Cross electro-nape-acupuncture ameliorates cerebral hemorrhage-induced brain damage by inhibiting necroptosis
Autor: | Guofeng Cai, Li-Li Shang, Gao Shan, Wen-Li Song, Kun-Ping Jia, Zhong-Ren Sun, Haichun Zhou, Kai Liu, Hui Zhao, Sheng-Nan Xu, Zhe Zhuang, Cai Guoliang, Xiu-Zhen Wang |
---|---|
Rok vydání: | 2020 |
Předmět: |
Cross electro-nape acupuncture
genetic structures Nape business.industry Necroptosis Quantitative real-time polymerase chain reaction General Medicine Brain damage Pharmacology Cerebral hemorrhage eye diseases RIPK1 medicine.anatomical_structure Enzyme-linked immunosorbent assay Clinical and Translational Research Receptor interacting protein kinase 1 Acupuncture medicine sense organs medicine.symptom Quantitative Real-Time Polymerase Chain Reaction business |
Zdroj: | World Journal of Clinical Cases |
ISSN: | 2307-8960 |
Popis: | BACKGROUND Receptor interacting protein kinase 1 (RIPK1)-mediated cell death, including apoptosis and necroptosis, belongs to programmed cell death. It has been reported that RIPK1-mediated necroptosis exists in lesions of cerebral hemorrhage (CH). Electroacupuncture, a treatment derived from traditional Chinese medicine, could improve neurological impairment in patients with brain injury. AIM To investigate the protective role of cross electro-nape acupuncture (CENA) in CH, and clarify the potential mechanism. METHODS CH rat models were established, and CENA was applied to the experimental rats. Neurological functions and encephaledema were then measured. Necrotic cells in the brain of rats with CH were evaluated by propidium iodide staining. Necroptosis was assessed by immunofluorescence. Activation of the necroptosis-related pathway was detected by western blot. Extraction of brain tissue, cerebrospinal fluid and serum samples was conducted to measure the expression and secretion of inflammatory cytokines by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. RESULTS The necroptotic marker p-MLKL was detectable in the brains of rats with CH. Next, we found that CENA could ameliorate neurological functions in rat models of CH. Moreover, the upregulation of RIPK1-mediated necroptosis-related molecules in the brains of rats with CH were inhibited by CENA. Further investigation revealed that CENA partially blocked the interaction between RIPK1 and RIPK3. Finally, in vivo assays showed that CENA decreased the expression of the inflammatory cytokines tumor necrosis factor-α, interleukin-6 and interleukin-8 in CH rat models. CONCLUSION These findings revealed that CENA exerts a protective role in CH models by inhibiting RIPK1-mediated necroptosis. |
Databáze: | OpenAIRE |
Externí odkaz: |