The protective effects of lycopus lucidus turcz in diabetic retinopathy and its possible mechanisms

Liu, Jinlu; Bhuvanagiri, Sai; Qu, Xiaohan

doi:10.1080/21691401.2019.1640230

Cited by 12 publications

(6 citation statements)

References 35 publications

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“…As shown in Figure 4B,D, the retinas in the model group exhibited increased numbers of TUNEL-positive cells in the INL. In comparison, the retinas in the GRg1 group contained fewer TUNEL-positive cells, which was consistent with a previous study (22).…”

Section: Grg1 Decreased Retinal Gcl and Inl Cell Apoptosissupporting

confidence: 92%

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

et al. 2020

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Background: Diabetic retinopathy (DR), a diabetic vascular complication, is prone to developing into blindness. Ginsenoside Rg1 (GRg1), a major saponin in ginseng, exerts high anti-apoptotic activity.Methods: This study aimed to explore the protective effects of GRg1 against diabetes-induced retinal damage. Measurements of blood glucose, blood lipids and vascular permeability were performed, as well as assessments of pathological changes, and the retinal thickness of each layer. Retinal cell apoptosis related protein expression levels were measured by immunofluorescence and western blot assays.Results: Our data demonstrated that GRg1 effectively reduced blood glucose and triglyceride levels and maintained normal retinal permeability and physiological structure. GRg1 maintained the thickness of the ganglion cell layer (GCL) and the inner nuclear layer (INL) by reducing cell apoptosis.Conclusions: These data strongly indicate that GRg1 prevents diabetic retinal changes by decreasing GCL and INL cell apoptosis. GRg1 may be a promising drug for early DR treatment.

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Section: Grg1 Decreased Retinal Gcl and Inl Cell Apoptosissupporting

confidence: 92%

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

et al. 2020

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“…Previously data showed that VEGF could be produced by RPE cells, endothelial cells, and pericytes of retinal vessels. RPE cells played a more important role in VEGF production [40]. Studies found that targeted inhibition of VEGF and HIF-1α expression could inhibit pathological retinal angiogenesis in DR [41].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of KCTD10 Affects Diabetic Retinopathy Progression by Reducing VEGF and Affecting Angiogenesis

Feng

Wang

2022

Genetics Research

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Aim. We purposed to evaluate the KCTD10 effects of angiogenesis in diabetic retinopathy (DR). Methods. We induced a DR cell model using high glucose (HG) treatment of HRECs and ARPE-19 cells. A DR rat was established by injecting streptozotocin. Small interference RNA targeted KCTD10 (si-KCTD10) was used to mediate KCTD10 inhibition in cell and animal models. The roles of KCTD10 on cell viability, apoptosis, angiogenesis, and related proteins (VEGF and HIF-1α) were observed by RT-qPCR, Western blot, CCK-8 assay, TUNEL staining, tube formation assay, ELISA, and immunohistochemistry assay. Results. KCTD10 expression was upregulated in DR cells and retinal tissue of DR rats. Treatment of the cells with si-KCTD10 increased cell viability and decreased apoptosis and angiogenesis in DR cells. Inhibition of KCTD10 could reduce the expression of VEGF and HIF-1α in DR cells. Furthermore, KCTD10 inhibition reduced VEGF levels in the retinal tissue of DR rats. Conclusion. This work showed that inhibition of KCTD10 relieved angiogenesis in DR.

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“…41,42 In this study, we discovered that the levels of p-JNK and p-p38 were increased in HG-induced HRECs, consistent with the results of previous studies. [43][44][45] Combined treatment with exogenous salusin-β and HG resulted in higher levels of p-JNK and p-p38 than treatment with HG alone, whereas both knockdown salusin-β and NAC pretreatment reduced these levels. These results demonstrate that salusin-β induced by HG can activate the JNK and p38 MAPK signalling pathways in a ROS-dependent manner.…”

Section: Dovepressmentioning

confidence: 98%

Salusin-β Mediates High Glucose-Induced Inflammation and Apoptosis in Retinal Capillary Endothelial Cells via a ROS-Dependent Pathway in Diabetic Retinopathy

Wang¹,

Zhang²,

Zhou³

et al. 2021

DMSO

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Background: Diabetic retinopathy (DR) is characterized by retinal vascular endothelial cell death and vascular inflammation, which are microvascular complications of diabetes mellitus (DM). Salusin-β, a newly identified peptide, is closely associated with hypertension, atherosclerosis and diabetic cardiomyopathy. However, the exact role of salusin-β in high glucose (HG)-induced retinal capillary endothelial cell (REC) inflammation and apoptosis remains unclear.Patients and Methods: A total of 60 patients with type 2 diabetes and 20 healthy controls were included in this study. Based on fundus fluorescein angiography findings, the diabetic patients were divided into three subgroups: diabetes without retinopathy (DWR), nonproliferative DR (NPDR) and proliferative DR (PDR). Serum salusin-β levels were measured by enzyme-linked immunosorbent assay. Human RECs (HRECs) were cultured in normal glucose (NG) and HG medium with or without salusin-β. Salusin-β expression was analysed by Western blotting and immunofluorescence staining. Expression of the pro-inflammatory cytokines MCP-1, IL-1β, TNF-α, and VCAM-1 was analysed by Western blotting. Reactive oxygen species (ROS) production was measured with 2′,7′-dichlorofluorescein diacetate (DCFH-DA). Cell apoptosis rates were determined by flow cytometry. The levels of p38, JNK, p-p38, and p-JNK and the apoptosis-related proteins cleaved caspase-3, Bax, and cl2 were analysed by Western blotting. Results: Serum salusin-β levels were higher in diabetic patients than in healthy controls (p = 0.0027), especially in patients with NPDR and PDR (both p<0.01). HG upregulated salusin-β expression in HRECs in a time-dependent manner. Salusin-β exacerbated inflammation and apoptosis, upregulated intracellular ROS production in HG-induced HRECs, and activated ROS-dependent JNK and p38 MAPK signalling, while knockdown of salusin-β suppressed these effects. Conclusion:Our findings indicate that salusin-β can promote inflammation and apoptosis via ROS-dependent JNK and p38 MAPK signalling in HG-induced HRECs and could be a therapeutic target for DR.

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The protective effects of lycopus lucidus turcz in diabetic retinopathy and its possible mechanisms

Cited by 12 publications

References 35 publications

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

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

Inhibition of KCTD10 Affects Diabetic Retinopathy Progression by Reducing VEGF and Affecting Angiogenesis

Salusin-β Mediates High Glucose-Induced Inflammation and Apoptosis in Retinal Capillary Endothelial Cells via a ROS-Dependent Pathway in Diabetic Retinopathy

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