scholarly journals Protective Effects of Melatonin on Retinal Inflammation and Oxidative Stress in Experimental Diabetic Retinopathy

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Tingting Jiang ◽  
Qing Chang ◽  
Jiyang Cai ◽  
Jiawen Fan ◽  
Xiaozhe Zhang ◽  
...  

Oxidative stress and inflammation are important pathogenic factors contributing to the etiology of diabetic retinopathy (DR). Melatonin is an endogenous hormone that exhibits a variety of biological effects including antioxidant and anti-inflammatory functions. The goals of this study were to determine whether melatonin could ameliorate retinal injury and to explore the potential mechanisms. Diabetes was induced by a single intraperitoneal (i.p.) injection of STZ (60 mg/kg) in Sprague-Dawley rats. Melatonin (10 mg kg−1daily, i.p.) was administered from the induction of diabetes and continued for up to 12 weeks, after which the animals were sacrificed and retinal samples were collected. The retina of diabetic rats showed depletion of glutathione and downregulation of glutamate cysteine ligase (GCL). Melatonin significantly upregulated GCL by retaining Nrf2 in the nucleus and stimulating Akt phosphorylation. The production of proinflammatory cytokines and proteins, including interleukin 1β, TNF-α, and inducible nitric oxide synthase (iNOS), was inhibited by melatonin through the NF-κB pathway. At 12 weeks, melatonin prevented the significant decrease in the ERG a- and b-wave amplitudes under the diabetic condition. Our results suggest potent protective functions of melatonin in diabetic retinopathy. In addition to being a direct antioxidant, melatonin can exert receptor-mediated signaling effects to attenuate inflammation and oxidative stress of the retina.

2014 ◽  
Vol 70 (3) ◽  
pp. 713-723 ◽  
Author(s):  
Mohamed Salah Allagui ◽  
Anouer Feriani ◽  
Zouhour Bouoni ◽  
Hichem Alimi ◽  
Jean Claud Murat ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Claudio Bucolo ◽  
Giuseppina Marrazzo ◽  
Chiara Bianca Maria Platania ◽  
Filippo Drago ◽  
Gian Marco Leggio ◽  
...  

Diabetic retinopathy is a complex condition where inflammation and oxidative stress represent crucial pathways in the pathogenesis of the disease. Aim of the study was to investigate the effects of a fortified extract of red berries,Ginkgo bilobaand white willow bark containing carnosine andα-lipoic acid in early retinal and plasma changes of streptozotocin-induced diabetic rats. Diabetes was induced by a single streptozotocin injection in Sprague Dawley rats. Diabetics and nondiabetic (control) rats were treated daily with the fortified extract for the ten days. Retina samples were collected and analyzed for their TNF-αand VEGF content. Moreover, plasma oxidative stress was evaluated by thiobarbituric acid reacting substances (TBARS). Increased TNF-αand VEGF levels were observed in the retina of diabetic rats. Treatment with the fortified extract significantly lowered retinal cytokine levels and suppressed diabetes-related lipid peroxidation. These data demonstrate that the fortified extract attenuates the degree of retinal inflammation and plasma lipid peroxidation preserving the retina in early diabetic rats.


2019 ◽  
Vol 17 ◽  
pp. 205873921984783 ◽  
Author(s):  
Xian Zhang ◽  
En Shi ◽  
Lan Yang ◽  
Weina Fu ◽  
Feng Hu ◽  
...  

