WU Rihui, HU Fangzhu, XIE Li, et al. Effect of electroacupuncture at the acupoints of pericardium meridian on oxidative stress-related proteins in ischemic stroke rats[J]. Chinese Acupuncture & Moxibustion, 2026, 46(5): 753-761.
DOI:
WU Rihui, HU Fangzhu, XIE Li, et al. Effect of electroacupuncture at the acupoints of pericardium meridian on oxidative stress-related proteins in ischemic stroke rats[J]. Chinese Acupuncture & Moxibustion, 2026, 46(5): 753-761.DOI: 10.13703/j.0255-2930.20250327-0006.
Effect of electroacupuncture at the acupoints of pericardium meridian on oxidative stress-related proteins in ischemic stroke rats
To investigate the effect and potential mechanism of electroacupuncture (EA) at the acupoints of the hand-
jueyin
pericardium meridian on oxidative stress-related proteins in ischemic stroke rats.
Methods
2
Of 108 SD male rats
27 rats were randomly assigned to a sham-operation group
and the rest 81 rats were in a modeling group and prepared the middle cerebral artery occlusion (MCAO) models by inserting a suture into the carotid artery. The 81 successfully modeled rats were randomized into a model group
a pericardium meridian group and a non-meridian point group
27 rats in each one; and each group was subdivided into a 1-day group (12 rats) and a 7-day group (15 rats) according to intervention duration. In the pericardium meridian group
EA was delivered at "Tianquan" (PC2)
"Quze" (PC3)
"Neiguan" (PC6)
and "Daling" (PC7) on the right side; and the electric stimulation was attached to two pairs of points "Tianquan" (PC2) and "Quze" (PC3)
and "Neiguan" (PC6) and "Daling" (PC7)
respectively
with continuous wave
at the frequency of 1 Hz to 20 Hz and a current intensity of 4 mA to 6 mA
30 min each time. In the non-meridian point group
the sites 1.5 mm lateral to "Tianquan" (PC2)
"Quze" (PC3)
"Neiguan" (PC6) and "Daling" (PC7) on the right side were located and stimulated with the same procedure as the pericardium meridian group. The intervention in each subgroup was conducted for 1 day and 7 days respectively. The Zea Longa score and Bederson score were used to evaluate the neurological deficits in rats. TTC staining was adopted to determine the infarct volume
HE staining and Nissl staining were employed to observe the morphology of brain tissue
and transmission electron microscopy was utilized to examine the ultrastructure of mitochondria in neurons on the ischemic side. Using ELISA
the levels of nuclear factor E2-related factor 2 (Nrf2)
heme oxygenase 1 (HO-1)
and peroxisome proliferator-γ coactivator-1α (PGC-1α) in serum were detected. Using Western blot and real-time fluorescent quantitative PCR
the protein and mRNA expression of Nrf2
HO-1
and PGC-1α in brain tissue on the ischemic side was detected.
Results
2
The neurological deficits and pathological changes were not found in the sham-operation group. In 1 and 7 days of intervention
in the model group
the neuronal density in the infarcted area was reduced and neuronal edema was obvious; and when compared with the sham-operation group
the neurological deficit scores were higher (
P
<
0.001)
the volume of cerebral infarction increased (
P
<
0.001) and the number of cortical neurons decreased (
P
<
0.001). In 7 days of intervention
compared with the sham-operation group
the levels of serum Nrf2
HO-1
and PGC-1α were reduced (
P
<
0.01)
and the protein and mRNA expression of Nrf2
HO-1
and PGC-1α in brain tissue on the ischemic side decreased (
P
<
0.001) in the model group; neuronal cell edema was alleviated
necrotic cells were declined
and mitochondrial morphology was improved in the pericardium meridian group
and the number of neurons in the cerebral cortex was higher than that in the model group (
P
<
0.01). When compared with the model group and non-meridian point group
the levels of serum Nrf2
HO-1 and PGC-1α were elevated (
P
<
0.001)
and the protein and mRNA expression of Nrf2
HO-1 and PGC-1α in brain tissue on the ischemic side increased in the pericardium meridian group (
P
<
0.001).
Conclusion
2
Electroacupuncture at the acupoints of hand-
jueyin
pericardium meridian alleviates neurological deficits and promotes neurological functional recovery in MCAO rats
which may be mediated by upregulating the expression of Nrf2