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Electroacupuncture attenuates cerebral ischemia/reperfusion injury by regulating oxidative stress, neuronal death and neuroinflammation via stimulation of PPAR-γ.
Cheng, Nanfang; Cheng, Xinyuan; Tan, Feng; Liang, Yangui; Xu, Lihong; Wang, Jian; Tan, Jiuqing.
Affiliation
  • Cheng N; Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Foshan, China.
  • Cheng X; The Fourth Clinical Medical College, Guangzhou University of Traditional Chinese Medicine, Guangzhou, China.
  • Tan F; Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Foshan, China.
  • Liang Y; Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Foshan, China.
  • Xu L; Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Foshan, China.
  • Wang J; Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Foshan, China.
  • Tan J; Department of Neurology, Foshan Hospital of Traditional Chinese Medicine, Foshan, China.
Acupunct Med ; 42(3): 133-145, 2024 Jun.
Article de En | MEDLINE | ID: mdl-38351622
ABSTRACT

BACKGROUND:

Oxidative stress and inflammatory responses play essential roles in cerebral ischemia/reperfusion (I/R) injury. Electroacupuncture (EA) is widely used as a rehabilitation method for stroke in China; however, the underlying mechanism of action remains unclear. Peroxisome proliferator-activated receptor gamma (PPAR-γ) has been reported to impact anti-inflammatory and anti-oxidative effects.

OBJECTIVE:

This study investigated the role of PPAR-γ in EA-mediated effects and aimed to illuminate its possible mechanisms in cerebral I/R.

METHODS:

In this study, male Sprague-Dawley (SD) rats with middle cerebral artery occlusion/reperfusion (MCAO/R) injury were treated with EA at LI11 and ST36 for 30 min daily after MCAO/R for seven consecutive days. The neuroprotective effects of EA were measured by neurobehavioral evaluation, triphenyltetrazolium chloride staining, hematoxylin-eosin staining and transmission electron microscopy. Oxidative stress, inflammatory factors, neural apoptosis and microglial activation were examined by enzyme-linked immunosorbent assay, immunofluorescence and reverse transcriptase polymerase chain reaction. Western blotting was used to assess PPAR-γ-mediated signaling.

RESULTS:

We found that EA significantly alleviated cerebral I/R-induced infarct volume, decreased neurological scores and inhibited I/R-induced oxidative stress, inflammatory responses and microglial activation. EA also increased PPAR-γ protein expression. Furthermore, the protective effects of EA were reversed by injection of the PPAR-γ antagonist T0070907.

CONCLUSION:

EA attenuates cerebral I/R injury by regulating oxidative stress, neuronal death and neuroinflammation via stimulation of PPAR-γ.
Sujet(s)
Mots clés

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Lésion d'ischémie-reperfusion / Électroacupuncture / Encéphalopathie ischémique / Rat Sprague-Dawley / Stress oxydatif / Récepteur PPAR gamma Limites: Animals / Humans / Male Langue: En Journal: Acupunct Med Sujet du journal: TERAPIAS COMPLEMENTARES Année: 2024 Type de document: Article Pays d'affiliation: Chine Pays de publication: Royaume-Uni

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Lésion d'ischémie-reperfusion / Électroacupuncture / Encéphalopathie ischémique / Rat Sprague-Dawley / Stress oxydatif / Récepteur PPAR gamma Limites: Animals / Humans / Male Langue: En Journal: Acupunct Med Sujet du journal: TERAPIAS COMPLEMENTARES Année: 2024 Type de document: Article Pays d'affiliation: Chine Pays de publication: Royaume-Uni