Effect of Sex Hormones on Diabetic Microangiopathy (Diffuse Glomerulosclerosis and Diabetic Retinopathy) in the Cohen Diabetic Rat

2015 ◽  
pp. 137-153
Author(s):  
A. M. Cohen ◽  
L. Yanko ◽  
E. Rosenmann
Keyword(s):  
Diabetic Retinopathy ◽  
Sex Hormones ◽  
Diabetic Microangiopathy ◽  
Diabetic Rat

scholarly journals Serum levels of mac-2 binding protein are associated with diabetic microangiopathy and macroangiopathy in people with type 2 diabetes

2020 ◽  
Vol 8 (1) ◽  
pp. e001189
Author(s):  
Yoshitaka Hashimoto ◽  
Masahide Hamaguchi ◽  
Ayumi Kaji ◽  
Ryosuke Sakai ◽  
Noriyuki Kitagawa ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Retinopathy ◽  
Liver Fibrosis ◽  
Proliferative Diabetic Retinopathy ◽  
Binding Protein ◽  
Protein Glycosylation ◽  
Diabetic Microangiopathy ◽  
Alcoholic Fatty Liver ◽  
Increased Risk

IntroductionNon-alcoholic fatty liver disease is reportedly associated with type 2 diabetes and progressive liver fibrosis, as evaluated by transient elastography, and has been linked with micro- and macroangiopathy in people with type 2 diabetes. The purpose of this cross-sectional study was to investigate the association between serum mac-2 binding protein glycosylation isomer (M2BPGi) levels and diabetic complications in people with type 2 diabetes.Research design and methodsSerum M2BPGi levels were measured in terms of cut-off index (C.O.I.) units. Urinary albumin excretion (UAE) was calculated and nephropathy was graded as normoalbuminuria, microalbuminuria, or macroalbuminuria. Retinopathy was divided into three groups: no-diabetic retinopathy (NoDR), non-proliferative-diabetic retinopathy (NPDR), or proliferative-diabetic retinopathy (PDR) .ResultsThe mean age for the 363 studied subjects (212 males) was 66.4±10.6 years, the median serum M2BPGi level was 0.77 (0.57–1.04) C.O.I., and the median UAE was 22 (9–82.1) mg/g creatinine. M2BPGi levels in microalbuminuria (0.83 (0.61 to 1.18) C.O.I.) and macroalbuminuria (0.88 (0.67 to 1.22) C.O.I.) cases were higher than those in normoalbuminuria cases (0.71 (0.54 to 0.92) C.O.I.). M2BPGi levels in NPDR (0.93 (0.68 to 1.28) C.O.I.) and PDR (0.95 (0.71 to 1.31) C.O.I.) cases were higher than in cases with NoDR (0.73 (0.56 to 0.99) C.O.I.). Furthermore, M2BPGi levels in subjects with a history of cardiovascular diseases were higher than in those with no such history (0.82 (0.65 to 1.22) vs 0.76 (0.55 to 1.03) C.O.I., p=0.019). The logarithm of (M2BPGi+1) was associated with the logarithm of UAE values after adjusting for covariates (standardized β=0.107, p=0.031).ConclusionsThis study reveals a close association between serum M2BPGi levels and diabetic microangiopathy and macroangiopathy in people with type 2 diabetes. The results also show that liver fibrosis, evaluated by M2BPGi, is independently associated with an increased risk of albuminuria.

scholarly journals Nanoparticles C60 fullerene prevent reactive gliosis in retina of aged rats under hyperglycemia

2015 ◽  
Vol 6 (2) ◽  
pp. 113-118
Author(s):  
I. V. Prischepa ◽  
O. G. Prokushenkova ◽  
V. S. Nedzvetsky
Keyword(s):  
Diabetic Retinopathy ◽  
Glial Cells ◽  
Glycosylated Hemoglobin ◽  
Initial Period ◽  
Protective Action ◽  
Diabetic Rats ◽  
Water Soluble ◽  
Reactive Gliosis ◽  
C60 Fullerene ◽  
Diabetic Rat

Reactivation of glial cells, induced by metabolic disorders of glucose utilization and development of oxidative stress in retina under diabetes mellitus, is the key pathogenetic factor of diabetic retinopathy. Nanoparticles of C60 fullerene and some of their water-soluble derivates are known as one of the strongest antioxidants having neuroprotective effect in a number of pathologies and harmful influences. In the present study, for the first time, the effects of nanostructures of hydrated C60 fullerene (C60HyFn) on the expression and polypeptide composition of glial fibrillary acidic protein (GFAP) in retina of rats with streptozotocin (STZ)-induced diabetes have been evaluated. Using immunoblotting, 1.93-fold up-regulation of GFAP in diabetic rat retina as compared with control was shown, as a result of retinal glial cells reactivation induced by hyperglycemia. Increase in GFAP-immunolabeling associated with the reactive gliosis development in retina of diabetic rats was also confirmed by immuno-histochemical method. Consumption of C60HyFn solution (90 nM) as drinking water by diabetic rats for 12 weeks caused 1.51-fold decrease of GFAP level compared to untreated diabetic animals. In addition, C60HyFn caused statistically significant lowering of glycosylated hemoglobin concentration in blood serum of STZ-diabetic rats 1.58-fold. However, nanoparticles C60 did not affect neither insulin nor glucose levels in blood of diabetic rats. In conclusion, results obtained indicate that protective action of hydrated fullerene in the initial period of diabetic retinopathy of aged animals is realized through suppression of excessive activation of GFAP-positive retinal cells. 

