Call for Papers  

Article Details


Procyanidin B2 Protects TR-iBRB2 Cells Against Hyperglyc emia Stress by Attenuating Oxidative Stress and Inflammasome Activation <i>via</i> Regulation of Redoxosomes/NF-kB Signaling

[ Vol. 23 , Issue. 10 ]

Author(s):

Wenjun Zou, Qianyi Lu, Xue Zhu, Ying Pan, Quan Xu* and Ke Wang*   Pages 1095 - 1103 ( 9 )

Abstract:


<p>Background: Microvascular dysfunction is a hallmark of diabetic retinopathy (DR), which may lead to visual impairment and blindness. Procyanidin B2 (PB2) is a subclass of flavonoids and is widely known due to its anti-oxidant and antiinflammatory effects. However, little is known about the effect of PB2 on hyperglycemia stress-induced retinal microvascular dysfunction. <p> Objective: The purpose of this study was to investigate the effect of PB2 against hyperglycemia stress in rat retinal capillary endothelial cells (TR-iBRB2) as well as the underpinning mechanism. <p> Methods: Cell viability was determined using MTT assay. ROS, NOX activity analysis, Western blot analysis, and immunofluorescence analysis were applied in the study. <p> Results: The results showed that PB2 pre-treatment significantly reduced high glucose- induced cytotoxicity in TR-iBRB2 cells by suppressing oxidative stress and inflammasome activation. Mechanistical study revealed that redoxosomes were formed and activated in TR-iBRB2 cells upon hyperglycemia stress, resulting in activation of NF- κB and thus induction of oxidative stress and inflammasomes activation. However, PB2 pre-treatment dose-dependently attenuated the above events, indicating the protective effect of PB2 against hyperglycemia stress was achieved by regulating redoxosomes/ NF-kB signaling. <p> Conclusion: Our findings may contribute to the potential clinical use of PB2 in treating DR and suggest redoxosomes/NF-kB signaling may be a potential therapeutic target of this disease.</p>

Keywords:

Diabetic retinopathy, microvascular dysfunction, procyanidin B2, redoxosomes/NF-kB signaling, procyanidin B2 (PB2), diabetes mellitus (DM).

Affiliation:



Read Full-Text article