3-Iodothyronamine Acting through an Anti-Apoptotic Mechanism Is Neuroprotective Against Spinal Cord Injury in Rats.

This study aims to show how 3-iodothyronamine (T1AM) protects against spinal cord injury (SCI) in rats. We randomly divided adult female Sprague-Dawley rats (N=54) into three equal groups: (1) untreated control (n=18) (2) T1AM (n=18) (3) T1AM+EPPTB (n=18). The clamp method was used to produce SCI at the T10 segment, and the following data were collected 3, 5, and 7 days after the injury plus treatment. The mean BBB scores of both the control and T1AM+ EPPTB groups were 1.5 +/- 0.5, 3.5 +/- 0.5, and 4.5 +/- 0.5 on days 3, 5, and 7 after SCI, respectively, whereas those for the T1AM group were 3.3 +/- 0.5, 5.3 +/- 0.5, and 7.5 +/- 0.5, a significant difference from the first two groups mentioned on each day (all P values <0.05). Although HE staining indicated that all three groups displayed neuronal degeneration and necrosis, disorganized spinal cord tissue structure, proliferation of glial cells, and spinal cord porosis, the damage was less in the T1AM group than in the other two groups. The number of apoptotic cells gradually increased in all three groups. However, while the mean numbers of apoptotic cells in the control (9.8%+/- 2.6%, 14.2%+/- 5.9%, 57.2%+/- 15.1%) and T1AM+ EPPTB groups (9.1%+/- 3.0%, 13.4%+/- 6.3%, 57.4%+/- 11.1%) on days 3, 5, and 7, respectively, were not significantly different from each other, those in the T1AM group (2.3%+/- 1.4%, 7.6%+/- 1.8%, 36.1%+/- 9.9%) were significantly lower than those in both the other groups at each time point (all P values <0.05). Thus, T1AM is involved in the apoptosis pathway through stimulation of TAAR1. The T1AM-TAAR1 interaction decreased spinal cord neuron apoptosis, reduced secondary SCI, and promoted hind limb motor function recovery in rats with SCI.