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

2019 ◽  
Vol 47 (1) ◽  
pp. 2900-2908
Author(s):  
Jinlu Liu ◽  
Sai Bhuvanagiri ◽  
Xiaohan Qu
Keyword(s):  
Diabetic Retinopathy ◽  
Protective Effects ◽  
Lycopus Lucidus

scholarly journals Reduced Levels of Drp1 Protect against Development of Retinal Vascular Lesions in Diabetic Retinopathy

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1379
Author(s):  
Dongjoon Kim ◽  
Hiromi Sesaki ◽  
Sayon Roy
Keyword(s):  
Diabetic Retinopathy ◽  
Cell Loss ◽  
Vascular Lesions ◽  
Protective Effects ◽  
Diabetic Mice ◽  
Wild Type ◽  
Apoptotic Genes ◽  
Retinal Vascular Lesions ◽  
Acellular Capillaries ◽  
Pericyte Loss

High glucose (HG)-induced Drp1 overexpression contributes to mitochondrial dysfunction and promotes apoptosis in retinal endothelial cells. However, it is unknown whether inhibiting Drp1 overexpression protects against the development of retinal vascular cell loss in diabetes. To investigate whether reduced Drp1 level is protective against diabetes-induced retinal vascular lesions, four groups of mice: wild type (WT) control mice, streptozotocin (STZ)-induced diabetic mice, Drp1+/− mice, and STZ-induced diabetic Drp1+/− mice were examined after 16 weeks of diabetes. Western Blot analysis indicated a significant increase in Drp1 expression in the diabetic retinas compared to those of WT mice; retinas of diabetic Drp1+/− mice showed reduced Drp1 level compared to those of diabetic mice. A significant increase in the number of acellular capillaries (AC) and pericyte loss (PL) was observed in the retinas of diabetic mice compared to those of the WT control mice. Importantly, a significant decrease in the number of AC and PL was observed in retinas of diabetic Drp1+/− mice compared to those of diabetic mice concomitant with increased expression of pro-apoptotic genes, Bax, cleaved PARP, and increased cleaved caspase-3 activity. Preventing diabetes-induced Drp1 overexpression may have protective effects against the development of vascular lesions, characteristic of diabetic retinopathy.

scholarly journals Analysis of Lipid Peroxidation by UPLC-MS/MS and Retinoprotective Effects of the Natural Polyphenol Pterostilbene

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 168
Author(s):  
Isabel Torres-Cuevas ◽  
Iván Millán ◽  
Miguel Asensi ◽  
Máximo Vento ◽  
Camille Oger ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Diabetic Retinopathy ◽  
Redox Homeostasis ◽  
Ultra Performance Liquid Chromatography ◽  
Protective Effects ◽  
Diabetic Retina ◽  
Key Factor ◽  
Adrenic Acid ◽  
Diabetic Rabbits ◽  
High Level

The loss of redox homeostasis induced by hyperglycemia is an early sign and key factor in the development of diabetic retinopathy. Due to the high level of long-chain polyunsaturated fatty acids, diabetic retina is highly susceptible to lipid peroxidation, source of pathophysiological alterations in diabetic retinopathy. Previous studies have shown that pterostilbene, a natural antioxidant polyphenol, is an effective therapy against diabetic retinopathy development, although its protective effects on lipid peroxidation are not well known. Plasma, urine and retinas from diabetic rabbits, control and diabetic rabbits treated daily with pterostilbene were analyzed. Lipid peroxidation was evaluated through the determination of derivatives from arachidonic, adrenic and docosahexaenoic acids by ultra-performance liquid chromatography coupled with tandem mass spectrometry. Diabetes increased lipid peroxidation in retina, plasma and urine samples and pterostilbene treatment restored control values, showing its ability to prevent early and main alterations in the development of diabetic retinopathy. Through our study, we are able to propose the use of a derivative of adrenic acid, 17(RS)-10-epi-SC-Δ15-11-dihomo-IsoF, for the first time, as a suitable biomarker of diabetic retinopathy in plasmas or urine.

scholarly journals Protective Effects ofPanax notoginsengSaponins against High Glucose-Induced Oxidative Injury in Rat Retinal Capillary Endothelial Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Yue Fan ◽  
Yuan Qiao ◽  
Jianmei Huang ◽  
Minke Tang
Keyword(s):  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
High Glucose ◽  
Microvascular Dysfunction ◽  
Panax Notoginseng ◽  
Protective Effects ◽  
Pronounced Increase ◽  
Nadph Oxidase 4 ◽  
Retinal Capillary ◽  
Capillary Endothelial Cells

