour of patients with primary open‐angle glaucoma

Liu

Wang

Feng

et al. 2021

J Cellular Molecular Medi

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Primary open‐angle glaucoma (POAG) is characterized by irreversible neurodegeneration accompanied by visual field defects and high intraocular pressure. Currently, an effective treatment is not available to prevent the progression of POAG, other than treatments to decrease the high intraocular pressure. We performed proteomic analysis of aqueous humour (AH) samples from patients with POAG combined with cataract and patients with cataract to obtain a better understanding of the pathogenesis of POAG and explore potential treatment targets for this condition. Samples were collected from 10 patients with POAG combined with cataract and 10 patients with cataract. Samples from each group were pooled. A high‐resolution, label‐free, liquid chromatography‐tandem mass spectrometry‐based quantitative proteomic analysis was performed. In total, 610 proteins were identified in human AH samples from the two groups. A total of 48 up‐regulated proteins and 49 down‐regulated proteins were identified in the POAG combined with cataract group compared with the control group. Gene Ontology (GO) analysis revealed key roles for these proteins in inflammation, immune responses, growth and development, cellular movement and vesicle‐mediated transport in the biological process category. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated the down‐regulated expression of glutathione S‐transferase P (GSTP1) in the glutathione metabolism signalling pathway in the POAG combined with cataract group. Additionally, certain significantly differentially expressed proteins in the proteomic profile were verified by enzyme‐linked immunosorbent assay (ELISA). GSTP1 levels were reduced in the human AH samples from the POAG combined with cataract group, based on the results of ELISA and proteomic profiling. Therefore, GSTP1, a redox‐related marker, may be involved in the pathological process of POAG and may become a treatment target in the future.

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DL-3-n-butylphthalide Protected Retinal Müller Cells Dysfunction from Oxidative Stress

Cited by 19 publications

References 23 publications

Inhibition of Autophagy Facilitates XY03-EA-Mediated Neuroprotection against the Cerebral Ischemia/Reperfusion Injury in Rats

Inhibition of Autophagy Facilitates XY03-EA-Mediated Neuroprotection against the Cerebral Ischemia/Reperfusion Injury in Rats

YAP is essential for TGF‐β‐induced retinal fibrosis in diabetic rats via promoting the fibrogenic activity of Müller cells

Low expression of GSTP1 in the aqueous humour of patients with primary open‐angle glaucoma

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