Objective

2

To investigate the effect of moxibustion on central insulin resistance related proteins of the rats suffering from diabetic cognitive decline

and analyze the underlying mechanism of moxibustion for cognition improvement.

Methods

2

Using the intraperitoneal injection of STZ combined with a high-fat diet

the rat model of diabetic cognitive decline were prepared. Twenty successfully-modeled rats were assigned randomly into a model group and a moxibustion group

10 rats in each one. Besides

a blank group was set up with 10 rats collected. In the moxibustion group

suspending moxibustion was applied to "Baihui" (GV20)

"Shenting" (GV24) and "Dazhui" (GV14) at the same time

20 min in each intervention

once a day

and 6 interventions were delivered weekly and the duration of treatment was consecutive 4 weeks. The random blood glucose was measured using glucometer

and the learning-memory ability was detected by water maze test. HE staining was used to observe the morphology of neurons in the hippocampal tissue

real-time PCR assay was to detect mRNA expression of insulin receptor substrate 1 (IRS1)

phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) in the hippocampal tissue. The Western blot method was employed to detect the protein expression of IRS1

PI3K

AKT

phosphorylated IRS1 (p-IRS1)

phosphorylated PI3K (p-PI3K) and phosphorylated AKT (p-AKT) in the hippocampal tissue

and the ratio of p-IRS1/IRS1

p-PI3K/PI3K and p-AKT/AKT was calculated separately. The immunofluorescence intensity of p-IRS1

p-PI3K

and p-AKT was measured using immunofluorescence.

Results

2

Compared with the blank group

the rats of the model group exhibited higher random blood glucose (

P

<

0.001)

longer escape latency (

P

<

0.001)

severe pathological damage in the hippocampus

lower mRNA expression of IRS1

PI3K

and AKT (

P

<

0.001)

reduced ratio of p-IRS1/IRS1

p-PI3K/PI3K and p-AKT/AKT (

P

<

0.001)

and declined immunofluorescence intensity of p-IRS1

p-PI3K

and p-AKT in the hippocampal tissue (

P

<

0.001). In comparison with the model group

for the rats of the moxibustion group

the random blood glucose decreased (

P

<

0.05)

the escape latency was shortened (

P

<

0.01)

the hippocampal pathological damage was attenuated

the mRNA expression of IRS1

PI3K and AKT increased (

P

<

0.01)

the ratio of p-IRS1/IRS1

p-PI3K/PI3K and p-AKT/AKT was elevated (

P

<

0.01

P

<

0.05)

and the immunofluorescence intensity of p-IRS1

p-PI3K

and p-AKT in the hippocampal tissue was strengthened (

P

<

0.01

P

<

0.05).

Conclusion

2

In diabetic rats experiencing cognitive decline

moxibustion can enhance the learning-memory ability

which may be attributed to modulating the protein expression of IRS1

PI3K

and AKT

and their phosphorylation

activating insulin signal transduction

and reducing central insulin resistance.