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Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood–Retina Barrier Functions

Diabetic retinopathy (DR) primarily progresses into retinal degeneration caused by microvascular dysfunction. The pathophysiology of DR progression is still uncertain. This study investigates the function of beta-carotene (PBC) originating from palm oil mill effluent in the treatment of diabetes in...

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Autores principales: Paramaswaran, Yamunna, Subramanian, Aswinprakash, Paramakrishnan, Nallupillai, Ramesh, Muthusamy, Muthuraman, Arunachalam
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10224388/
https://www.ncbi.nlm.nih.gov/pubmed/37242430
http://dx.doi.org/10.3390/ph16050647
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author Paramaswaran, Yamunna
Subramanian, Aswinprakash
Paramakrishnan, Nallupillai
Ramesh, Muthusamy
Muthuraman, Arunachalam
author_facet Paramaswaran, Yamunna
Subramanian, Aswinprakash
Paramakrishnan, Nallupillai
Ramesh, Muthusamy
Muthuraman, Arunachalam
author_sort Paramaswaran, Yamunna
collection PubMed
description Diabetic retinopathy (DR) primarily progresses into retinal degeneration caused by microvascular dysfunction. The pathophysiology of DR progression is still uncertain. This study investigates the function of beta-carotene (PBC) originating from palm oil mill effluent in the treatment of diabetes in mice. An intraperitoneal injection of streptozotocin (35 mg/kg) was used to induce diabetes, which was then accelerated by an intravitreal (i.vit.) injection of STZ (20 µL on day 7). PBC (50 and 100 mg/kg) and dexamethasone (DEX: 10 mg/kg) were also administered orally (p.o.) for 21 days. At various time intervals, the optomotor response (OMR) and visual-cue function test (VCFT) responses were evaluated. Biomarkers, such as reduced glutathione (GSH), thiobarbituric acid reactive substances (TBARSs), and catalase activity were determined in retinal tissue samples. DR significantly lowers the spatial frequency threshold (SFT) and time spent in the target quadrant (TSTQ), increases the reaching time in the visual-cue platform (RVCP), lowers retinal GSH and catalase activity levels, and elevates TBARS levels. The treatments of PBC and DEX also ameliorate STZ-induced DR alterations. The potential ameliorative activity of PBC in DR is attributed to its anti-diabetic, anti-oxidative, and control of blood–retinal barrier layer properties.
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spelling pubmed-102243882023-05-28 Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood–Retina Barrier Functions Paramaswaran, Yamunna Subramanian, Aswinprakash Paramakrishnan, Nallupillai Ramesh, Muthusamy Muthuraman, Arunachalam Pharmaceuticals (Basel) Article Diabetic retinopathy (DR) primarily progresses into retinal degeneration caused by microvascular dysfunction. The pathophysiology of DR progression is still uncertain. This study investigates the function of beta-carotene (PBC) originating from palm oil mill effluent in the treatment of diabetes in mice. An intraperitoneal injection of streptozotocin (35 mg/kg) was used to induce diabetes, which was then accelerated by an intravitreal (i.vit.) injection of STZ (20 µL on day 7). PBC (50 and 100 mg/kg) and dexamethasone (DEX: 10 mg/kg) were also administered orally (p.o.) for 21 days. At various time intervals, the optomotor response (OMR) and visual-cue function test (VCFT) responses were evaluated. Biomarkers, such as reduced glutathione (GSH), thiobarbituric acid reactive substances (TBARSs), and catalase activity were determined in retinal tissue samples. DR significantly lowers the spatial frequency threshold (SFT) and time spent in the target quadrant (TSTQ), increases the reaching time in the visual-cue platform (RVCP), lowers retinal GSH and catalase activity levels, and elevates TBARS levels. The treatments of PBC and DEX also ameliorate STZ-induced DR alterations. The potential ameliorative activity of PBC in DR is attributed to its anti-diabetic, anti-oxidative, and control of blood–retinal barrier layer properties. MDPI 2023-04-26 /pmc/articles/PMC10224388/ /pubmed/37242430 http://dx.doi.org/10.3390/ph16050647 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Paramaswaran, Yamunna
Subramanian, Aswinprakash
Paramakrishnan, Nallupillai
Ramesh, Muthusamy
Muthuraman, Arunachalam
Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood–Retina Barrier Functions
title Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood–Retina Barrier Functions
title_full Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood–Retina Barrier Functions
title_fullStr Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood–Retina Barrier Functions
title_full_unstemmed Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood–Retina Barrier Functions
title_short Therapeutic Investigation of Palm Oil Mill Effluent-Derived Beta-Carotene in Streptozotocin-Induced Diabetic Retinopathy via the Regulation of Blood–Retina Barrier Functions
title_sort therapeutic investigation of palm oil mill effluent-derived beta-carotene in streptozotocin-induced diabetic retinopathy via the regulation of blood–retina barrier functions
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10224388/
https://www.ncbi.nlm.nih.gov/pubmed/37242430
http://dx.doi.org/10.3390/ph16050647
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