Abstract
Objective C1q/CTRP1 is a newly discovered adiponectin protein, which is highly expressed in adipose and heart tissues. Recent studies have revealed that C1q/CTRP1 can regulate metabolism and inhibit inflammation. CTRP1 is also expressed in brain tissues and vascular cells of human and rat, and research on cerebral hemorrhage and cerebral ischemia-reperfusion injury demonstrates that the CTRP family can attenuate secondary brain injury and exert neuroprotective effects. Thus, this study was designed to explore the role of CTRP1 in traumatic brain injury (TBI) and the underlying mechanism.
Main methods Rats were assigned into rCTRP1 group, vehicle group, and sham group. Modified Feeney’s method was used to establish a closed traumatic brain injury model. Morris water maze was used for directional navigation, reverse searching and space exploration tests in rats. In addition, Golgi-Cox staining was utilized to visualize neurons, dendrites and dendritic spines. ELISA was conducted to detect the levels of inflammatory factors (IL-6 and TNF-α). Finally, Western blot was adopted to detect the relative expression of p-mTOR and autophagy-related proteins (Beclin-1 and LC3-II).
Results CTRP1 improved the behavioral and histopathological outcomes, inhibited the inflammatory response, activated mTOR and decreased autophagy-associated protein synthesis in TBI rats.
Conclusion CTRP1 exerts neuroprotective effects in TBI rats by regulating inflammation and autophagy and has potential therapeutic properties after TBI.
