scholarly journals Quercetin protects against diabetic encephalopathy via SIRT1/NLRP3 pathway in db/db mice

2020 ◽  
Vol 24 (6) ◽  
pp. 3449-3459 ◽  
Author(s):  
Tian Hu ◽  
Xin‐Yi Lu ◽  
Jing‐Jing Shi ◽  
Xiao‐Qi Liu ◽  
Qu‐Bo Chen ◽  
...  
Keyword(s):  
Diabetic Encephalopathy

D-Ribose Plays a Crucial Role in Type 1 Diabetic Encephalopathy

2019 ◽  
Author(s):  
Lexiang Yu ◽  
Yao Chen ◽  
Yan Wei ◽  
Rongqiao He
Keyword(s):  
Crucial Role ◽  
Diabetic Encephalopathy

scholarly journals A Novel Role for the Calcium Sensing Receptor in Rat Diabetic Encephalopathy

2015 ◽  
Vol 35 (1) ◽  
pp. 38-50 ◽  
Author(s):  
Shiyun Dong ◽  
Gang Li ◽  
Dan Zheng ◽  
Jichao Wu ◽  
Dianjun Sun ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Laser Scanning ◽  
Laser Scanning Confocal Microscopy ◽  
Diabetic Rats ◽  
Neonatal Rat ◽  
Protective Mechanism ◽  
Diabetic Encephalopathy ◽  
Calcium Sensing Receptor ◽  
Scanning Confocal Microscopy ◽  
Calcium Sensing

Background: Diabetic encephalopathy is a common complication of diabetes, and it may be involved in altering intracellular calcium concentrations ([Ca2+]i) at its onset. The calcium sensing receptor (CaSR) is a G-protein coupled receptor, however, the functional involvement of CaSR in diabetic encephalopathy remains unclear. Methods: In this study, diabetic rats were modeled by STZ (50 mg/kg). At the end of 4, 8 and 12 weeks, the CaSR expression in hippocampus was analyzed by Western blot. In neonatal rat hippocampal neurons, the [Ca2+]i was detected by laser scanning confocal microscopy, the production of reactive oxygen species (ROS) in mitochondria, the level of NO and the mitochondrial transmembrane potential were measured by MitoSOX, DAF-FM and JC-1, respectively. Results: Our results showed in hippocampal neurons treated with high glucose, CaSR regulated [Ca2+]i through the PLC-IP3 pathway. CaSR expression was decreased and was involved in the changes in [Ca2+]i. Mitochondrial membrane potential, NO release and expression of p-eNOS decreased, while the production of ROS in mitochondria increased. Conclusion: Down-regulation of CaSR expression was accompanied by neuronal injury, calcium disturbance, increased ROS production and decreased release of NO. Up-regulation of CaSR expression attenuated these changes through a positive compensatory protective mechanism to inhibit and delay diabetic encephalopathy in rats.

Dynamics of the Initial Signs of Experimental Diabetic Encephalopathy

2015 ◽  
Vol 45 (3) ◽  
pp. 276-282
Author(s):  
I. A. Volchegorskii ◽  
L. M. Rassokhina ◽  
I. Yu. Miroshnichenko
Keyword(s):  
Diabetic Encephalopathy

scholarly journals Role of glial metabolism in diabetic encephalopathy as detected by high resolution13C NMR

2003 ◽  
Vol 16 (67) ◽  
pp. 440-449 ◽  
Author(s):  
María A. García-Espinosa ◽  
María L. García-Martín ◽  
Sebastián Cerdán
Keyword(s):  
Diabetic Encephalopathy

C-Peptide and Type 1 Diabetic Encephalopathy

2011 ◽  
pp. 93-109 ◽  
Author(s):  
Anders A. F. Sima ◽  
Wei-Xian Zhang
Keyword(s):  
Diabetic Encephalopathy ◽  
C Peptide

scholarly journals Ameliorative Effect of Saffron Aqueous Extract on Hyperglycemia, Hyperlipidemia, and Oxidative Stress on Diabetic Encephalopathy in Streptozotocin Induced Experimental Diabetes Mellitus

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Saeed Samarghandian ◽  
Mohsen Azimi-Nezhad ◽  
Fariborz Samini
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Serum Proteins ◽  
Advanced Glycation Endproducts ◽  
Antioxidant Properties ◽  
Diabetic Encephalopathy ◽  
Beneficial Effects ◽  
Glucose Levels ◽  
Ameliorative Effect ◽  
Saffron Extract

Diabetic encephalopathy is one of the severe complications in patients with diabetes mellitus. Findings indicate that saffron extract has antioxidant properties but its underlying beneficial effects on diabetic encephalopathy were unclear. In the present study, the protective activities of saffron were evaluated in diabetic encephalopathy. Saffron at 40 and 80 mg/kg significantly increased body weight and serum TNF-αand decreased blood glucose levels, glycosylated serum proteins, and serum advanced glycation endproducts (AGEs) levels. Furthermore, significant increase in HDL and decrease (P<0.05) in cholesterol, triglyceride, and LDL were observed after 28 days of treatment. At the end of experiments, the hippocampus tissue was used for determination of glutathione content (GSH), superoxide dismutase (SOD), and catalase (CAT) activities. Furthermore, saffron significantly increased GSH, SOD, and CAT but remarkably decreased cognitive deficit, serum TNF-α, and induced nitric oxide synthase (iNOS) activity in hippocampus tissue. Our findings indicated that saffron extract may reduce hyperglycemia and hyperlipidemia risk and also reduce the oxidative stress in diabetic encephalopathy rats. This study suggested that saffron extract might be a promising candidate for the improvement of chemically induced diabetes and its complications.

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