Histone deacetylase 6 interference protects mice against experimental stroke-induced brain injury via activating Nrf2/HO-1 pathway. Issue 3 (4th May 2019)

• Record Type: Journal Article
• Authors: Li, Jie; Zhao, Yanping; Shi, Junfeng; Ren, Zhanyun; Chen, Feng; Tang, Wuzhuang
• Is Part Of: Animal cells and systems. Volume 23:Issue 3(2019)
• Page Start: 192
• Page End: 199
• Publication Date: 2019-05-04
• Subjects: Histone deacetylase 6 -- Nrf2/HO-1 -- cerebral ischemia/reperfusion injury -- oxidative stress; Systems biology -- Periodicals; Biology -- Periodicals; Cytology -- Periodicals; Zoology -- Periodicals; 590
• DOI: 10.1080/19768354.2019.1601132
• Languages: English
• ISSNs: 1976-8354

Abstract

ABSTRACT: Cerebral stroke is a fatal disease with increasing incidence. The study was to investigate the role and mechanism of Histone deacetylase 6 (HDAC6) on experimental stroke-induced brain injury. The recombinant shRNA-HDAC6 or scramble shRNA lentivirus was transfected to ICR mice. Then, the ischemia/reperfusion injury (I/RI) mice were constructed using middle cerebral artery occlusion (MCAO) method. Brain TTC staining was used to determine infarct areas. Serum levels of oxidative stress-related factors were detected by enzyme linked immunosorbnent assay (ELISA). Realtime-qPCR (RT-qPCR) and Western blot were used to respectively detect mRNA and protein levels. HDAC6 was up-regulated in brain I/RI mice (MCAO group), and down-regulated again in MCAO mice transfected with shRNA-HDAC6 (MCAO + shRNA group). The infarct area of the MCAO mice was increased, neurological scores were higher, and serum protein levels of 3-NT, 4-HNE and 8-OHdG were higher. HDAC6 interference attenuated above effects. Though protein levels of Nrf2 and HO-1 in cytoplasm increased slightly in MCAO group, they increased significantly by HDAC6 interference. The protein levels of Nrf2 in cytoblast decreased significantly in MCAO group, and increased markedly by HDAC6 interference. HDAC6 interference protected mice against experimental stroke-induced brain injury via Nrf2/HO-1 pathway.