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Neuroprotective effects of resveratrol on retinal ganglion cells in glaucoma in rodents: A narrative review

Maryam GolmohammadiSchool of Medicine Shahid Beheshti University of Medical Sciences Tehran IranSeyed Arash Aghaei MeibodiSchool of Medicine Shahid Beheshti University of Medical Sciences Tehran IranSulieman Ibraheem Shelash Al‐HawaryDepartment of Business Administration, Business School Al al‐Bayt University Mafraq JordanJitendra GuptaInstitute of Pharmaceutical Research GLA University Mathura IndiaIbrohim B. SapaevNew Uzbekistan University Tashkent UzbekistanMazin A. A. NajmPharmaceutical Chemistry Department, College of Pharmacy Al‐Ayen University Thi‐Qar IraqMarim AlwaveMedical Technical College Al‐Farahidi University Baghdad IraqMozhgan NazifiDepartment of Neurology Hamadan University of Medical Sciences Hamadan IranMohammad Reza RahmaniDepartment of Physiology and Pharmacology, School of Medicine Rafsanjan University of Medical Sciences Rafsanjan IranMohammad Yasin ZamanianDepartment of Pharmacology and Toxicology, School of Pharmacy Hamadan University of Medical Sciences Hamadan IranGervason MoriasiDepartment of Medical Biochemistry, School of Medicine, College of Health Sciences Mount Kenya University Thika Kenya
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Abstract Glaucoma, an irreversible optic neuropathy, primarily affects retinal ganglion cells (RGC) and causes vision loss and blindness. The damage to RGCs in glaucoma occurs by various mechanisms, including elevated intraocular pressure, oxidative stress, inflammation, and other neurodegenerative processes. As the disease progresses, the loss of RGCs leads to vision loss. Therefore, protecting RGCs from damage and promoting their survival are important goals in managing glaucoma. In this regard, resveratrol (RES), a polyphenolic phytoalexin, exerts antioxidant effects and slows down the evolution and progression of glaucoma. The present review shows that RES plays a protective role in RGCs in cases of ischemic injury and hypoxia as well as in ErbB2 protein expression in the retina. Additionally, RES plays protective roles in RGCs by promoting cell growth, reducing apoptosis, and decreasing oxidative stress in H 2 O 2 ‐exposed RGCs. RES was also found to inhibit oxidative stress damage in RGCs and suppress the activation of mitogen‐activated protein kinase signaling pathways. RES could alleviate retinal function impairment by suppressing the hypoxia‐inducible factor‐1 alpha/vascular endothelial growth factor and p38/p53 axes while stimulating the PI3K/Akt pathway. Therefore, RES might exert potential therapeutic effects for managing glaucoma by protecting RGCs from damage and promoting their survival.

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