Rabbit Anti-Human RNF6 (a.a. 580-685) Polyclonal antibody

Background Traumatic brain injury (TBI) has ranked as one of the leading causes of disability and death in the world. The neuroinflammation mediated by signal transducer and activator of transcription 3 (STAT3) signaling during the progression of TBI leads to long-term neurodegeneration. Ring finger protein 6 (RNF-6) is an E3 ubiquitin ligase and can regulate the activity of STAT3 signaling pathway by targeting its inhibitors. However, the mechanism underlying this process in TBI remains poorly understood. Methods In this research, cortical impact injury was used to construct the TBI rat model. Western blot assay was performed to evaluate the protein levels of RNF6, Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1), and STAT3/pSTAT3. QRT-PCR assay was performed to assess the RNA levels of RNF6 and other cytokines. The neural function of TBI rats was estimated by modified Neurological Severity Scores test. Results The expression of RNF-6 was up-regulated in the brain tissues of TBI rats. Down-regulation of RNF6 alleviated the symptoms and improved the neural recovery postinjury in TBI rats. Inhibition of RNF6 suppressed the cerebral inflammation by up-regulating the protein level of SHP-1 and down-regulating the phosphorylation level of STAT3. Conclusion Inhibition of RNF6 alleviated TBI by suppressing the STAT3 signaling in TBI rats.