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Scholars Academic Journal of Biosciences | Volume-7 | Issue-08
Class II selective Histone deacetylase inhibitors (HDACi) as therapeutics for Type 2 Diabetic Retinopathy: An in silico approach
Devkinandan Sharma, Priyanka Mishra, Dr. Archana tiwari
Published: Aug. 21, 2019 | 250 195
DOI: 10.36347/sajb.2019.v07i08.006
Pages: 345-354
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Abstract
From chronically diabetic retinopathy upsurge the augur of diabetes can lead to irreversible vision loss. In the present chronological time, no cure in early-stage is possible in case of Diabetic Retinopathy (DR). Decreased the level of BDNF gene association between type II diabetes and class II Histone deacetylase (HDACs) as both increases; Histone deacetylases (HDACs) regulate epigenetic gene expression programs by modulating chromatin architecture and are required for neuronal development. Dysregulation of HDACs and aberrant chromatin acetylation homeostasis have been implicated in various diseases ranging from cancer to neurodegenerative disorders, for instance, DR. Class- II selective Histone deacetylase inhibitors (HDACi) have implications in increasing synaptic plasticity, decreasing angiogenesis, triggering neuroprotective signaling and positively suppress abnormal development of blood vessels. HDACi also shows promise as therapeutics for neurodegenerative. Here, we propose in-silico research that-there is a strong rationale for early treatment of diabetic retinopathy with aim and objective of this erudite research is insilico approach to investigate the binding affinity of Class- II selective Histone Deacetylase towards BDNF-TrKB pathway. The docking was done using “AutoDock vina and Swissdock” and visualized it through “UCSF chimera & Discovery Studio 2017 R2 Client”. Protein-protein analysis and visualization of docking simulation results were done using “HEX Server”. Molecular docking results of every Class- II Histone Deacetylase Inhibitors towards Trk-B receptor have negative binding energy, whereas E-total and E-shape value with greater than -7 and RMS values having negative ~0.5 ≤ 1.This research concludes that our findings implicate class II selective HDAC inhibitors in triggering neuroprotective signaling that can be increased expression of BDNF gene and indicate that class II selective HDAC inhibitors are an approach towards personalized medicine