Pterostilbene Attenuates Cocultured BV-2 Microglial Inflammation-Mediated SH-SY5Y Neuronal Oxidative Injury via SIRT-1 Signalling

• Published in: Oxidative medicine and cellular longevity Vol. 2020; no. 2020; pp. 1 - 11
• Main Authors: Chen, Zhao, Lei, Qiang, Song, Mingyang, Wang, Bodong, Lei, Zhijie, Yang, Long, Liu, Qiang, Wang, Xiaogang, Sun, Yinxue, Liu, Haixiao, Tang, Tao, Zhu, Qiang, Huang, Zhao
• Format: Journal Article
• Language: English
• Published: Cairo, Egypt Hindawi Publishing Corporation 2020; Hindawi; John Wiley & Sons, Inc; Hindawi Limited
• Subjects: Antibodies; Apoptosis; Cell culture; Homeostasis; Inflammation; Ischemia; Metabolism; Mitogens; Nervous system diseases; Neurodegeneration; Neurological disorders; Neurons; Oxidative stress; Stroke; Stroke (Disease); Trauma; Tumor necrosis factor-TNF; China; United States > US
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2020/3986348

Microglial inflammation plays an important part in the progression of multiple neurological diseases, including neurodegenerative diseases, stroke, depression, and traumatic encephalopathy. Here, we aimed to explore the role of pterostilbene (PTE) in the microglial inflammatory response and subsequent damage of cocultured neural cells and partially explain the underlying mechanisms. In the coculture system of lipopolysaccharide-activated BV-2 microglia and SH-SY5Y neuroblastoma, PTE (only given to BV-2) exhibited protection on SH-SY5Y cells, evidenced by improved SH-SY5Y morphology and viability and LDH release. It also attenuated SH-SY5Y apoptosis and oxidative stress, evidenced by TUNEL and DCFH-DA staining, as well as MDA, SOD, and GSH levels. Moreover, PTE upregulated SIRT-1 expression and suppressed acetylation of NF-κB p65 subunit in BV-2 microglia, thus decreasing the inflammatory factors, including TNF-α and IL-6. Furthermore, the effects above were reversed by SIRT-1 inhibitor EX527. These results suggest that PTE reduces the microglia-mediated inflammatory response and alleviates subsequent neuronal apoptosis and oxidative injury via increasing SIRT-1 expression and inhibiting the NF-κB signalling pathway.