Pterostilbene inhibits inflammation and ROS production in chondrocytes by activating Nrf2 pathway

Xue, EX; Lin, JP; Zhang, Y; Sheng, SR; Liu, HX; Zhou, YL; Xu, H

HERO ID

10703059

Reference Type

Journal Article

Year

2017

Language

English

PMID

28410217

HERO ID 10703059
In Press No
Year 2017
Title Pterostilbene inhibits inflammation and ROS production in chondrocytes by activating Nrf2 pathway
Authors Xue, EX; Lin, JP; Zhang, Y; Sheng, SR; Liu, HX; Zhou, YL; Xu, H
Journal Oncotarget
Volume 8
Issue 26
Page Numbers 41988-42000
Abstract Pterostilbene has been reported as a potential drug to inhibit oxidative stress and inflammation. However, the effect of pterostilbene on chondrocytes and osteoarthritis remains to be elucidated. We sought to investigate whether pterostilbene could protect chondrocytes from inflammation and ROS production through factor erythroid 2-related factor 2 (Nrf2) activation. The pterostilbene toxicity on chondrocytes collected from cartilages of Sprague-Dawley rats was assessed by CCK-8 test. Immunofluorescence and Western blotting explored the nuclear translocation of Nrf2. Nrf2 expression was silenced by siRNA to evaluate the involvement of Nrf2 in the effect of pterostilbene on chondrocytes. Finally, osteoarthritis model was established by the transection of anterior cruciate ligament and partial medial meniscectomy in rats, and then these rats received pterostilbene 30 mg/kg, daily, p.o. for 8 weeks. Histology and immunohistochemistry were used to assess histopathological change and Nrf2 expression in cartilage. Nuclear translocation of Nrf2 was stimulated by pterostilbene without cellular toxicity. Pterostilbene inhibited the level of COX-2, iNOS, PGE2, and NO, as well as the mitochondrial and total intracellular ROS production induced by IL-1β in chondrocytes, partially reversed by the Nrf2 silencing. Pterostilbene prevented cartilage degeneration and promoted the nuclear translocation of Nrf2 in cartilage. These results suggest that pterostilbene could inhibit the IL-1β-induced inflammation and ROS production in chondrocytes by stimulating the nuclear translocation of Nrf2.
Doi 10.18632/oncotarget.16716
Pmid 28410217
Wosid WOS:000405493400022
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English