Triad1 Promotes the Inflammatory Response and Neuronal Apoptosis to Aggravate Acute Spinal Cord Injury in Rats.

Abstract

Objective Spinal cord injury (SCI) is one of the most devastating central injuries, resulting in serious locomotor deficits. Triad1 is known to play an important role in SCI, but its effects on the inflammatory response and physiological behavior have not been thoroughly studied. This study is aimed at examining the effects of Triad1 on the inflammatory response and neuronal injury in acute SCI in rats. Methods Twenty-four male Sprague–Dawley (SD) rats were randomly divided into a control group, SCI group, sh-NC group, and Triad1 knockout group (sh-Triad1). The Basso Beattie Bresnahan locomotor rating scale was utilized for the assessment of the motor ability of rats. Hematoxylin and eosin (H&E), Luxol fast blue (LFB), and TUNEL staining were used to assess the pathological injury, demyelination, and neuronal apoptosis, respectively. ELISA was used to detect the levels of IL-1β, IL-10, and TNF-α, and qRT-PCR was used to examine the expression level of Triad1. Furthermore, the protein levels of Triad1, Bax, Bcl-2, and cleaved caspase-3 were determined using western blotting. Results The Triad1 expression level was upregulated in damaged spinal cord tissue. Knockdown of Triad1 improved motor function and reduced SCI as well as apoptosis of spinal cord neurons. In addition, the knockdown of Triad1 inhibited the inflammatory response caused by SCI. Conclusion Knockdown of Triad1 can reduce SCI in rats with acute SCI by inhibiting the inflammatory response and apoptosis.