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High-frequency spinal cord stimulation produces longlasting analgesic effects by restoring lysosomal function and autophagic flux in the spinal dorsal horn

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Neural Regeneration Research 2022年第2期17卷 370-377页

作者： Zhi-Bin Wang Yong-Da Liu Shuo Wang Ping Zhao Department of Anesthesiology and Pain Management Shengjing Hospital of China Medical UniversityShenyangLiaoning ProvinceChina Department of Anesthesiology Zhongshan HospitalFudan UniversityShanghaiChina

High-frequency spinal cord stimulation(HF-SCS) has been established as an effective therapy for neuropathic pain. However, the analgesic mechanisms involved in HF-SCS remain to be clarified. In our study, adult rat neuropathic pain was induced by spinal nerve ligation. Two days after modeling, the rats were subjected to 4 hours of HF-SCS(motor threshold 50%, frequency 10,000 Hz, and pulse width 0.024 ms) in the dorsal horn of the spinal cord. The results revealed that the tactile allodynia of spinal nerve-injured rats was markedly alleviated by HFSCS, and the effects were sustained for 3 hours after the stimulation had ceased. HF-SCS restored lysosomal function, increased the levels of lysosome-associated membrane protein 2(LAMP2) and the mature form of cathepsin D(matu-CTSD), and alleviated the abnormally elevated levels of microtubule-associated protein 1 A/B-light chain 3(LC3)-II and sequestosome 1(P62) in spinal nerve-injured rats. HF-SCS also mostly restored the immunoreactivity of LAMP2, which was localized in neurons in the superficial layers of the spinal dorsal horn in spinal nerve-injured rats. In addition, intraperitoneal administration of 15 mg/kg chloroquine for 60 minutes reversed the expression of the aforementioned proteins and shortened the timing of the analgesic effects of HF-SCS. These findings suggest that HF-SCS may exhibit longlasting analgesic effects on neuropathic pain in rats through improving lysosomal dysfunction and alleviating autophagic flux. This study was approved by the Laboratory Animal Ethics Committee of China Medical University, Shenyang, China(approval No. 2017 PS196 K) on March 1, 2017.

关键词： autolysosome dorsal horn of spinal cord dysfunction electrical stimulation high-frequency spinal cord stimulation neuropathic pain spinal nerve ligation

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autolysosome dysfunction regulates inflammatory response in ankylosing spondylitis monocytes

Autolysosome dysfunction regulates inflammatory response in ...

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第十二届全国免疫学学术大会

作者： Zhai Yue Lin Peng Feng Zhuan Han Qing Luo Xing Chen Zhinan Zhu Ping Department of Clinical Immunology PLA Specialized Research Institute of Rheumatology &ImmunologyXijing HospitalFourth Military Medical University National Translational Science Center for Molecular Medicine Department of Cell Biology Fourth Military Medical University

Background:autolysosome is a stage of autophagy,which includes the fusion of a autophagosome and a lysosome.The dysfunction of autolysosome will facilitate the infection of pathogens.However,the role of autolysosome i... 详细信息

关键词： autolysosome Autophagy Ankylosing spondylitis A20 IL-1

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Chlorpromazine protects against acetaminophen-induced liver injury in mice by modulating autophagy and c-Jun N-terminal kinase activation

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Liver Research 2019年第1期3卷 65-74页

作者： Yuan Li Hong-Min Ni Hartmut Jaeschke Wen-Xing Ding Department of Pharmacology Toxicology and TherapeuticsThe University of Kansas Medical CenterKansas CityKSUSA

Background and aim:Overdose of acetaminophen(APAP)leads to liver injury,which is one of the most common causes of liver failure in the United States.We previously demonstrated that pharmacological activation of autophagy protects against APAP-induced liver injury in mice via removal of damaged mitochondria and APAP-adducts(APAP-ADs).Using an image-based high-throughput screening for autophagy modulators,we recently identified that chlorpromazine(CPZ),a dopamine inhibitor used for anti-schizophrenia,is a potent autophagy inducer in vitro.Therefore,the aim of the present study is to determine whether CPZ may protect against APAP-induced liver injury via inducing autophagy.Methods:Wild type C57BL/6J mice were injected with APAP to induce liver injury.CPZ was administrated either at the same time with APAP(co-treatment)or 2 h later after APAP administration(post-treat-ment).Hemotoxyline and eosin(H&E)staining of liver histology,terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling(TUNEL)staining of necrotic cell death as well as serum levels of alanine aminotransferase(ALT)were used to monitor liver injury.Results:We found that CPZ markedly protected against APAP-induced liver injury as demonstrated by decreased serum levels of ALT,liver necrotic areas as well as TUNEL-positive cells in mice that were either co-treated or post-treated with CPZ.Mechanistically,we observed that CPZ increased the number of autolysosomes and decreased APAP-induced c-Jun N-terminal kinase activation without affecting the metabolic activation of APAP.Pharmacological inhibition of autophagy by chloroquine partially weak-ened the protective effects of CPZ against APAP-induced liver injury.Conclusions:Our results indicate that CPZ ameliorates APAP-induced liver injury partially via activating hepatic autophagy and inhibiting JNK activation.

关键词： Chlorpromazine(CPZ) Acetaminophen(APAP) Drug-induced liver injury Necrosis autolysosome Hepatotoxicity Glutathione(GSH) Oxidant stress

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