Abstract
To investigate the effects of aquaporin 4 (AQP4) and inward rectifier potassium channel 4.1 (Kir4.1) on medullospinal edema after treatment with methylprednisolone (MP) to suppress acute spinal cord injury (ASCI) in rats. Sprague Dawley rats were randomly divided into control, sham, ASCI, and MP-treated ASCI groups. After the induction of ASCI, we injected 30 mg/kg MP via the tail vein at various time points. The Tarlov scoring method was applied to evaluate neurological symptoms, and the wet-dry weights method was applied to measure the water content of the spinal cord. The motor function score of the ASCI group was significantly lower than that of the sham group, and the spinal water content was significantly increased. In addition, the levels of AQP4 and Kir4.1 were significantly increased, as was their degree of coexpression. Compared with that in the ASCI group, the motor function score and the water content were significantly increased in the MP group; in addition, the expression and coexpression of AQP4 and Kir4.1 were significantly reduced. Methylprednisolone inhibited medullospinal edema in rats with acute spinal cord injury, possibly by reducing the coexpression of aquaporin 4 and Kir4.1 in medullospinal tissues.
Highlights
Acute spinal cord injury (ASCI) is a trauma-induced spinal cord disorder; current research mainly focuses on preventing secondary spinal cord injuries, promoting regeneration of the spinal cord, and replacing the injured medullospinal tissues[1]
The comparison between the sham and control groups showed no significant difference in the water content, indicating that the surgery did not result in medullospinal edema in rats (60.85±5.37 vs. 60.65±4.27, P > 0.05)
Our results showed that in the MP group, the boundaries between spinal gray matter and white matter were clearer than ASCI group
Summary
Acute spinal cord injury (ASCI) is a trauma-induced spinal cord disorder; current research mainly focuses on preventing secondary spinal cord injuries, promoting regeneration of the spinal cord, and replacing the injured medullospinal tissues[1]. Aquaporins (AQPs) are closely related to tissue edema and AQP4 is the most studied isoform in the central nervous system, as it is widely distributed in the brain and spinal cord; it is closely related to trauma-induced brain and medullospinal edema. AQP4 participates in the transportation of water molecules in the brain, as well as the regulation of electrolytes and osmotic pressure, in the physiological state; under pathological conditions, it is involved in tissue edema caused by bodily injury[4]. The expression of Kir4.1 in rats with focal cerebral ischemia/reperfusion positively correlated with the degree of brain edema, and Kir4.1 was transported by AQP4-coupled mediating water[6]. The combined effects of Kir4.1 and AQP4 on medullospinal edema secondary to spinal cord injury have not been reported
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