The protective effects of lycium barbarum polysaccharides on retinal neurons in diabetic rats and its mechanism.
10.12047/j.cjap.5749.2019.014
- Author:
Hong PAN
1
;
Zhen SHI
1
;
Tai-Guo YANG
2
;
La-Mei YU
1
;
Ai-Li XU
1
Author Information
1. Department of Physiology, Binzhou Medical College, Yantai 264003.
2. The People's Hospital of Pingyi County, Pingyi 273300, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Diabetes Mellitus, Experimental;
Drugs, Chinese Herbal;
pharmacology;
Heme Oxygenase (Decyclizing);
drug effects;
NF-E2-Related Factor 2;
drug effects;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Retina;
drug effects
- From:
Chinese Journal of Applied Physiology
2019;35(1):55-59
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To clarify whether lycium barbarum polysaccharides (LBP) have protective effects on retina neuronal cells in diabetic rats and to identify the related mechanism involved in this process.
METHODS:Eighteen SD rats were randomly divided into 3 groups ( n= 6): normal control group (NC), diabetes mellitus group (DM) and LBP-treatment group (DM+LBP). The diabetic rat model was induced by single intraperitoneal injection of streptozotocin (STZ). The rats in DM+LBP group were treated with LBP at the dose of 1 mg/kg by gavage, once a day for 12 weeks. After the treatment, the weight and blood glucose, the generation of reactive oxygen species (ROS), the surviving retinal ganglion cells (RGCs) and amacrine cells and the protein expressions of nuclear factor E2-related factor 2 (Nrf2) and the heme oxygenase-1 (HO-1) were detected.
RESULTS:The successful rate of diabetic model was 100%. Compared with NC group, the rats of DM group caused weight loss, elevated blood glucose, a marked increase of ROS generation and a significant decrease in the number of RGCs and amacrine cells (P＜0.01), and these effects were diminished or abolished by LBP treatment. Meanwhile, LBP significantly increased the expressions of Nrf2 and HO-1 in the retinas of diabetic rats (P＜0.01).
CONCLUSION:LBP can improve retinal oxidative stress and exert beneficial neuroprotective effects in diabetic rats, and its mechanism may be associated with the activation of the Nrf2/HO-1 antioxidant pathway.
