To evaluate the protective effects of dexmedetomidine on the colon and spinal cord of rats with functional
chronic visceral pain and its regulatory mechanism on extracellular signal-regulated kinase 1-cyclic
adenosine monophosphate response element-binding protein signaling pathway. A rat model of irritable
bowel syndrome was established by colorectal distention stimulation. Animals were categorized into
normal group, model group, experimental group and control group. No treatment was given in normal
group, while colorectal distention stimulation was utilized in model group, experimental group and control
group. After successful modeling, the animals in experimental group were injected intraperitoneally
with 5 μg/kg of dexmedetomidine hydrochloride injection daily, those in control group were injected
intraperitoneally with 5 μg/kg pinaverium bromide daily and those in normal group and model group
were injected intraperitoneally daily with the same volume of normal saline, for 14 consecutive days.
Abdominal withdrawal reflex score and pain threshold of rats were measured. Cell apoptosis in the spinal
cord of rats was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling
staining. The messenger ribonucleic acid expressions of extracellular signal-regulated kinase 1 and cyclic
adenosine monophosphate response element-binding protein in the spinal cord were detected by real-
time quantitative polymerase chain reaction and phosphorylated-extracellular signal-regulated kinase 1
and phosphorylated-cyclic adenosine monophosphate response element-binding protein expressions in the
spinal cord of rats were tested by Western blotting. Compared with normal group, abdominal withdrawal
reflex score, cell apoptosis rate, messenger ribonucleic acid expressions of extracellular signal-regulated
kinase 1 and cyclic adenosine monophosphate response element-binding protein, phosphorylated-
extracellular signal-regulated kinase 1 and phosphorylated-cyclic adenosine monophosphate response
element-binding protein expressions were significantly higher (p<0.05) and pain threshold value was
significantly lower (p<0.05) in model group, experimental group and control group at 20 mmHg, 40
mmHg, 60 mmHg and 80 mmHg pressures. Abdominal withdrawal reflex score, cell apoptosis rate,
messenger ribonucleic acid expressions of extracellular signal-regulated kinase 1 and cyclic adenosine
monophosphate response element-binding protein, phosphorylated-extracellular signal-regulated kinase 1
and phosphorylated-cyclic adenosine monophosphate response element-binding protein expressions were
significantly lower (p<0.05) and pain threshold value was significantly higher (p<0.05) in experimental
group and control group than those in model group at 20 mmHg, 40 mmHg, 60 mmHg and 80 mmHg
pressures. Dexmedetomidine can prominently ameliorate the clinical symptoms of rats with functional
chronic visceral pain and may protect the colon and spinal cord by inhibiting the extracellular signal-
regulated kinase 1/cyclic adenosine monophosphate response element-binding protein signaling pathway.