Abstract
Introduction: Spinal cord injury (SCI) involves a primary trauma and secondary cellular processes that can lead to severe damage to the nervous system, resulting in long-term spinal deficits. At the cellular level, SCI causes astrogliosis, of which glial fibrillary acidic protein (GFAP) is a major index.Objective: The aim of this study was to investigate the neuroprotective effects of Lavandula angustifolia (Lav) on the repair of spinal cord injuries in Wistar rats.Materials and Methods: Forty-five female rats were randomly divided into six groups of seven rats each: the intact, sham, control (SCI), Lav 100, Lav 200, and Lav 400 groups. Every week after SCI onset, all animals were evaluated for behavior outcomes by the Basso, Beattie, and Bresnahan (BBB) score. H&E staining was performed to examine the lesions post-injury. GFAP expression was assessed for astrogliosis. Somatosensory evoked potential (SEP) testing was performed to detect the recovery of neural conduction.Results: BBB scores were significantly increased and delayed responses on sensory tests were significantly decreased in the Lav 200 and Lav 400 groups compared to the control group. The greatest decrease of GFAP was evident in the Lav 200 and Lav 400 groups. EMG results showed significant improvement in the hindlimbs in the Lav 200 and Lav 400 groups compared to the control group. Cavity areas significantly decreased and the number of ventral motor neurons significantly increased in the Lav 200 and Lav 400 groups.Conclusion: Lav at doses of 200 and 400 mg/kg can promote structural and functional recovery after SCI. The neuroprotective effects of L. angustifolia can lead to improvement in the contusive model of SCI in Wistar rats.
Highlights
Spinal cord injury (SCI) involves a primary trauma and secondary cellular processes that can lead to severe damage to the nervous system, resulting in long-term spinal deficits
The pathogenesis of spinal cord injuries (SCI) after the primary trauma plays an important role in initial tissue disruption, and the subsequent initiation of a series of secondary cellular processes beyond the injury site can lead to long-term spinal deficits and disabilities (Beattie et al, 2002; Dumont et al, 2002)
Astrogliosis is a cellular response that creates a barrier to axonal regeneration, and the major index of astrogliosis is marked upregulation of glial fibrillary acidic protein (GFAP; Bharne et al, 2013)
Summary
Spinal cord injury (SCI) involves a primary trauma and secondary cellular processes that can lead to severe damage to the nervous system, resulting in long-term spinal deficits. SCI causes astrogliosis, of which glial fibrillary acidic protein (GFAP) is a major index. The pathogenesis of SCI after the primary trauma plays an important role in initial tissue disruption, and the subsequent initiation of a series of secondary cellular processes beyond the injury site can lead to long-term spinal deficits and disabilities (Beattie et al, 2002; Dumont et al, 2002). Astrogliosis is a cellular response that creates a barrier to axonal regeneration, and the major index of astrogliosis is marked upregulation of glial fibrillary acidic protein (GFAP; Bharne et al, 2013). SCI results in increased tissue oxidative stress and production of reactive oxygen species (ROS; Azbill et al, 1997), and antioxidant protection after SCI has improved outcomes in experimental animals (Kamencic et al, 2001)
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