Diabetic retinopathy, a leading cause of visual loss and blindness, is characterized by microvascular dysfunction. Hyperglycemia is considered the major pathogenic factor for diabetic retinopathy and is associated with increased oxidative stress in the retina. In this study, we investigated the potential protective effects ofPanax notoginsengSaponins (PNS) in retinal capillary endothelial cells (RCECs) exposed to high glucose conditions. We found a pronounced increase in cell viability in rat RCECs incubated with both PNS and high glucose (30 mM) for 48 h or 72 h. The increased viability was accompanied by reduced intracellular hydrogen peroxide (H2O2) and superoxide (O2-), decreased mitochondrial reactive oxygen species (ROS), and lowered malondialdehyde (MDA) levels. PNS also increased the activities of total superoxide dismutase (SOD), MnSOD, catalase (CAT), and glutathione peroxidase (GSH-PX). The glutathione (GSH) content also increased after PNS treatment. Furthermore, PNS reduced NADPH oxidase 4 (Nox4) expression. These results indicate that PNS exerts a protective effect against high glucose-induced injury in RCECs, which may be partially attributed to its antioxidative function.

scholarly journals Notoginsenoside R1 Ameliorates Diabetic Retinopathy through PINK1-Dependent Activation of Mitophagy

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 213 ◽  
Author(s):  
Ping Zhou ◽  
Weijie Xie ◽  
Xiangbao Meng ◽  
Yadong Zhai ◽  
Xi Dong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Oral Treatment ◽  
Müller Cells ◽  
Panax Notoginseng ◽  
Protective Effects ◽  
Muller Cells ◽  
Beneficial Effects ◽  
Pre Treatment ◽  
Lc3 Puncta

: Accumulating evidence has indicated that inflammation, oxidative stress, apoptosis, and autophagy in retinal Müller cells are involved in diabetic retinopathy (DR). Notoginsenoside R1 (NGR1), a novel saponin extracted from Panax notoginseng, posesses pharmacological properties, including treating diabetic encephalopathy and improving microcirculatory disorders. Nevertheless, its beneficial effects on DR and the potential mechanism remain to be elucidated. In this study, we found retinal vascular degeneration, reduced retinal thickness, and impaired retinal function in db/db mice were all dramatically attenuated by oral treatment with NGR1 (30 mg/kg) for 12 weeks. NGR1 pretreatment also significantly inhibited apoptosis, markedly suppressed the VEGF expression, markedly increased PEDF expression and markedly inhibited oxidative stress and inflammation in rat retinal Müller cells (rMC-1) subjected to high glucose (HG) and in the retinas of db/db mice. Furthermore, NGR1 pre-treatment upregulated the level of PINK1 and Parkin, increased the LC3-II/LC3-I ratio, and downregulated the level of p62/SQSTM1 in rMC-1 cells induced by HG and in the retinas of db/db mice. Moreover, NGR1 administration enhanced the co-localization of GFP-LC3 puncta and MitoTracker in rMC-1 cells. Importantly, knockdown of PINK1 abolished the protective effects of NGR1. In conclusion, these phenomena suggested that NGR1 prevented DR via PINK1-dependent enhancement of mitophagy.

A novel regulatory network of linc00174/miR-150-5p/VEGFA modulates pathological angiogenesis in diabetic retinopathy

2021 ◽  
Author(s):  
JuanJuan Wang ◽  
Kunfang Wu ◽  
Dingding Wang
Keyword(s):  
Diabetic Retinopathy ◽  
Regulatory Network ◽  
Vascular Dysfunction ◽  
Underlying Mechanism ◽  
Tube Formation ◽  
Vascular Complication ◽  
Luciferase Reporter ◽  
Protective Effects ◽  
Downstream Effector ◽  
Non Coding Rnas

