Abstract
This study evaluated the effect of microglia transplantation on neurological functional recovery in rats subjected to traumatic spinal cord injury (SCI). The rat model of SCI was established using a weight drop device. Forty SCI rats were randomly divided into the microglia group and the saline group. Then, rat-derived microglial cells or normal saline was injected into the injured site 7 days after surgery. The Basso-Beattie-Bresnahan (BBB) score, inclined plate test, and motor-evoked potentials (MEPs) were applied to assess the recovery of motor function. Hematoxylin and eosin (H&E) staining was used to assess the therapeutic effect. Microglia transplantation significantly improved BBB scores and functional scores at 2, 3, 4, 6, and 8 weeks after surgery compared to saline injection (P<0.05). Meanwhile, a prolonged MEP latency and decreased MEP amplitude were observed at 4 and 8 weeks in the microglia group (P<0.05). Histological analysis showed less damage and better prognosis in SCI rats of the microglia group. BrdU+ cell tracing experiments showed that microglia were recruited to the injured area of the spinal cord at 7 and 14 days after transplantation. The intensity of immunofluorescence was increased in CD68+ and OX42+ microglia at 2 days, 1 week, and 2 weeks, and then decreased at 3 and 4 weeks after transplantation in the microglia group. The transplantation of activated microglia played a key role in promoting the recovery of spinal cord function in a rat model of SCI.
Highlights
Spinal cord injury (SCI) is a serious clinical problem
We aimed to explore the therapeutic potential of rat-derived microglia transplantation into a rat model of traumatic SCI
Rat microglial cells were isolated from the early postnatal specific pathogen-free (SPF) Wistar rat brain, and images of the 1st and 2nd generation of cultured cells are shown in Figure 1A (a,b)
Summary
Spinal cord injury (SCI) is a serious clinical problem. An injury to the spinal cord disrupts the conduction of motor and sensory information between the brain and body [1,2]. The pathophysiology of SCI involves primary and secondary mechanisms of injury. The primary injury is typically restricted to immediate physical injury to the spinal cord due to the laceration, contusion, compression, or contraction of the neural tissue. Pathological changes associated with the primary injury include severed axons, direct mechanical damage to cells, and ruptured blood vessels. The secondary injury is characterized by further destruction of neuronal and glial cells, mainly due to inflammatory responses, leading to the expansion of the injury site and loss of neurologic function. Studies exploring therapeutic strategies for patients with SCI are needed to improve neurological outcomes
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