Expression of hyperphosphorylated Tau protein in retrograde degeneration of neurons

Objective To explore the expression of hyperphosphorylated Tau protein in the retrograde degeneration of spinal central neurons after cervical 7 nerve transection, so as to provide a new idea for the protection of retrograde degeneration of central neurons after peripheral nerve injury. Methods Thirty-six adult female Sprague-Dawley rats were randomly divided into three groups (sham operation group, transection group, transection+drug intervention group). The rats in transection group and transection+drug intervention group were treated with bilateral cervical 7 nerve cutting to make models, and the rats in transection+drug intervention group were treated with 1 mmol/kg lithium chloride intraperitoneally every day. After 2 and 4 weeks, the spinal cords of cervical 7 of the rats were taken, and the apoptosis of neurons was analyzed by HE staining and flow cytometry. The expression of Tau protein and related protein was analyzed by Western blot. Results HE staining and flow cytometry showed that the apoptotic degree of the transection group at 2 weeks was less than that at 4 weeks. The resutls of Western blot showed that as time went on, the amount of total Tau protein decreased due to the transection of cervical 7 nerve, and the proportion of phosphorylated Tau protein increased. The difference was statistically significant. After lithium chloride administration, the degree of apoptosis and the proportion of phosphorylated Tau protein decreased significantly. Conclusion The mechanism of Tau protein hyperphosphorylation lies in the process of retrograde degeneration of spinal cord central neurons after cervical 7 transection, and lithium chloride can reduce the degree of retrograde degeneration. Key words: Tau proteins; Brachial plexus; Neuron retrograde degeneration; Hyperphosphorylation