Background: Diabetic retinopathy (DR) has been regarded as a sight-threatening vascular complication of diabetes mellitus (DM). Accumulating evidence has identified the involvement of long non-coding RNAs (lncRNAs) in DR pathogenesis. We aim to investigate the role and underlying mechanism of linc00174 in DR process. Methods: Samples of human vitreous humour from proliferative DR and non-diabetic individuals were collected to examine the levels of linc00174. Human retinal microvascular endothelial cells (HRMECs) exposed with high glucose were employed to simulate the pathological statues of DR. shRNA specifically targeting linc00174 was applied. CCK-8, transwell, and matrigel tube formation were performed to evaluate cell proliferation, migration and angiogenesis. Bioinformatics analysis and luciferase reporter assay were conducted to verify the linc00174/miR-150-5p/VEGFA regulatory network. Western blotting was employed to determine the expression of VEGFA. Results: Linc00174 was significantly elevated in patients with DR, as well as HG-stimulated HRMECs, of which knockdown repressed HG-induced proliferation, migration and angiogenesis. miR-150-5p was identified as a downstream effector to be involved in linc00174-mediated protective effects. miR-150-5p directly bound to the 3’-UTR of VEGFA. The linc00174/miR-150-5p/VEGFA axis was confirmed in retinal vascular dysfunction. Conclusion: Linc00174 deteriorates diabetic retinal microangiopathy via regulating miR-150-5p/VEGFA pathway, indicating a novel therapeutic target for DR treatment.

scholarly journals Protective Effect of Fenofibrate on Oxidative Stress-Induced Apoptosis in Retinal–Choroidal Vascular Endothelial Cells: Implication for Diabetic Retinopathy Treatment

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 712 ◽  
Author(s):  
Ying-Jung Hsu ◽  
Chao-Wen Lin ◽  
Sheng-Li Cho ◽  
Wei-Shiung Yang ◽  
Chung-May Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Diabetic Retinopathy ◽  
B Cell ◽  
Cell Lymphoma ◽  
Vascular Endothelial Cells ◽  
B Cell Lymphoma ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Amino Terminal

Diabetic retinopathy (DR) is an important microvascular complication of diabetes and one of the leading causes of blindness in developed countries. Two large clinical studies showed that fenofibrate, a peroxisome proliferator-activated receptor type α (PPAR-α) agonist, reduces DR progression. We evaluated the protective effects of fenofibrate on retinal/choroidal vascular endothelial cells under oxidative stress and investigated the underlying mechanisms using RF/6A cells as the model system and paraquat (PQ) to induce oxidative stress. Pretreatment with fenofibrate suppressed reactive oxygen species (ROS) production, decreased cellular apoptosis, diminished the changes in the mitochondrial membrane potential, increased the mRNA levels of peroxiredoxin (Prx), thioredoxins (Trxs), B-cell lymphoma 2 (Bcl-2), and Bcl-xl, and reduced the level of B-cell lymphoma 2-associated X protein (Bax) in PQ-stimulated RF/6A cells. Western blot analysis revealed that fenofibrate repressed apoptosis through cytosolic and mitochondrial apoptosis signal-regulated kinase-1 (Ask)-Trx-related signaling pathways, including c-Jun amino-terminal kinase (JNK) phosphorylation, cytochrome c release, caspase 3 activation, and poly (ADP-ribose) polymerase-1 (PARP-1) cleavage. These protective effects of fenofibrate on RF/6A cells may be attributable to its anti-oxidative ability. Our research suggests that fenofibrate could serve as an effective adjunct therapy for ocular oxidative stress-related disorders, such as DR.

scholarly journals HuoXueJieDu Formula Alleviates Diabetic Retinopathy in Rats by Inhibiting SOCS3-STAT3 and TIMP1-A2M Pathways

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Hongliang Wang ◽  
Wei Xing ◽  
Shijie Tang ◽  
Zhenglin Wang ◽  
Tiantian Lv ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetic Retinopathy ◽  
Immunohistochemical Staining ◽  
Expression Profiles ◽  
Enrichment Analysis ◽  
Underlying Mechanism ◽  
Diabetic Rats ◽  
Pathway Enrichment Analysis ◽  
Protective Effects ◽  
Matrix Metabolism

HuoXueJieDu (HXJD) formula exerts protective effects against diabetic retinopathy (DR) in rats, but its underlying mechanism remains unknown. In the present study, the diabetic rats were established using streptozocin. The administration of HXJD was initiated at 20 weeks after diabetes induction and continued for 12 weeks. Whole genome expression profiles in rat retinas were examined using microarray technology. Differential gene expression and pathway enrichment analysis were conducted on the microarray data, with validation through real-time PCR and immunohistochemical staining. The results showed that 170 genes and several IPA canonical pathways related to inflammation, matrix metabolism, and phototransduction were regulated by HXJD. PCR validation of selected genes, including SOCS3, STAT3, TIMP1, and A2M, confirmed the gene expression changes influenced by HXJD. In addition, the immunohistochemical staining results suggested that critical members of the SOCS3-STAT3 pathway were also affected by HXJD. Taken together, these results indicated that SOCS3-STAT3 and TIMP1-A2M pathways might mediate the alleviation of HXJD activities in rats with diabetic retinopathy.

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