Abstract
Chrysin (CH), a natural plant flavonoid, has shown a variety of beneficial effects. Our present study was conducted to evaluate the therapeutic potential of CH three days after spinal cord injury (SCI) in rats and to probe the underlying neuroprotective mechanisms. SCI was induced using the modified weight-drop method in Wistar rats. Then, they were treated with saline or CH by doses of 30 and 100 mg/kg for 26 days. Neuronal function was assessed with the Basso Beattle Bresnahan locomotor rating scale (BBB). The water content of spinal cord was determined after traumatic SCI. The NF-κB p65 unit, TNF-α, IL-1β and IL-6 in serums, as well as the apoptotic marker, caspase-3, of spinal cord tissues were measured using commercial kits. The protein level and activity of inducible nitric oxide synthase (iNOS) were detected by western blot and a commercial kit, respectively. NO (nitric oxide) production was evaluated by the determination of nitrite concentration. The rats with SCI showed marked reductions in BBB scores, coupled with increases in the water content of spinal cord, the NF-κB p65 unit, TNF-α, IL-1β, IL-6, iNOS, NO production and caspase-3. However, a CH supplement dramatically promoted the recovery of neuronal function and suppressed the inflammatory factors, as well as the iNOS pathway in rats with SCI. Our findings disclose that CH improved neural function after SCI in rats, which might be linked with suppressing inflammation and the iNOS pathway.
Highlights
It is well established that spinal cord injury (SCI) serves as a devastating health problem that affects thousands of individuals [1] each year and causes primary and secondary injuries [2]
Our findings disclose that CH improved neural function after SCI in rats, which might be linked with suppressing inflammation and the inducible nitric oxide synthase (iNOS) pathway
The rats induced by SCI exhibited a severe impairment with remarkable reductions of the Basso Beattle Bresnahan locomotor rating scale (BBB) scores (p < 0.01) at the selected time points
Summary
It is well established that spinal cord injury (SCI) serves as a devastating health problem that affects thousands of individuals [1] each year and causes primary and secondary injuries [2]. The delayed secondary impairment is made up of multiple pathophysiological processes, including ischemia, edema, hemorrhage, inflammatory responses, energy metabolism system disorder, excitotoxicity and oxidative damage [3], which generates reversible nerve injury. NO could cause marked inflammation in the regulation of immune responses [7]. Emerging evidence has illustrated that inflammation-induced iNOS is highly expressed, and this isoform produces great amounts of NO after traumatic SCI, causing cytotoxicity to spinal cord [8,9]. The present investigation aimed to evaluate the protection of CH and elucidate the roles of inflammation and the iNOS pathway in CH-mediated neuroprotection against traumatic SCI in rats
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