Table 1.
In vitro studies on resveratrol effect on cultured retinal cells.
| Author, Year (Country) | Cells | Origin | Identification of Cells/Authentication of Cell Line | Insult | Resveratrol Concentration (Incubation Time) | Laboratory Techniques | Major Findings |
|---|---|---|---|---|---|---|---|
| Chan Chi-Ming, 2013 (Taiwan, USA) [26] | ARPE-19 | Human cell line (retinal pigment epithelial cells) obtained from Food Industry Research and Development Institute (Hsinchu, Taiwan) |
No data | PDGF-BB (20 ng/mL) at 37 °C for 30 minutes | 1, 3 or 10 µM | ECIS migration assay, MTT assay, dot binding assay, WB, in vitro scratch wound healing assay | Resveratrol inhibited PDGF- BB-induced migration and signaling in ARPE19 cells possibly through via PDGFRb, PI3K/Akt and MAPK pathways. Resveratrol had no effect on the RPE cell adhesion to fibronectin. |
| Chang Yo-Chen, 2017 (Taiwan) [21] | ARPE-19 | Human cell line (retinal pigment epithelial cells) obtained from ATCC | No data | CoCl2 (100–1000 μM)—hypoxic mimetic treatment | 20 µM | IP, WB, gelatin zymography, ELISA, RT PCR | Resveratrol reduced hypoxia-induced secretion of HMGB1.Oxidative and hypoxic stresses reduction; angiogenetic and fibrotic changes and tissue remodeling |
| Chen Yuhua, 2019 (China) [20] | Rat retinal endothelial cell (RREC) culture | Primary culture of rat cells | No data | High glucose conditions (30 mM glucose for 7 days) | 10, 50, 100, 200 or 500 μM (24 h) | MTT assay, WB, RT PCR | Incubation with resveratrol did not affect cell viability up to 100 µM in normal glucose concentration conditions. Inflammation suppression and increased expression of PON1 as well as suppression of active caspase-3 upregulation driven by culturing in exposure to elevated glucose levels. |
| Kowluru Renu A., 2014 (USA) [27] | Bovine retinal capillary endothelial cells (BRECs) | Primary culture of bovine cells | No data | H2O2 exposure (250 µM for 1 h) and high glucose conditions (20 mM for 4 days) | 25 µM | IP, RT PCR, WB, enzyme activity assay, ROS assay | Resveratrol ameliorated high glucose-induced inhibition of Sirt1 activity and prevented increase in the acetylation of p65, binding of p65 with MMP-9 promoter and activation of MMP-9. |
| Li Jun, 2017 (China) [23] | Bovine retinal capillary endothelial cells (BRECs) | Primary culture of bovine cells | Expression of Von Willebrand factor (IHC) | High glucose conditions (30mM glucose) | 1, 5, 10 or 20μM (48 h) | Flow cytometry, RT PCR, WB | Reduction of high glucose-induced intracellular ROS elevation through the activation of AMPK/Sirt1/PGC-1α pathway and apoptosis suppression. |
| Liu Shulin, 2016 (China) [17] | Peripheral blood mononuclear cells (PBMCs) |
19 patients with proliferative diabetic retinopathy and 20 controls |
No data | No insult | 10 µM (72 h) | ELISA, WB, RT PCR | IL-17 expression was upregulated and SIRT1 expression levels were decreased in the PBMCs of patients with proliferative diabetic retinopathy |
| Losso Jack, 2010 (USA) [24] | ARPE-19 | Human cell line (retinal pigment epithelial cells) obtained from ATCC | No data | High glucose conditions (33 mM glucose) | 1.25, 2.5, 5, 10 µM (9 days) | crystal violet cell viability assay, ELISA, WB, scrape-Loading/dye transfer assay | Inhibitory effect on hyperglycemia-induced inflammation in retinal pigment epithelial cells: ameliorated decreased GJIC, secretion of cytokines IL-6 and IL-8, downregulation of Cx43, activation of TGF-β,PKCβ, and COX-2. |
| Shen Hongjie, 2015 (China) [22] | hRECs (Human Retinal Endothelial Cells) | Human cell line (retinal pigment epithelial cells) obtained from Angio-Proteomie (USA) | No data | High glucose conditions (33 mM glucose for 72 h) | homologous derivative of resveratrol, pterostilbene 1 mM (72 hours) |
MTT assay, ELISA, enzyme activity assay, ROS assay | Regulation of oxidation balance by decreasing inflammation, and further regulation retinal cells over proliferation to delay diabetic retinopathy progress. |
| Subramani Murali, 2017 (India) [25] | ARPE-19 | Human cell line (retinal pigment epithelial cells) obtained from Karolinska Institute, Sweden | No data | Bevacizumab (0.25 mg/ml for 2 h) | 100 µM (48 h) | Trypan blue assay, MTT assay, FLICA, RT PCR, BrdU assay, IHC, WB, scratch assay | Downregulation of VEGFR-2 and its activation, reduction by 50% of VEGF-A, decrease in the proliferation of cultured RPE cells, restoring the membrane integrity of blood-retinal barrier |
| Zeng Kaihong, 2016 (China) [19] | Rat Müller cells | Primary culture of rat cells | Müller cells were identified by expression of glutamine synthetase, vimentin and glutamate transporter (IHC) |
High glucose conditions (25 mM for at least 3 days) | 10, 20 or 30 mM (for at least 3 days) | Glutamate uptake assay, enzymatic activity assay, IHC, RT PCR | Resveratrol prevented high glucose –induced decrease of glutamate transporters (GLAST) expression and decrease in glutamate uptake. |
| Zeng Kaihong, 2017 (China) [18] | Rat Müller cells | Primary culture of rat cells | Müller cells were identified by expression of glutamine synthetase, vimentin and glutamate transporter (IHC) |
High glucose conditions (25 mM for at least 3 days) | 10, 20 or 30 mM (for at least 3 days) | RT PCR, enzymatic activity assay, IHC | Resveratrol prevented high glucose-induced retinal Müller cells apoptosis via microRNA-29b (miR-29b): decreased Bax and specificity protein 1 (SP1) expression and increased Bcl-2. miR-29b inhibitor reversed the anti-apoptotic effect of resveratrol. |