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Effects of intrathecal and intravenous administration of dexmedetomidine on motor function recovery and inflammatory response in rats with spinal cord injury

By: Chai, Y.
Contributor(s): Wei, Shuxin.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2021Edition: Vol.83(2), March-April.Description: 380-386p.Subject(s): PHARMACEUTICSOnline resources: Click here In: Indian journal of pharmaceutical sciencesSummary: To analyze the e ffects of intrathecal and intravenous dexmedetomidine on motor function recovery and in flammatory response in rats with spinal cord injury. The rats were divided into three groups, the right femoral sheath injection group (3 μg/kg), the right femoral sheath injection group (3 μg/kg) Dexmedetomidine ( μg/kg), Inhibitor kappa B kinase inhibitor group (intrathecal injection of 50 μl/kg BMS-345541). Neuromotor function, pathological changes of spinal cord tissue, apoptosis rate of spinal cord tissue and changes of in flammatory factors were observed. The neuromotor function scores of rats in intrathecal group, intravenous group and intrathecal+intravenous group were significantly higher than those in model group at 24 h and 48 h after treatment (p<0.05) and those in intrathecal+intravenous group were significantly higher than those in intrathecal group at 24 h and 48 h after treatment, with statistical significance (p<0.05). In intrathecal group, vein group and intrathecal+vein group, the injury of nerve tissue structure was mild, the cells were slightly swollen and the cytoplasm was uniform. The apoptosis number of spinal cord injury tissue in intrathecal group, intravenous group and intrathecal+venous group was significantly lower than that of model group (p<0.05), and the apoptosis number of intrathecal+venous group was signi ficantly lower than that of intrathecal group (p<0.05). The expression of interleukin-1 β, interleukin-6 and tumor necrosis factor- α messenger RNA in intrathecal group, intravenous group and intrathecal+venous group was signi ficantly lower than that in model group (p<0.05), while the mRNA expression of interleukin-1 β, interleukin-6 and tumor necrosis factor- α in intrathecal+venous group was significantly lower than that in intrathecal group (p<0.05). The expressions of inhibitor kappa B kinase β, nuclear factor kappa-light-chain-enhancer of activated B cells messenger RNA and protein in the Inhibitor kappa B kinase β inhibitor group and dexmedetomidine group were signi ficantly lower than those in the model group (p<0.05) and the expressions of inhibitor kappa B kinaseβ, nuclear factor kappa-light-chain- enhancer of activated B cells messenger RNA and protein in the dexmedetomidine group were significantly lower than those in the inhibitor kappa B kinase β inhibitor group (p<0.05). Intrathecal and intravenous dexmedetomidine can significantly improve the recovery of neuromotor function and reduce inflammatory response in rats with spinal cord injury. The mechanism may be related to the inhibition of inhibitor kappa B kinase/ nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway.
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To analyze the e ffects of intrathecal and intravenous dexmedetomidine on motor function recovery
and in flammatory response in rats with spinal cord injury. The rats were divided into three groups,
the right femoral sheath injection group (3 μg/kg), the right femoral sheath injection group (3 μg/kg)
Dexmedetomidine ( μg/kg), Inhibitor kappa B kinase inhibitor group (intrathecal injection of 50 μl/kg
BMS-345541). Neuromotor function, pathological changes of spinal cord tissue, apoptosis rate of spinal
cord tissue and changes of in flammatory factors were observed. The neuromotor function scores of rats
in intrathecal group, intravenous group and intrathecal+intravenous group were significantly higher than
those in model group at 24 h and 48 h after treatment (p<0.05) and those in intrathecal+intravenous group
were significantly higher than those in intrathecal group at 24 h and 48 h after treatment, with statistical
significance (p<0.05). In intrathecal group, vein group and intrathecal+vein group, the injury of nerve
tissue structure was mild, the cells were slightly swollen and the cytoplasm was uniform. The apoptosis
number of spinal cord injury tissue in intrathecal group, intravenous group and intrathecal+venous group
was significantly lower than that of model group (p<0.05), and the apoptosis number of intrathecal+venous
group was signi ficantly lower than that of intrathecal group (p<0.05). The expression of interleukin-1 β,
interleukin-6 and tumor necrosis factor- α messenger RNA in intrathecal group, intravenous group and
intrathecal+venous group was signi ficantly lower than that in model group (p<0.05), while the mRNA
expression of interleukin-1 β, interleukin-6 and tumor necrosis factor- α in intrathecal+venous group was
significantly lower than that in intrathecal group (p<0.05). The expressions of inhibitor kappa B kinase β,
nuclear factor kappa-light-chain-enhancer of activated B cells messenger RNA and protein in the Inhibitor
kappa B kinase β inhibitor group and dexmedetomidine group were signi ficantly lower than those in the
model group (p<0.05) and the expressions of inhibitor kappa B kinaseβ, nuclear factor kappa-light-chain-
enhancer of activated B cells messenger RNA and protein in the dexmedetomidine group were significantly
lower than those in the inhibitor kappa B kinase β inhibitor group (p<0.05). Intrathecal and intravenous
dexmedetomidine can significantly improve the recovery of neuromotor function and reduce inflammatory
response in rats with spinal cord injury. The mechanism may be related to the inhibition of inhibitor kappa
B kinase/ nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway.

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