Abstract

 
 
 
 Purpose: To investigate the protective effect of Crataegus songarica extract (CSCE) against traumatic brain injury (TBI) in rats, and the underlying mechanism of action.
 Methods: A rat model of TBI was established via tracheal intubation procedure, and the rats were treated with graded doses of CSCE. Neuronal survival was determined by Nissl staining, while neuronal apoptosis was measured using TUNEL-staining. Neurological impairments were determined based on neurological severity score (NSS).
 Results: Treatment of TBI rats with CSCE enhanced neuronal survival and decreased TUNEL-positive cell fraction in the brain cortex. The treatment prevented elevation of NSS and suppressed mRNA and protein expression levels of IL-6 and TNF-α in brain cortex. Moreover, CSCE treatment prevented TBI-mediated suppression of activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx), and attenuated hydrogen peroxide (H2O2) levels in TBI rat brain cortex. Treatment of TBI rats with CSCE down-regulated NF-κB expression, increased Nrf2 expression and up-regulated mRNA expressions of heme oxygenase 1 (HO-1) and quinine oxidoreductase 1 (NQO-1).
 Conclusion: These results suggest that CSCE prevents TBI-mediated reduction in neuronal survival and inhibits brain cortical neuronal death in rats. It improves NSS and inhibits inflammatory response via activation of Nrf2 pathway and targeting of NF-κB expression. Therefore, CSCE is a potential therapeutic agent for TBI.
 
 
 
Highlights
Traumatic brain injury (TBI) results from a blow to the head or piercing of brain tissue with a sharp-edged object, leading to impaired brain function [1,2]
Primary injury refers to immediate damage following TBI, while secondary injury comprises long-term injuries associated with oxidative stress, inflammatory reactions and neuronal apoptosis [2]
Treatment of TBI rats with Crataegus songarica extract (CSCE) led to dose-dependent increases in neuronal survival, as was evident in significantly higher count of Nissl- positive stained cells
Summary
Traumatic brain injury (TBI) results from a blow to the head or piercing of brain tissue with a sharp-edged object, leading to impaired brain function [1,2]. Primary injury refers to immediate damage following TBI, while secondary injury comprises long-term injuries associated with oxidative stress, inflammatory reactions and neuronal apoptosis [2]. Knockdown of Nrf at the genetic level has been found to promote severity of injury in mice with TBI via oxidative stress mechanism [9]. The rat brain tissues were excised fixed in 4 % paraformaldehyde at 4 ̊C for 24 h, followed by paraffin embedding. Presence of apoptotic cells in the brain cortex of rats was determined using an in situ cellular death detection kit (Catalog number: 1168481710; Roche Diagnostics). The brain cortical tissues of rats were homogenized and centrifuged for 20 min at 12,000 g. The brain cortical tissues of rats were lysed using RIPA buffer, followed by protein extraction using protein extraction kit (Beyotime). Differences were taken as statistically significant at p < 0.05
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