scholarly journals Gender, sex hormones and diabetic retinopathy: A review

2021 ◽  
Vol 7 (1) ◽  
pp. 181-189
Author(s):  
Rajendra P Maurya ◽  
Ashish Gupta ◽  
Anup Singh ◽  
Virendra P Singh ◽  
Sanjay Bosak ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Sex Hormones

The STZ-induced diabetic rat as a model for studying neuronal pathologies of diabetic retinopathy

2015 ◽  
Vol 93 ◽  
pp. n/a-n/a
Author(s):  
R. Herrmann ◽  
N. Zippel ◽  
J. Haller ◽  
R. Streicher
Keyword(s):  
Diabetic Retinopathy ◽  
Diabetic Rat

scholarly journals Network Pharmacology-based Investigation of the Underlying Mechanism of Panax notoginseng Treatment of Diabetic Retinopathy

2020 ◽  
Vol 23 (4) ◽  
pp. 334-344
Author(s):  
Chunli Piao ◽  
Zheyu Sun ◽  
De Jin ◽  
Han Wang ◽  
Xuemin Wu ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Molecular Mechanisms ◽  
Topological Analysis ◽  
Enrichment Analysis ◽  
Panax Notoginseng ◽  
Diabetic Microangiopathy ◽  
Network Pharmacology ◽  
Pathway Enrichment Analysis ◽  
Annotation Database ◽  
Cox 2

Background: Panax notoginseng, a Chinese herbal medicine, has been widely used to treat vascular diseases. Diabetic retinopathy (DR) is one of the complications of diabetic microangiopathy. According to recent studies, the application of Panax notoginseng extract and related Chinese patent medicine preparations can significantly improve DR. However, the pharmacological mechanisms remain unclear. Therefore, the purpose of this study was to decipher the potential mechanism of Panax notoginseng treatment of DR using network pharmacology. Methods: We evaluated and screened the active compounds of Panax notoginseng using the Traditional Chinese Medicine Systems Pharmacology database and collected potential targets of the compounds by target fishing. A multi-source database was also used to organize targets of DR. The potential targets as the treatment of DR with Panax notoginseng were then obtained by matching the compound targets with the DR targets. Using protein-protein interaction networks and topological analysis, interactions between potential targets were identified. In addition, we also performed gene ontology-biological process and pathway enrichment analysis for the potential targets by using the Biological Information Annotation Database. Results: Eight active ingredients of Panax notoginseng and 31 potential targets for the treatment of DR were identified. The screening and enrichment analysis revealed that the treatment of DR using Panax notoginseng primarily involved 28 biological processes and 10 related pathways. Further analyses indicated that angiogenesis, inflammatory reactions, and apoptosis may be the main processes involved in the treatment of DR with Panax notoginseng. In addition, we determined that the mechanism of intervention of Panax notoginseng in treating DR may involve five core targets, VEGFA, MMP-9, MMP-2, FGF2, and COX-2. Conclusion: Panax notoginseng may treat diabetic retinopathy through the mechanism of network pharmacological analysis. The underlying molecular mechanisms were closely related to the intervention of angiogenesis, inflammation, and apoptosis with VEGFA, MMP-9, MMP-2, FGF2, and COX-2 being possible targets.

Ranibizumab prevents Müller cell edema by decreasing VEGF-A in diabetic retinopathy

2020 ◽  
Author(s):  
Tianqin Wang ◽  
Chaoyang Zhang ◽  
Hai Xie ◽  
Qiuxue Yi ◽  
Dandan Liu ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Potassium Level ◽  
Müller Cells ◽  
Müller Cell ◽  
Intracellular Sodium ◽  
K Channel ◽  
Diabetic Rat ◽  
Muller Cells ◽  
Intracellular Potassium ◽  
Muller Cell

