Asiaticoside Inhibits Neuronal Apoptosis and Promotes Functional Recovery After Spinal Cord Injury in Rats

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Asiaticoside Inhibits Neuronal Apoptosis and Promotes Functional Recovery After Spinal Cord Injury in Rats Lei Fan 1,2 & Xiaobin Li 1,2 & Tao Liu 1,2 Received: 9 July 2019 / Accepted: 10 October 2019 # Springer Science+Business Media, LLC, part of Springer Nature 2020

Abstract Spinal cord injury is a critical traumatic injury. This study aimed to investigate the possible protective effects of asiaticoside on neuronal injury in a rat model of spinal cord injury and to clarify the possible molecular mechanisms underlying these protective effects. Rats were randomly divided into the following four groups: naïve, sham, spinal cord injury (moderate mechanical compression injury model), and spinal cord injury + asiaticoside. Time to spontaneous urination after spinal cord injury was measured. The Basso–Beattie–Bresnahan scoring method, inclined plate grasp experiments, and footprint experiments were used to evaluate motor function. Neuritin and TNF-α levels in the spinal cord were detected via ELISA, and caspase-3 level was detected via Western blotting. Spinal cord morphology was assessed via hematoxylin–eosin staining. Apoptosis in the spinal cord was assessed using Fluoro–Jade B staining. Recovery times for spontaneous urination and motor function were shorter in the spinal cord injury + asiaticoside group than in the spinal cord injury group. The neuritin level was increased and TNF-α and caspase-3 levels were decreased in the spinal cord injury + asiaticoside group. Morphological integrity of neurons was better in the spinal cord injury + asiaticoside group than in the spinal cord injury group. It can thus be said that asiaticoside decreased apoptosis of spinal cord neurons. Asiaticoside exerts protective effects against spinal cord injury in rats, possibly by inhibiting the apoptosis of neurons and anti-inflammatory mechanisms. Keywords Spinal cord injury . Asiaticoside . TNF-α . Neuritin . Caspase-3 . Apoptosis . Anti-inflammatory . In vivo . Morphological integrity . Protective effect

Introduction Spinal cord injury (SCI) is a common cause of neurological dysfunction and disability, and its incidence has dramatically increased to approximately 15–40 cases/ million people worldwide. In the modern society, acute SCI is a critical traumatic injury owing to its poor prognosis with motor, sensory, and sphincter dysfunction; dystonia; and pathological reflex changes (Capogrosso et al. 2016; Harkema et al. 2011; Jiang et al. 2018). Despite the tremendous progress in surgical and medical

* Tao Liu [email protected] 1

Department of Orthopedic Surgery, Henan Provincial People’s Hospital, Zhengzhou 450003, Henan, China

2

Department of Orthopedic Surgery, People’s Hospital of Zhengzhou University, Zhengzhou 450003, Henan, China

methods, there are still no effective treatment modalities for neurological deficits after SCI (Kiehn 2016). Several noxious factors involved in SCI interact via multiple pathways at the molecular level, and induction of apoptosis increases damage, eventually developing into irreversible inju