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Retinal neuroprotective effects of quercetin in streptozotocin-induced diabetic rats.
Exp Eye Res. 2014 Aug; 125:193-202.EE

Abstract

The aim of the present study was to evaluate the effects of Quercetin (Qctn), a plant based flavonol, on retinal oxidative stress, neuroinflammation and apoptosis in streptozotocin-induced diabetic rats. Qctn treatment (25- and 50 mg/kg body weight) was given orally for six months in diabetic rats. Retinal glutathione (GSH) and antioxidant enzymes [superoxide dismutase (SOD) and catalase (CAT)] were estimated using commercially available assays, and inflammatory cytokines levels [tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β)] were estimated by ELISA method. Immunofluorescence and western blot studies were performed for nuclear factor kappa B (NF-kB), caspase-3, glial fibrillary acidic protein (GFAP) and aquaporin-4 (AQP4) expressions. Structural changes were evaluated by light microscopy. In the present study, retinal GSH levels and antioxidant enzyme (SOD and CAT) activities were significantly decreased in diabetic group as compared to normal group. However, in Qctn-treated rats, retinal GSH levels were restored close to normal levels and positive modulation of antioxidant enzyme activities was observed. Diabetic retinas showed significantly increased expression of pro-inflammatory cytokines (TNF-α and IL-1β) as compared to that in normal retinas, while Qctn-treated retinas showed significantly lower levels of cytokines as compared to diabetic retinas. Light microscopy showed significantly increased number of ganglion cell death and decreased retinal thickness in diabetic group compared to those in normal retina; however, protective effect of Qctn was seen. Increased apoptosis in diabetic retina is proposed to be mediated by overexpression of NF-kB and caspase-3. However, Qctn showed inhibitory effects on NF-kB and caspase-3 expression. Microglia showed upregulated GFAP expression, and inflammation of Müller cells resulted in edema in their endfeet and around perivascular space in nerve fiber layer in diabetic retina, as observed through AQP4 expression. However, Qctn treatments inhibited diabetes-induced increases in GFAP and AQP4 expression. Based on these findings, it can be concluded that bioflavonoids, such as Qctn can be effective for protection of diabetes induced retinal neurodegeneration and oxidative stress.

Authors+Show Affiliations

Ocular Pharmacology Laboratory, Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences & Research, University of Delhi, New Delhi 110017, India; School of Medicine, Wayne State University, MI, USA. Electronic address: binitkumar35@gmail.com.Ocular Pharmacology Laboratory, Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences & Research, University of Delhi, New Delhi 110017, India. Electronic address: skgup@hotmail.com.Department of Anatomy, All India Institute of Medical Sciences, New Delhi 110029, India.Ocular Pharmacology Laboratory, Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences & Research, University of Delhi, New Delhi 110017, India.Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi 110029, India.Department of Anatomy, All India Institute of Medical Sciences, New Delhi 110029, India.Ocular Pharmacology Laboratory, Department of Pharmacology, Delhi Institute of Pharmaceutical Sciences & Research, University of Delhi, New Delhi 110017, India.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24952278

Citation

Kumar, Binit, et al. "Retinal Neuroprotective Effects of Quercetin in Streptozotocin-induced Diabetic Rats." Experimental Eye Research, vol. 125, 2014, pp. 193-202.
Kumar B, Gupta SK, Nag TC, et al. Retinal neuroprotective effects of quercetin in streptozotocin-induced diabetic rats. Exp Eye Res. 2014;125:193-202.
Kumar, B., Gupta, S. K., Nag, T. C., Srivastava, S., Saxena, R., Jha, K. A., & Srinivasan, B. P. (2014). Retinal neuroprotective effects of quercetin in streptozotocin-induced diabetic rats. Experimental Eye Research, 125, 193-202. https://doi.org/10.1016/j.exer.2014.06.009
Kumar B, et al. Retinal Neuroprotective Effects of Quercetin in Streptozotocin-induced Diabetic Rats. Exp Eye Res. 2014;125:193-202. PubMed PMID: 24952278.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Retinal neuroprotective effects of quercetin in streptozotocin-induced diabetic rats. AU - Kumar,Binit, AU - Gupta,Suresh Kumar, AU - Nag,Tapas Chandra, AU - Srivastava,Sushma, AU - Saxena,Rohit, AU - Jha,Kumar Abhiram, AU - Srinivasan,Bharthu Parthasarthy, Y1 - 2014/06/18/ PY - 2014/02/25/received PY - 2014/06/10/revised PY - 2014/06/11/accepted PY - 2014/6/22/entrez PY - 2014/6/22/pubmed PY - 2014/9/27/medline KW - GFAP KW - apoptosis KW - aquaporin-4 KW - bioflavonoid KW - neuroinflammation KW - quercetin SP - 193 EP - 202 JF - Experimental eye research JO - Exp Eye Res VL - 125 N2 - The aim of the present study was to evaluate the effects of Quercetin (Qctn), a plant based flavonol, on retinal oxidative stress, neuroinflammation and apoptosis in streptozotocin-induced diabetic rats. Qctn treatment (25- and 50 mg/kg body weight) was given orally for six months in diabetic rats. Retinal glutathione (GSH) and antioxidant enzymes [superoxide dismutase (SOD) and catalase (CAT)] were estimated using commercially available assays, and inflammatory cytokines levels [tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β)] were estimated by ELISA method. Immunofluorescence and western blot studies were performed for nuclear factor kappa B (NF-kB), caspase-3, glial fibrillary acidic protein (GFAP) and aquaporin-4 (AQP4) expressions. Structural changes were evaluated by light microscopy. In the present study, retinal GSH levels and antioxidant enzyme (SOD and CAT) activities were significantly decreased in diabetic group as compared to normal group. However, in Qctn-treated rats, retinal GSH levels were restored close to normal levels and positive modulation of antioxidant enzyme activities was observed. Diabetic retinas showed significantly increased expression of pro-inflammatory cytokines (TNF-α and IL-1β) as compared to that in normal retinas, while Qctn-treated retinas showed significantly lower levels of cytokines as compared to diabetic retinas. Light microscopy showed significantly increased number of ganglion cell death and decreased retinal thickness in diabetic group compared to those in normal retina; however, protective effect of Qctn was seen. Increased apoptosis in diabetic retina is proposed to be mediated by overexpression of NF-kB and caspase-3. However, Qctn showed inhibitory effects on NF-kB and caspase-3 expression. Microglia showed upregulated GFAP expression, and inflammation of Müller cells resulted in edema in their endfeet and around perivascular space in nerve fiber layer in diabetic retina, as observed through AQP4 expression. However, Qctn treatments inhibited diabetes-induced increases in GFAP and AQP4 expression. Based on these findings, it can be concluded that bioflavonoids, such as Qctn can be effective for protection of diabetes induced retinal neurodegeneration and oxidative stress. SN - 1096-0007 UR - https://www.unboundmedicine.com/medline/citation/24952278/Retinal_neuroprotective_effects_of_quercetin_in_streptozotocin_induced_diabetic_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(14)00170-5 DB - PRIME DP - Unbound Medicine ER -