Objective

2

To observe the effects of electroacupuncture (EA) on the expression of serum interleukin-1β (IL-1β)

tumor necrosis factor-α (TNF-α)

and the pancreatic nuclear factor-κB (NF-κB) pathway in type 2 diabetes mellitus (T2DM) rats

and to explore the possible mechanism by which EA improving the dedifferentiation of pancreatic β-cells in the treatment of T2DM.

Methods

2

Among 18 SPF-grade male Wistar rats

6 rats were randomly selected as the control group

and the remaining 12 rats were fed with high-sugar and high-fat diet combined with intraperitoneal injection of 2% streptozotocin solution (35 mg/kg) to establish T2DM model. After successful modeling

the 12 rats were randomly divided into a model group and an EA group

with 6 rats in each group. The EA group received EA at bilateral "Zusanli" (ST 36)

"Sanyinjiao" (SP 6)

"Weiwanxiashu" (EX-B 3)

and "Pishu" (BL 20)

with continuous wave

frequency of 15 Hz

current intensity of 2 mA

for 20 min each time

once a day

6 times a week

for a total of 6 weeks. Fasting blood glucose (FBG) levels were measured before modeling and before and after intervention. After intervention

ELISA was used to detect the serum fasting insulin (FINS)

IL-1β and TNF-α levels

and the β-cell function index (HOMA-β) and insulin resistance index (HOMA-IR) were calculated; HE staining was used to observe the morphology of the pancreatic islets; Western blot was used to detect the protein expression of pancreatic forkhead box protein O1 (FoxO1)

pancreatic and duodenal homeobox 1 (PDX-1)

neurogenin 3 (NGN3)

and NF-κB p65.

Results

2

After intervention

the FBG in the model group was higher than that in the control group (

P

<

0.01)

and the FBG in the EA group was lower than that in the model group (

P

<

0.01). Compared with the control group

the model group had increased levels of serum FINS

IL-1β

TNF-α

and HOMA-IR (

P

<

0.01)

and decreased HOMA-β (

P

<

0.01)

reduced protein expression of pancreatic FoxO1 and PDX-1 (

P

<

0.01)

and increased protein expression of pancreatic NGN3 and NF-κB p65 (

P

<

0.01

P

<

0.05). Compared with the model group

the EA group had lower serum FINS

IL-1β

TNF-α levels

and HOMA-IR (

P

<

0.01)

higher HOMA-β (

P

<

0.05)

increased protein expression of pancreatic FoxO1 and PDX-1 (

P

<

0.01

P

<

0.05)

and decreased protein expression of pancreatic NGN3 and NF-κB p65 (

P

<

0.01

P

<

0.05). The control group's pancreatic islets showed no obvious abnormalities; the model group's pancreatic islets were irregular in shape and had unclear boundaries with the surrounding area

with immune cell infiltration

reduced β-cell nuclei

disordered arrangement of islet cells

and increased intercellular spaces; the EA group showed improvements in islet morphology

immune cell infiltration

β-cell nuclei count

and the arrangement and spacing of islet cells approaching normal.

Conclusion

2

EA could lower the blood glucose levels in T2DM rats

alleviate chronic inflammatory responses in the islets

and improve the dedifferentiation of pancreatic β-cells

which may be related to the inhibition of pancreatic NF-κB pathway expression.