Diabetic retinopathy, an inflammatory condition, is one of the devastating complication associated with diabetes that can lead to irreversible blindness. Gentiopicroside (GP), a secoiridoid glycoside, exhibits anti-inflammatory and antioxidant activity. The investigation was carried out to explore whether GP could attenuate diabetic retinopathy in diabetic rats. Diabetes was induced by injecting streptozotocin (STZ) (65 mg/kg) intraperitoneally in 8-weeks-old male rats (200–240 g). The treatment group received GP (20, 40, 80 mg/kg) orally for a duration of 10 weeks in diabetic rats (n = 10), and the diabetic group animals received phosphate buffer solution (n = 20). Effect of GP on cell viability study was performed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Oxidative stress markers, inflammatory mediators, and angiogenic factors were quantified in the retinal tissues of diabetic animals. All data were analyzed by one-way analysis of variance (ANOVA) at P < 0.05. Cytoprotective effect of GP was observed in MTT assay. GP effectively downregulated inflammatory cytokine, nuclear factor κB (NF-κB), tumor necrosis factor-α (TNF-α), interleukin 1 beta (IL-1β), and intercellular adhesion molecules-1 (ICAM-1), and upregulated antioxidant markers glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) in the retina of diabetic rats. GP equilibrated the disturbed angiogenic factors in the diabetic retinal tissues. Results clearly indicated defensive role of GP in the treatment of diabetic retinopathy by inhibition of NF-κB and oxidative stress.


2014 ◽  
Vol 31 (4) ◽  
pp. 233-243
Author(s):  
Ivana Stojanović ◽  
Srđan Ljubisavljević ◽  
Ivana Stevanović ◽  
Slavica Stojnev ◽  
Radmila Pavlović ◽  
...  

Summary The aim of this study was to investigate the exogenous agmatine influence on nitrosative and oxidative stress parameters in acute phase of multiple sclerosis (MS) experimental model, experimental autoimmune encephalomyelitis (EAE). EAE was induced by subcutaneous injection of myelin basic protein (50 μg per animal). Sprague-Dawley rats were divided into five groups: I group - (CG), treated by PBS (i.p.), II group - (EAE), III group - (CFA), treated with Complete Freund’s adjuvant (0.2 ml subcutaneously), IV group - (EAE+AGM), treated by agmatine (75 mg/kg bw i.p.) upon EAE induction and V group - (AGM), received only agmatine in the same dose. The animals were treated every day during experiment - from day 0 to 15, and clinically scored every day. They were sacrificed on day 16 from MBP application. NO2+NO3, S-nitrosothiols (RSNO), malondyaldehide (MDA) and reduced glutathione (GSH) concentrations and superoxide dismutase (SOD) activity were determined in rat whole encephalitic mass (WEM) and cerebellum homogenates. Agmatine exerted strong protective effects on EAE clinical symptoms (p<0.05). In EAE brain homogenates, NO2+NO3, RSNO and MDA concentrations were increased compared to CG values. Agmatine treatment diminished NO2+NO3, RSNO and MDA levels in EAE animals (p<0.05). In EAE rats, GSH level and SOD activity were decreased compared to CG values, but agmatine treatment increased both parameters compared to EAE untreated animals (p<0.05). Immunohistochemical staining supported the clinical and biochemical findings in all groups. The CNS changes in EAE are successfully supressed by agmatine application, which could be the the new aspect of the neuroprotective effects of agmatine.


Author(s):  
Maryem Ben Salem ◽  
Rihab Ben Abdallah Kolsi ◽  
Raouia Dhouibi ◽  
Kamilia Ksouda ◽  
Slim Charfi ◽  
...  

2012 ◽  
Vol 8 (2) ◽  
pp. 1555-1565 ◽  
Author(s):  
Najla Hfaiedh ◽  
Sabah Dhibi ◽  
Sakria Mbarki ◽  
Jean-Claude Murat ◽  
Abdel Fattah Elfeki

Protective effects of Fenugreek seeds (Trigonella foenum graecum L), added in the diet, upon oxidative stress and dysfunctions in kidney, thyroid and liver of alloxan-diabetic rats were investigated.In our study, the alloxan-induced diabetes triggered 1) increased levels of glucose, total cholesterol and triglycerides in blood, 2) increased activities of alkaline phosphatase and transaminases in blood, 3) increased levels of creatinine, urea and protein in blood, 4) a decreased level of TSH and an increased level of free thyroxin in plasma.In addition, an oxidative stress, evidenced by an increase of lipids peroxidation level and superoxide dismutase activity associated with a decrease of glutathione peroxidase and catalase activities in hepatic and renal tissues, was observed.When Fenugreek seeds powder (100g/kg) was added in the food for 30 days, all this parameters were significantly shifted to more normal values.In conclusion, fenugreek seeds powder displays beneficial effects upon hepatotoxicity, nephropathy, thyroid dysfunction and oxidative stress in alloxan-diabetic rats. This property could be attributed to the presence of antioxidant components, such as complex polysaccharides and phenolic acids, as confirmed by analyses. 


