Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats

xlomafota13 shared this article with you from Inoreader Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):35. doi: 10.3892/etm.2021.10957. Epub 2021 Nov 9. ABSTRACT C1q/TNF-related protein-3 (CTRP3) is a novel adipokine that serves an important role in oxidative stress, anti-apoptosis, anti-inflammation and immune regulation. The aim of the present study was to investigate the protective role of CTRP3 against intracerebral hemorrhage (ICH)-induced brain injury. A model of autologous arterial blood-induced ICH was constructed in rats. Intracerebral infusion of a lentivirus carrying the CTRP3 gene was used to induce CTRP3 overexpression in the brain. The effects and mechanisms of CTRP3 overexpression on brain injury were investigated by detecting brain edema, blood-brain barrier (BBB) integrity, neurological function and inflammatory-associated factors 3 days after ICH. The present results demonstrated that CTRP3 overexpression ameliorated ICH-induced neurological dysfunction, decreased brain edema, maintained BB B integrity and attenuated inflammation. The protective effect of CTRP3 overexpression was associated with increased activation of silent information regulator 1 (SIRT1). In conclusion, the present study demonstrated that CTRP3 overexpression protected against ICH-induced brain injury in rats, potentially via activating the SIRT1 signaling pathway. PMID:34849150 | PMC:PMC8613529 | DOI:10.3892/etm.2021.10957 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.