Ginsenoside Rg1 prevents early diabetic retinopathy via reducing retinal ganglion cell layer and inner nuclear layer cell apoptosis in db/db mice

Gao, Ye; Yu-bin, JI; Luo, Yun; Sun, Junqi; Sun, Guibo

doi:10.21037/atm.2019.12.155

Cited by 22 publications

(14 citation statements)

References 26 publications

(32 reference statements)

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“…Regarding the gene expression level, Rg1 increased SIRT3 but decreased VEGF in rat retinal tissue and inhibited HRECs proliferation, migration and angiogenesis. It is consistent with the finding by Gao et al [ 17 ] that Rg1 can prevent DR by reducing apoptosis.…”

Section: Discussionsupporting

confidence: 93%

“…Moreover, Rg1 can improve endoplasmic reticulum stress-induced apoptosis in diabetic cardiomyopathy induced by streptozotocin (STZ) [ 16 ]. Rg1 prevents retinal damage by inhibiting retinal cell apoptosis [ 17 ]. Moreover, experimental studies have shown that ginsenoside Rg1 plays a role in promoting vascular regeneration and enhancing endothelial progenitor cell angiogenesis [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

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Ginsenoside Rg1 Inhibits High Glucose-Induced Proliferation, Migration, and Angiogenesis in Retinal Endothelial Cells by Regulating the lncRNA SNHG7/miR-2116-5p/SIRT3 Axis

Xue

et al. 2022

Journal of Oncology

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Background. Diabetic retinopathy (DR), including retinal angiogenesis and endothelial cell proliferation and migration, is a serious complication in diabetic patients. It has been reported that ginsenoside Rg1 can prevent retinal damage. However, the mechanism by which Rg1 prevents retinal damage is unknown. Therefore, the aim of the present study was to investigate the mechanism by which Rg1 inhibits high glucose-induced complications through the regulation of the lncRNA SNHG7/miR-2116-5p/SIRT3 axis. Methods. Under high glucose (HG) conditions, human retinal endothelial cells (HRECs) were cultured to simulate a DR environment, and Rg1 was added after 48 h. Negative control (NC), miR-2116-5p mimic, si-SNHG7, pc-DNA SIRT3, and miR-2116-5p inhibitor were transfected into HRECs, and CCK-8 assay was used to detect the cell viability. Angiogenesis and transwell assays were used to evaluate angiogenesis and cell migration, respectively. qRT–PCR and Western blot were used to detect the expression of related genes and proteins. Luciferase reporter assays and bioinformatics were used to analyze the target binding sites of miR-2116-5p to lncRNA SNHG7 and SIRT3. Results. The proliferation, migration and angiogenesis of HRECs were induced by HG. As expected, HG upregulated miR-2116-5p and VEGF expression but downregulated lncRNA SNHG7 and SIRT3 expression. Importantly, Rg1 inhibited HG-induced HREC proliferation, migration, and angiogenesis by upregulating the lncRNA SNHG7, and miR-2116-5p had a target regulatory relationship with both lncRNA SNHG7 and SIRT3. Conclusion. Rg1 inhibits HG-induced proliferation, migration, angiogenesis, and VEGF expression in retinal endothelial cells through the lncRNA SNG7/miR-2116-5p/SIRT3 axis. This finding provides theoretical evidence for the clinical application of Rg1 in DR.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 Inhibits High Glucose-Induced Proliferation, Migration, and Angiogenesis in Retinal Endothelial Cells by Regulating the lncRNA SNHG7/miR-2116-5p/SIRT3 Axis

Xue

et al. 2022

Journal of Oncology

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“…This retinal thinning correlated with the increased apoptosis observed in each of the retinal models. 15 , 25 , 26 …”

Section: Discussionmentioning

confidence: 99%

Correlation of Retinal Structure and Visual Function Assessments in Mouse Diabetes Models

Sheskey

Antonetti

Renterı́a

et al. 2021

Invest. Ophthalmol. Vis. Sci.

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“…Mice fed a high-fat diet exhibit impairments in a-wave, b-wave, and oscillatory potentials (OPs) on ERG testing, suggesting neuronal injury, though inner retinal thinning was not noted [33][34][35]. On the other hand, the db/db leptin-receptor-deficient mouse manifests both retinal functional deficits on ERG as well as RGC loss as early as 8 weeks of age [36][37][38]. Finally, diabetic retinal neurodegeneration has been documented, though less wellstudied, in other animal models.…”

Section: Animal Models Of Early Diabetic Retinal Neurodegenerationmentioning

confidence: 99%

Retinal Neurodegeneration in Diabetes: an Emerging Concept in Diabetic Retinopathy

Sachdeva

2021

Curr Diab Rep

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Purpose of Review Diabetic retinopathy (DR), the leading cause of blindness in working-aged adults, remains clinically defined and staged by its vascular manifestations. However, early retinal neurodegeneration may precede vascular pathology, suggesting that this neuronal damage may contribute to disease pathogenesis and represent an independent target for intervention. This review will discuss the evidence and implications for diabetic retinal neurodegeneration. Recent Findings A growing body of literature has identified progressive retinal thinning and visual dysfunction in patients with diabetes even prior to the onset of DR, though advances in retinal vascular imaging suggest that vascular remodeling and choroidal changes occur during these early stages as well. Animal models of diabetes and in vitro studies have also suggested that diabetes may directly affect the retinal neural and glial tissue, providing support to the concept that diabetic retinal neurodegeneration occurs early in the disease and suggesting potentially relevant molecular pathways. Summary Diabetic retinal neurodegeneration may represent a “preclinical” manifestation of diabetic retinal disease and remains an active area of investigation. As the natural history and molecular mechanisms become increasingly understood, it may lead to upcoming developments in not only the treatment options but also the clinical definition of DR.

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Ginsenoside Rg1 prevents early diabetic retinopathy via reducing retinal ganglion cell layer and inner nuclear layer cell apoptosis in db/db mice

Cited by 22 publications

References 26 publications

Ginsenoside Rg1 Inhibits High Glucose-Induced Proliferation, Migration, and Angiogenesis in Retinal Endothelial Cells by Regulating the lncRNA SNHG7/miR-2116-5p/SIRT3 Axis

Ginsenoside Rg1 Inhibits High Glucose-Induced Proliferation, Migration, and Angiogenesis in Retinal Endothelial Cells by Regulating the lncRNA SNHG7/miR-2116-5p/SIRT3 Axis

Correlation of Retinal Structure and Visual Function Assessments in Mouse Diabetes Models

Retinal Neurodegeneration in Diabetes: an Emerging Concept in Diabetic Retinopathy

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