Cinnamaldehyde mitigates spinal cord injury in rats through anti-inflammatory and anti-apoptotic pathways.

Abstract

BACKGROUND: Spinal cord injury (SCI) is a destructive neuropathological condition. Cinnamaldehyde (CA), a major bioactive component in Cinnamon essential oil, is known for its neuroprotective effects by inhibiting neuroinflammation, oxidative stress, and apoptosis. However, CA specific role in SCI remains unclear. The purpose of this study was to examine the impact of CA on SCI. METHODS: We established a rat model of SCI and assessed nerve damage in rats using the Basso-Beattie-Bresnahan (BBB) locomotion scale, inclined plane test and Tarlov Scale. Neuronal loss was evaluated with Nissl and NeuN staining. Apoptotic damage was assessed using TUNEL staining and caspase3 analysis. The level of M1-type microglia activation was explored using Iba1. Additionally, TNF-α and IL-Iβ concentrations were measured to examine inflammation. Poly (ADP-ribose) polymerase (PARP) and proliferating cell nuclear antigen (PCNA) were used to assess DNA damage. RESULTS: The results demonstrated that CA effectively improves behavioral scores measured by the BBB assay, inclined plane test, and Tarlov trial after SCI. NeuN and Nissl staining showed that CA significantly increases the number of NeuN-stained neurons and Nissl bodies. Apoptosis detection revealed that CA markedly reduces caspase3 production and the number of TUNEL-positive cells. Moreover, CA not only reduced Iba1 levels but also significantly decreased the production of TNF-α and IL-Iβ. Additionally, CA notably decreased PARP levels and promoted PCNA expression. CONCLUSIONS: CA regulates pathways involved in anti-neuroinflammation, anti-apoptosis, and DNA repair to improve neurological deficits and pathological conditions after SCI. CA therapeutic effect of CA may depend on the dosage.