Electroacupuncture at GV20‑GB7 regulates mitophagy to protect against neurological deficits following intracerebral hemorrhage via inhibition of apoptosis
| Autor: | Xiaohong Dai, Hao Liu, Zhihao Li, Xiao-Ying Liu, Xueping Yu, Wei Teng, Shan-Shan Dong, Peng Liu, Qiuxin Chen, Ruiqiao Guan, Wei Zou |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Male
autophagy Cancer Research Electroacupuncture Ubiquitin-Protein Ligases medicine.medical_treatment Apoptosis PINK1 Pharmacology Severity of Illness Index Biochemistry Neuroprotection Parkin Mitochondrial Proteins Rats Sprague-Dawley electroacupuncture Mitophagy Genetics medicine Animals Molecular Biology Cerebral Hemorrhage bcl-2-Associated X Protein TUNEL assay Caspase 3 business.industry Autophagy Membrane Proteins Articles intracerebral hemorrhage Mitochondria nervous system diseases Disease Models Animal Proto-Oncogene Proteins c-bcl-2 Oncology Molecular Medicine Tumor Suppressor Protein p53 business Acupuncture Points Protein Kinases |
| Zdroj: | Molecular Medicine Reports |
| ISSN: | 1791-3004 1791-2997 |
| DOI: | 10.3892/mmr.2021.12131 |
| Popis: | The acupuncture penetrating line of Baihui (GV20) to Qubin (GB7) spans the parietal, frontal and temporal lobes. The present study aimed to elucidate the mechanism by which electroacupuncture (EA) at GV20‑GB7 regulates mitophagy in intracerebral hemorrhage (ICH) and whether it serves a neuroprotective role. A whole blood‑induced ICH model was used. Mitophagy‑regulating proteins, including BCL/adenovirus E1B 19 kDa‑interacting protein 3 (BNIP3), PTEN‑induced putative kinase 1 (PINK1), Parkin and apoptosis‑associated proteins were detected by western blotting; autophagy following ICH was evaluated by immunofluorescent techniques; morphological characteristics of mitophagy were observed using transmission electron microscopy; and TUNEL assay was performed to determine the number of apoptotic cells. Immunohistochemistry was used to detect p53 expression. The protective role of EA (GV20‑GB7) via enhanced mitophagy and suppressed apoptosis in ICH was further confirmed by decreased modified neurological severity score. The results showed that EA (GV20‑GB7) treatment upregulated mitochondrial autophagy following ICH and inhibited apoptotic cell death. The mechanism underlying EA (GV20‑GB7) treatment may involve inhibition of p53, an overlapping protein of autophagy and apoptosis. EA (GV20‑GB7) treatment decreased neurobehavioral deficits following ICH but pretreatment with 3‑methyladenine counteracted the beneficial effects of EA (GV20‑GB7) treatment. In conclusion, EA (GV20‑GB7) improved recovery from ICH by regulating the balance between mitophagy and apoptosis. |
| Databáze: | OpenAIRE |
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