Increased Nerve Growth Factor Signaling in Sensory Neurons of Early Diabetic Rats Is Corrected by Electroacupuncture
Figure 5
Variations of downstream NGF signaling after STZ and EA in DRGs. Representative Western blot of three samples for each experimental group is presented in each panel, together with data from densitometry analysis of three separate gel/blot runs (). The analysis of the total ERK1/2 and -ERK1/2 (p-ERK1/2) (a) and the total Akt and -Akt (p-Akt) (b) revealed that any significant variation in expression and the activation of these two TrkA-related downstream signaling kinases was induced by experimental treatments in the DRGs. The JNK that is known to be part of the downstream signaling machinery (c) was decreased four weeks after STZ, while -JNK (p-JNK) was increased. EA normalized both variations. The presence of the downstream signaling molecule and phosphorylated NF-κB-p65 complex—representing an index of the nuclear translocation activity of the transcription factor NF-κB—was unaffected by STZ (d), while EA greatly enhanced phospho-NF-κB-p65 presence in DRGs of diabetic rats, suggesting an augmented activity of the factor. Coherently, STZ lowered the phosphorylation of the IκB-α below controls level, suggesting an increase of its repressive activity upon NF-κB (d); EA in diabetic rats counteracted such an effect, significantly improving IκB-α phosphorylation versus STZ group, further indicating a decreased repression of NF-κB activity induced by EA. Data presented in ((a)–(d)) are percent variations from the mean of control group, obtained after normalization with GAPDH band integrated optical density. Data are expressed as % of the mean of controls () SD * versus control group. # versus STZ group.
