RGFP966 exerts neuroprotective effect via HDAC3/Nrf2 pathway after surgical brain injury in rats

• DOI: 10.1016/j.heliyon.2023.e18160
• Publication Date: 2023-07-12T01:30:00Z
• Authors: Hai-Ping Gu; Xiao-Feng Wu; Ya-Ting Gong; Mu-Yao Wu; Meng-Ying Shi; Ya-ming Sun; Bao-Qi Dang; Gang Chen
• Keywords: Social sciences (General); H1-99; Q1-390; Science (General); HDAC3/Nrf2 signal pathway; Oxidative stress; HDAC3; RGFP966; Surgical brain injury; Research Article

BackgroundHistone deacetylase 3 (HDAC3) restores chromatin nucleosomes to a transcriptional repression state, thereby inhibiting gene expression. Studies have found that HDAC3 expression is upregulated in variety of pathological states the central nervous system and related its neurotoxicity. However, role surgical brain injury (SBI) has not been thoroughly explored. Objective: To observe SBI outcome after suppression. Methods: Rat model was used, intraperitoneal injection RGFP966 (HDAC3 specific inhibitor) used detect changes neuronal apoptosis indexes surrounding cortex rats, cerebral edema neurological rats were observed. Results: The peripheral increased, inhibited upregulation saved nerve cells around damaged area. In addition, increased anti-oxidative stress proteins such as heme oxygenase-1 (HO-1) superoxide dismutase 2 (SOD2). At same time, apoptotic marker protein cleaved-caspase-3 (cle-caspase-3) decreased, while level protective B-cell lymphoma (Bcl-2) increased. this research demonstrated rat model, antioxidant modifier nuclear factor-erythroid 2-related factor (Nrf2) Conclusion: might activate HDAC3/Nrf2 signaling pathway by HDAC3, regulated oxidative cell induced reduced edema, had effect on injury. It be potential target pathology.