Fig. 5.
Spinal genetic knockdown of adenosine monophosphate–activated protein kinase α (AMPKα) decreased glial glutamate transporter-1 (GLT-1) protein expression and increased glial fibrillary acid protein promoter (GFAP) and interleukin-1β (IL-1β) protein expression, and glycogen synthase kinase 3β (GSK3β) activity in naive rats. Bar graphs show the mean (± SEM) relative density of GLT-1, GFAP, and IL-1β to β-actin and phosphorylated GSK3β (pGSK3β) to total GSK3β (tGSK3β) in the spinal dorsal horn of AMPKα small interfering RNA (siRNA), scrambled siRNA, or the iFect (Neuromics, USA) vehicle-treated rats. Data obtained from individual animals are shown in the scatter plot. Samples of each molecule protein expression in each group are shown. *P < 0.05.

Spinal genetic knockdown of adenosine monophosphate–activated protein kinase α (AMPKα) decreased glial glutamate transporter-1 (GLT-1) protein expression and increased glial fibrillary acid protein promoter (GFAP) and interleukin-1β (IL-1β) protein expression, and glycogen synthase kinase 3β (GSK3β) activity in naive rats. Bar graphs show the mean (± SEM) relative density of GLT-1, GFAP, and IL-1β to β-actin and phosphorylated GSK3β (pGSK3β) to total GSK3β (tGSK3β) in the spinal dorsal horn of AMPKα small interfering RNA (siRNA), scrambled siRNA, or the iFect (Neuromics, USA) vehicle-treated rats. Data obtained from individual animals are shown in the scatter plot. Samples of each molecule protein expression in each group are shown. *P < 0.05.

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