Objective

2

To observe the effects of eye acupuncture on neurological deficits and mitophagy in neurons of ischemic cortical brain tissue in rats with cerebral ischemia reperfusion injury (CIRI)

and to explore the possible mechanism of eye acupuncture in improving CIRI.

Methods

2

Forty-eight SD rats were randomly divided into a sham operation group

a model group

an eye acupuncture group

and an inhibitor group

with 12 rats in each group. The modified middle cerebral artery occlusion method was used to establish CIRI model in the model group

eye acupuncture group

and inhibitor group. Before modeling

the rats in the sham operation group

model group

and eye acupuncture group were intraperitoneally injected with phosphate-buffered solution

while the rats in the inhibitor group were intraperitoneally injected with Compound C solution (adenosine monophosphate-activated protein kinase [AMPK

]

inhibitor). After successful modeling

the rats in the eye acupuncture group and inhibitor group received eye acupuncture intervention. Bilateral Shangjiao

Xiajiao

Gan (CO

12

) and Shen (CO

10

) were selected

with needles retained for 30 min without manipulation

once every 12 h

for a total of 7 interventions. Longa and Bederson scores were used to evaluate neurological deficits in rats. TTC staining was used to observe cerebral infarction. Nissl staining was used to observe the number of Nissl bodies in cortical brain tissue in the ischemic penumbra area. Transmission elect

ron microscopy was used to observe the ultrastructure of neuronal mitochondria in cortical brain tissue in the ischemic penumbra area. Western blot was used to detect the protein expressions of AMPK

phosphorylated adenosine monophosphate-activated protein kinase (p-AMPK)

unc-51-like autophagy activating kinase 1 (ULK1)

phosphorylated unc-51-like autophagy activating kinase 1 (p-ULK1)

FUN14 domain containing 1 (FUNDC1)

phosphorylated FUN14 domain containing 1 (p-FUNDC1)

and microtubule-associated protein light chain 3βⅡ (LC3-Ⅱ).

Results

2

Compared with the sham operation group

Longa and Bederson scores in the model group were increased (

P

<

0.05)

cerebral infarct volume was increased (

P

<

0.05)

the number of Nissl bodies in cortical brain tissue in the ischemic penumbra area was reduced (

P

<

0.05)

autophagosomes appeared

and the ratios of p-AMPK/AMPK

p-ULK1/ULK1

p-FUNDC1/FUNDC1

as well as LC3-Ⅱ protein expression in cortical brain tissue in the ischemic penumbra area were increased (

P

<

0.05). Compared with the model group and inhibitor group

Longa and Bederson scores in the eye acupuncture group were reduced (

P

<

0.05)

cerebral infarct volume was reduced (

P

<

0.05)

the number of Nissl bodies in cortical brain tissue in the ischemic penumbra area was increased (

P

<

0.05)

a small number of autophagosomes were observed

and the ratios of p-AMPK/AMPK

p-ULK1/ULK1

p-FUNDC1/FUNDC1

as well as LC3-Ⅱ protein expression in cortical brain tissue in the ischemic penumbra area were increased (

P

<

0.05).

Conclusion

2

The eye acupuncture may improve CIRI by upregulating the AMPK/ULK1/FUNDC1 signaling axis

promoting mitophagy

and alleviating neuronal injury.