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Vitamin [D.sub.3] Inhibits High-Glucose-Induced Death of HRMECs by Inhibiting the Expression of the NLRP3 Inflammasome Pathway.
Furthermore, we found that the Bax/Bcl-2 protein ratio decreased after high-glucose-treated HRMECs were treated with vitamin [D.sub.3].
These findings suggest that vitamin [D.sub.3] protects HRMECs by inhibiting the increase in NLRP3 inflammasome protein levels and decreasing IL-1[beta] secretion.
We determined ROS levels and TXNIP expression in HRMECs incubated in the presence of high glucose and NAC.
Abbreviations BRB: Blood-retinal barrier ECM: Extracellular matrix ERG: Electroretinogram HRS: Hyperreflective spots HRMEC: Human retinal microvascular endothelial cells IVT: Intravitreal OCT: Optical coherence tomography PVD: Posterior vitreous detachment RPE: Retinal pigmented epithelium SRF: Subretinal fluid TEER: Transepithelial or transendothelial electrical resistance VMA/VMT: Vitreomacular adhesion/Vitreomacular traction.
Transendothelial or -epithelial resistance of HRMEC and ARPE19 monolayer cultures was monitored in function of time after applying the indicated treatments.
EGHB010 Inhibits VEGF-Induced Tube Formation in HRMECs. To investigate the cytotoxic effect of EGHB010 on HRMECs, we performed MTT assay with various concentrations of EGHB010 (1-100 [micro]g/mL).
We demonstrated for the first time that EGHB010 inhibited tube formation in HRMECs in vitro and retinal vascular leakage in vivo, mediated by VEGF.
In addition, in vitro studies showed that EGHB010 treatment inhibited VEGF-induced tube formation in HRMECs. Further studies may be required to determine the feasibility of using EGHB010 in the treatment of human wet AMD and diabetic macular edema.
Caption: Figure 1: EGHB010 inhibits tube formation in HRMECs. (a) Effect of EHGB010 on the viability of HRMECs was determined by MTS assay.
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