2020 ◽  
Author(s):  
Chengfeng Miao ◽  
Hanbin Chen ◽  
Yulian Li ◽  
Ying Guo ◽  
Feifei Xu ◽  
...  

Abstract Background: Diabetic encephalopathy is a severe diabetes complication with cognitive dysfunction and neuropsychiatric disability. The mechanisms underlying diabetic encephalopathy is believed to be relevant with oxidative stress, vascular amylin deposition, immune receptors, inflammation, etc. This study wanted to evaluate the ability of curcumin and its analog A13 to alleviate oxidative stress and inflammation in diabetes-induced damages in brain.Methods: Sixty adult male Sprague-Dawley rats were divided into 5 groups: normal control (NC) group, diabetes mellitus (DM) group, curcumin-treated diabetes mellitus (CUR) group, high dose of A13-treated diabetes mellitus (HA) group, low dose of A13-treated diabetes mellitus (LA) group. Activation of the nuclear factor kappa-B (NF-κB p65) pathway was detected by RT-qPCR, immunohistochemical (IHC) staining and Western blot; oxidative stress was detected by biochemical detection kit; brain tissue sections were stained with hematoxylin–eosin (HE) staining and Myelin staining. Results: RT-qPCR, IHC staining and Western blot showed that curcumin and A13 treatment could inhibit the NF-κB p65 pathway. Curcumin and A13 increased the activity of superoxide dismutase and decreased the malondialdehyde level in the brain of diabetic rats. Furthermore, HE staining and Myelin staining demonstrated that the histological lesions of the brain in diabetic rats could be significantly ameliorated by curcumin and A13.Conclusion: Curcumin analog A13 could alleviate the damages in the brain of diabetes rats by regulating the pathways of inflammation and oxidative stress. A13 may be a new potential therapeutic agent for diabetic encephalopathy.


Urology ◽  
2010 ◽  
Vol 75 (4) ◽  
pp. 902-906 ◽  
Author(s):  
Mehmet C. Ustuner ◽  
Sahin Kabay ◽  
Hilmi Ozden ◽  
Gul Guven ◽  
Mehmet Yucel ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Didem Onk ◽  
Oruc Alper Onk ◽  
Kultigin Turkmen ◽  
Huseyin Serkan Erol ◽  
Tulin Akarsu Ayazoglu ◽  
...  

Background.Inflammation and oxidative stress (OxS) contribute to the pathogenesis of diabetic kidney disease (DKD) and contrast-induced nephropathy (CIN). Patients with DKD were found to be more prone to CIN. Interleukin-33 (IL-33) is a proinflammatory cytokine, but its role in DKD and CIN is unknown.Methods.Thirty male Sprague-Dawley rats were enrolled. The first group was comprised of healthy rats (HRs), whereas the other four groups were made up of diabetic rats (DRs), diabetic rats with contrast-induced nephropathy (CIN + DRs), melatonin-treated diabetic rats (MTDRs), and melatonin-treated CIN + DRs (MTCIN + DRs). All groups except the HRs received 50 mg/kg/day streptozotocin (STZ). CIN + DRs were constituted by administrating 1.5 mg/kg of intravenous radiocontrast dye on the 35th day. MTDRs and MTCIN + DRs were given 20 mg/kg/day of intraperitoneal injection of melatonin (MT) from the 28th day for the constitutive seven days.Results.We observed increased IL-33 in the kidney tissue following induction of CIN in DRs. To determine whether MT is effective in preventing CIN, we administered MT in CIN + DRs and demonstrated that kidney tissue levels of OxS markers, inflammatory cytokines, and IL-33 were significantly diminished in MTCIN + DRs compared with other groups without MT treatment (p<0.05).Conclusion.Inhibition of IL-33 with MT provides therapeutic potential in DKD with CIN.


Sign in / Sign up

Export Citation Format

Share Document