Abstract Background: Diabetic macular edema (DME) is the most common cause of vision loss in patients with diabetic retinopathy. The efficacy of anti-VEGF therapy has been well demonstrated and become the standard of care in the management of DME. The present study is to explore the possible mechanism(s) of ranibizumab in protecting Müller cells from cellular edema in experimental diabetic retinopathy. Methods: Sprague-Dawley rats were rendered diabetes with intraperitoneal injection of streptozotocin. Intravitreal injection of ranibizumab was performed 8 weeks after diabetes onset. Four weeks later, the rats were killed and the retinas were harvested for examination. rMC-1 cells (rat Müller cell line) were treated with glyoxal for 24 hours, with or without ranibizumab. Cell viability was detected with CCK-8 assay. The expressions of inwardly rectifying K + channel 4.1 (Kir4.1), aquaporin 4 (AQP4), Dystrophin 71 (Dp71), vascular endothelial growth factor A (VEGF-A), glutamine synthetase (GS) and sodium-potassium-ATPase (Na + -K + -ATPase) were examined with Western blot. VEGF-A in the supernatant of cell culture was detected with ELISA. The intracellular potassium and sodium levels were detected with specific indicators. Results: Compared to the normal control, the protein expressions of Kir4.1, AQP4 and Dp71 were down-regulated significantly in diabetic rat retinas, which were prevented by ranibizumab. The above changes were recapitulated in vitro . As compared with the control, the intracellular potassium level in glyoxal-treated rMC-1 cells was increased, while the intracellular sodium level and Na + -K + -ATPase protein level remained unchanged. However, ranibizumab treatment increased Na + -K + -ATPase protein expression and decreased intracellular sodium, but not potassium level. Conclusion: Ranibizumab protected Müller cells from intracellular edema through up-regulation of Kir4.1, AQP4, and Dp71 by directly binding VEGF-A. It also increased the expression of Na + -K + -ATPase, contributing to reduction of the intracellular osmotic pressure.

scholarly journals The Role of SGLT2 Inhibitor on the Treatment of Diabetic Retinopathy

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Wenjun Sha ◽  
Song Wen ◽  
Lin Chen ◽  
Bilin Xu ◽  
Tao Lei ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Glucose Transporter ◽  
Early Stage ◽  
Sglt2 Inhibitor ◽  
Research Field ◽  
Research Progress ◽  
Diabetic Microangiopathy ◽  
Control Blood Glucose ◽  
Glucose Transporter 2 ◽  
Prevention And Treatment

Diabetic retinopathy (DR) is one of the most serious complications of diabetic microangiopathy. DR has an early onset and is not easy to detect. When visual impairment occurs, the optimal period for therapy is often missed. Therefore, the prevention and treatment of DR should start from the early stage of diabetes. Sodium-dependent glucose transporter 2 inhibitor (SGLT2i) is a new antidiabetic drug which is mainly used in clinical practice to control blood glucose of patients with type 2 diabetes prone to develop chronic heart failure. Recent studies have found that SGLT2 is also expressed in the human retina. Now, the prevention and treatment of diabetic retinopathy with SGLT2i while reducing blood sugar has become a new research field. Hence, this article reviewed the recent therapeutic and research progress of SGLT2 in the treatment of diabetic retinopathy.

scholarly journals Dual blockade of renin angiotensin system in reducing the early changes of diabetic retinopathy and nephropathy in a diabetic rat model

2014 ◽  
Vol 6 (12) ◽  
pp. 625 ◽  
Author(s):  
Pugazhenthan Thangaraju ◽  
Amitava Chakrabarti ◽  
Dibyajyoti Banerjee ◽  
Debasish Hota ◽  
Tamilselvan ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Rat Model ◽  
Renin Angiotensin System ◽  
Diabetic Rat ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Dual Blockade ◽  
Diabetic Rat Model

scholarly journals TBHQ Regulates the Nrf2/HO-1 Pathway to Enhance Stem Cell Treatment of Diabetic Retinopathy

2021 ◽  
Author(s):  
Ze-Peng XU ◽  
Ni TIAN ◽  
Song-Tiao LI ◽  
Kun-Meng LI ◽  
Xiao-Yu WANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Therapeutic Effect ◽  
Biological Effects ◽  
Combined Therapy ◽  
Diabetic Rats ◽  
Inflammatory Factors ◽  
Diabetic Rat ◽  
Human Umbilical Cord ◽  
Therapeutic Effects

Abstract Objective: To investigate the therapeutic effect of human umbilical cord mesenchymal stem cells (hUCMSCs) on diabetic retinopathy (DR) in diabetic rats, and to study the mechanism of hUCMSCs in treating diabetic retinopathy by tert-butylhydroquinone (tBHQ) regulation of the Nrf2/HO-1 pathway.Methods: The diabetic rat model was induced by intraperitoneal injection of streptozotocin (STZ). The experimental animals were divided into six groups: Normal, diabetes mellitus (DM), hUCMSCs, tBHQ, combined tBHQ-hUCMSCs, and all-trans-retinoid acid (ATRA)-hUCMSCs combined group. Visual function experiments and histological analyses were performed eight weeks post intravitreal injection. Biochemical and molecular analyses were used to assess the hUCMSCs composition and its biological effects.Results: Improvements in systemic oxidative stress and inflammation were found in the tBHQ group. Although hUCMSCs had no significant effect on oxidative stress, retinal structure was improved, visual defects reduced and expression of local retinal inflammatory factors were inhibited following its application. The effect of combined therapy was better than that of single therapy. Inhibition of the Nrf2/HO-1 pathway can promote the expression of systemic inflammatory factors and inhibit the therapeutic effect of hUCMSCs in the retina.Conclusions: Intravitreal administration of hUCMSCs triggers an effective cytoprotective microenvironment in the retina of diabetic mice. Alone, however, it may not significantly improve the systemic inflammatory response of diabetes. In combination with tBHQ it may promote Nrf2expression, systemic antioxidant stress and therapeutic effects of hUCMSCs.

Sign in / Sign up

Export Citation Format

Share Document