Alantolactone plays neuroprotective roles in traumatic brain injury in rats via anti-inflammatory, anti-oxidative and anti-apoptosis pathways.

Traumatic brain injury (TBI) is a common disease associated with a high rate of morbidity and mortality. Secondary brain injury following TBI triggers pathological, physiological, and biological reactions that lead to neurological dysfunctions. Alantolactone (ATL) is a well-known Chinese medicine that possesses strong anti-inflammatory properties, but its role in TBI remains poorly understood. The objective of this study was to evaluate the protective effect of ATL in a rat model of controlled cortical impact (CCI). We observed the neurological scores, brain water content, oxidative stress, neuroinflammation and apoptosis by performing an enzyme-linked immunosorbent assay, western blotting, quantitative real-time reverse transcription polymerase chain reaction (RT-qPCR), immunohistochemical (IHC) staining and other methods after CCI. The neurological scores, brain water content, levels of oxidative stress and inflammatory cytokines, and apoptosis index were markedly decreased following the ATL treatment in rats after TBI. Moreover, the antioxidant and anti-inflammatory effects of ATL in TBI may be partially mediated by inhibition of the NF-κB pathway and suppression of Cyclooxygenase 2 (COX-2). In addition, ATL attenuated TBI-induced neuronal apoptosis by suppressing the cytochrome c/caspase-dependent apoptotic pathway. Thus, ATL could exert neuroprotection in rats in a TBI model. Importantly, ATL has great potential in the clinical treatment of TBI.
Competing Interests: None.