PEDF Attenuates Ocular Surface Damage in Diabetic Mice Model Through Its Antioxidant Properties

2020 ◽  
pp. 1-7
Author(s):  
Xuemei Liu ◽  
Hui Liu ◽  
Xiaoxiao Lu ◽  
Joyce Tombran-Tink ◽  
Shaozhen Zhao
Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 2289-PUB
Author(s):  
EUN YOUNG LEE ◽  
YEOREE YANG ◽  
YUNJUNG CHO ◽  
SEUNG-HWAN LEE ◽  
JAE-HYOUNG CHO ◽  
...  

2021 ◽  
Author(s):  
Bochao Chen ◽  
Shumei Mao ◽  
Yanyan Sun ◽  
Liyuan Sun ◽  
Ning Ding ◽  
...  

A mitochondria-targeted near-infrared fluorescent probe NIR-V with 700 nm emission was designed to monitor cell viscosity changes, which was applied to detect the intracellular viscosity and imagine pancreatic tissue in diabetic mouse model.


2004 ◽  
Vol 36 (3) ◽  
pp. 156-165 ◽  
Author(s):  
Yumiko Takami ◽  
Huaqing Gong ◽  
Tsugio Amemiya

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Zhong-he Liu ◽  
Hong-guang Chen ◽  
Pan-feng Wu ◽  
Qing Yao ◽  
Hong-ke Cheng ◽  
...  

Objective. The effects of Flos Puerariae extract (FPE) on cognitive impairment associated with diabetes were assessed in C57BL/6J mice.Methods. Experimental diabetic mice model was induced by one injection of 50 mg/kg streptozotocin (STZ) for 5 days consecutively. FPE was orally administrated at the dosages of 50, 100, or 200 mg/kg/day, respectively. The learning and memory ability was assessed by Morris water maze test. Body weight, blood glucose, free fatty acid (FFA) and total cholesterol (TCH) in serum, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and acetylcholinesterase (AChE) activities in cerebral cortex and hippocampus were also measured.Results. Oral administration of FPE significantly improved cognitive deficits in STZ-induced diabetic mice. FPE treatment also maintained body weight and ameliorated hyperglycemia and dyslipidemia in diabetic mice. Additionally, decreased MDA level, enhanced CAT, and GSH-Px activities in cerebral cortex or hippocampus, as well as alleviated AChE activity in cerebral cortex, were found in diabetic mice supplemented with FPE.Conclusion. This study suggests that FPE ameliorates memory deficits in experimental diabetic mice, at least partly through the normalization of metabolic abnormalities, ameliorated oxidative stress, and AChE activity in brain.


2019 ◽  
Vol 62 (3) ◽  
pp. 166-172 ◽  
Author(s):  
Fang Fan ◽  
Zhihua Zhao ◽  
Xiaobin Zhao ◽  
Qingmin Ma ◽  
Kejun Li ◽  
...  

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Jee Young Han ◽  
Jin Joo Cha ◽  
Young Sun Kang ◽  
Jung Yeon Ghee ◽  
Ji Ae Yoo ◽  
...  

Abstract Background and Aims Activating Transcription Factor 3 (ATF3) is a stress-adaptive transcription factor, which has been suggested to be involved in maintaining glucose homeostasis. ATF3 respond rapidly to various stimuli like high glucose, fatty acids and oxidative stress, and is observed to either protective or detrimental effects in diabetic condition. Therefore to elucidate the exact role in diabetic nephropathy of ATF3, we investigated the role of ATF3 by inhibition with Raf-inhibitor GW5047 on diabetic mice model. Method ATF3 level was examined in the mouse podocytes and NRK cells with either overexpression or downregulation with ATF3. 8 week db/m and db/db mice as the model of diabetic mice were examined for the expression of ATF3 and were treated with GW5074, a Raf1 kinase inhibitor targeting the ATF3 intraperitoneally with a dose of 0.5mg/kg for 12 weeks. Results In cultured mouse podocytes and NRK cells, high glucose and angiotensin II markedly increased ATF3 expression. Gene Expressions of NOX4, MCP-1 and NF-kB were augmented by ATF3, and were attenuated by ATF3 siRNA. In db/db mice, plasma ATF3 level was not different from control db/m, however the urinary ATF3 excretion was significantly higher. Treatment of GW5074 decreased urinary ATF3 excretion. After 12 week treatment, serum creatinine level was significantly lower in the treatment db/db group, with less systemic oxidative stress. There were no significant differences in body weight, whereas the food intake was decreased in GW5047 group. Overall lipid profile or HOMA-IR, HbA1c level was not different from each group. Serum adiponectin were otherwise increased in GW5074 group. Urinary excretion of albumin at 2 month of treatment decreased with urinary nephrin excretion. Trend of increased gene expression of JNK, p-38, smad2, ERK which was downregulated by GW5074 was noted. Conclusion These findings suggest that in diabetic condition, the activation of ATF3 is associated pathogenesis of diabetic nephropathy and targeting ATF3 may have a protective role in the disease progression.


2019 ◽  
Vol 10 ◽  
Author(s):  
Babak Arjmand ◽  
Parisa Goodarzi ◽  
Hamid Reza Aghayan ◽  
Moloud Payab ◽  
Fakher Rahim ◽  
...  

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