Emodin Reduces Neuroinflammation in Rats with Acute Severe Craniocerebral Injury

Background: Acute severe craniocerebral injury (ASBI) is a leading cause of morbidity and mortality following trauma. Emodin has demonstrated a range of pharmacological effects, including anti-inflammatory and antioxidant properties. This study sought to investigate the effect of emodin on ASBI in rats and to elucidate its potential mechanisms. Methods: Thirty sprague-dawley (SD) rats were randomly assigned into five subgroups: the sham subgroup, the model subgroup, the low-dose emodin subgroup, the middle-dose subgroup, and the high-dose subgroup. Initially, we recorded the grip traction time and neurobehavioral scoring in each subgroup. Moreover, pathological injury in brain tissue was observed using hematoxylin-eosin (H&E) staining. Immunohistochemical staining was utilized to evaluate the levels of positive glial fibrillary acidic protein (GFAP) and ionized calcium-binding adapter molecule 1 (Iba1). Furthermore, the levels of cytokines were assessed using biochemical assays. The levels of reactive oxygen species (ROS) in the brain tissue were determined using a 2 ',7 '-dichlorodihydrofluorescein diacetate (DCFH-DA) probe. Additionally, the mRNA levels of inducible nitric oxide synthase (iNOS) and p38 mitogen-activated protein kinase (p38 MAPK) were evaluated employing quantitative real-time polymerase chain reaction (qRT-PCR). Heat shock proteins 70 (HSP70), B cell lymphoma-2 (Bcl-2), Bcl-2 associated X-protein (Bax), NOD-like receptor (NLR) family pyrin domain-containing protein 3 (NLRP3), caspase-1, iNOS, phosphorylated-p38 MAPK (p-p38 MAPK), p38 MAPK levels in the brain tissue were examined utilizing Western blot analysis. Results: Emodin treatment significantly improved the neurobehavioral and pathological damage of brain tissue in ASBI rats. HSP70, Bcl-2, glutathione (GSH), and superoxide dismutase (SOD) levels were substantially elevated in the brain tissue of the emodin subgroup. Conversely, emodin treatment reduced the levels of Bax, NLRP3, caspase-1, malondialdehyde (MDA), nitric oxide (NO), and ROS. Furthermore, serum levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, interferon-gamma (IFN-gamma), and IL-6 were significantly reduced in the emodin subgroup compared to the model subgroup (p < 0.05). Additionally, iNOS mRNA and protein levels were reduced in the brain tissue of the emodin subgroup compared to the model subgroup (p < 0.05). Similarly, the p-p38 MAPK protein concentrations were also alleviated in the brain tissue of the emodin subgroup compared to the model subgroup (p < 0.05). Conclusion: Emodin enhances motor function recovery, mitigates apoptosis and neuroinflammation, and reduces oxidative stress in ASBI rats, potentially through the p38 MAPK signaling pathway.