Neuritin Alleviates Diabetic Retinopathy by Regulating Endoplasmic Reticulum Stress in Rats
- Authors: Wen S.1, Hu M.1, Chen C.2, Li Z.1, Liu G.3
-
Affiliations:
- Department of Ophthalmology,, Jingmen No.1 People's Hospital
- , Renmin Hospital of Wuhan University, Hubei General Hospital
- Department of Ophthalmology,, Jingmen No. 1 Peoples Hospital, Jingmen
- Issue: Vol 27, No 16 (2024)
- Pages: 2454-2461
- Section: Chemistry
- URL: https://vietnamjournal.ru/1386-2073/article/view/644338
- DOI: https://doi.org/10.2174/0113862073275316231123060640
- ID: 644338
Cite item
Full Text
Abstract
Background:Neuritin, a small-molecule neurotrophic factor, maintains neuronal cell activity, inhibits apoptosis, promotes process growth, and regulates neural progenitor cell differentiation, migration, and synaptic maturation. Neuritin helps retinal ganglion cells (RGCs) survive optic nerve injury in rats and regenerate axons. However, the role of Neuritin in Diabetic retinopathy (DR) is unclear.
Objective:This study is intended to investigate the effect and mechanism of Neuritin in DR. For this purpose, we established DR rat models and injected Neuritin into them. This study provides a potential treatment for diabetic retinopathy.
Methods:The rat model of DR was established by streptozotocin (STZ) injection, and the effect of Neuritin on DR was detected by intravitreal injection. Histological analysis was performed by H&E and TUNEL methods. The mRNA and protein expressions of endoplasmic reticulum stress (ERS) pathway-related transcription factors were detected by qRT-PCR and western blot. The blood-retinal barrier (BRB) function was assessed using the patch-clamp technique and Evans blue leakage assay.
Results:Neuritin significantly improved the retinal structure, restrained the apoptosis of retinal cells, and protected the normal function of BRB in DR model rats. Mechanistically, Neuritin may function by inhibiting the expression of GRP78, ASK1, Caspase-12, VEGF, and so on.
Conclusion:Our results indicate that Neuritin alleviates retinal damage in DR rats via the inactive endoplasmic reticulum pathway. Our study provides a potential treatment for DR.
About the authors
Shu Wen
Department of Ophthalmology,, Jingmen No.1 People's Hospital
Email: info@benthamscience.net
Meng Hu
Department of Ophthalmology,, Jingmen No.1 People's Hospital
Email: info@benthamscience.net
Changzheng Chen
, Renmin Hospital of Wuhan University, Hubei General Hospital
Email: info@benthamscience.net
Zhen Li
Department of Ophthalmology,, Jingmen No.1 People's Hospital
Email: info@benthamscience.net
Guoli Liu
Department of Ophthalmology,, Jingmen No. 1 Peoples Hospital, Jingmen
Author for correspondence.
Email: info@benthamscience.net
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