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  1. Article: Focus on the Role of the NLRP3 Inflammasome in Multiple Sclerosis: Pathogenesis, Diagnosis, and Therapeutics.

    Cui, Yueran / Yu, Haiyang / Bu, Zhongqi / Wen, Lulu / Yan, Lili / Feng, Juan

    Frontiers in molecular neuroscience

    2022  Volume 15, Page(s) 894298

    Abstract: Neuroinflammation is initiated with an aberrant innate immune response in the central nervous system (CNS) and is involved in many neurological diseases. Inflammasomes are intracellular multiprotein complexes that can be used as platforms to induce the ... ...

    Abstract Neuroinflammation is initiated with an aberrant innate immune response in the central nervous system (CNS) and is involved in many neurological diseases. Inflammasomes are intracellular multiprotein complexes that can be used as platforms to induce the maturation and secretion of proinflammatory cytokines and pyroptosis, thus playing a pivotal role in neuroinflammation. Among the inflammasomes, the nucleotide-binding oligomerization domain-, leucine-rich repeat- and pyrin domain-containing 3 (NLRP3) inflammasome is well-characterized and contributes to many neurological diseases, such as multiple sclerosis (MS), Alzheimer's disease (AD), and ischemic stroke. MS is a chronic autoimmune disease of the CNS, and its hallmarks include chronic inflammation, demyelination, and neurodegeneration. Studies have demonstrated a relationship between MS and the NLRP3 inflammasome. To date, the pathogenesis of MS is not fully understood, and clinical studies on novel therapies are still underway. Here, we review the activation mechanism of the NLRP3 inflammasome, its role in MS, and therapies targeting related molecules, which may be beneficial in MS.
    Language English
    Publishing date 2022-05-25
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2452967-9
    ISSN 1662-5099
    ISSN 1662-5099
    DOI 10.3389/fnmol.2022.894298
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis.

    Cui, Yue-Ran / Bu, Zhong-Qi / Yu, Hai-Yang / Yan, Li-Li / Feng, Juan

    Neural regeneration research

    2022  Volume 18, Issue 7, Page(s) 1535–1541

    Abstract: Emodin, a substance extracted from herbs such as rhubarb, has a protective effect on the central nervous system. However, the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown. In this study, a rat model of ... ...

    Abstract Emodin, a substance extracted from herbs such as rhubarb, has a protective effect on the central nervous system. However, the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown. In this study, a rat model of experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis, and the rats were intraperitoneally injected with emodin (20 mg/kg/d) from the day of immune induction until they were sacrificed. In this model, the nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and the microglia exacerbated neuroinflammation, playing an important role in the development of multiple sclerosis. In addition, silent information regulator of transcription 1 (SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator (PGC-1α) was found to inhibit activation of the NLRP3 inflammasome, and SIRT1 activation reduced disease severity in experimental autoimmune encephalomyelitis. Furthermore, treatment with emodin decreased body weight loss and neurobehavioral deficits, alleviated inflammatory cell infiltration and demyelination, reduced the expression of inflammatory cytokines, inhibited microglial aggregation and activation, decreased the levels of NLRP3 signaling pathway molecules, and increased the expression of SIRT1 and PGC-1α. These findings suggest that emodin improves the symptoms of experimental autoimmune encephalomyelitis, possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial inflammation. These findings provide experimental evidence for treatment of multiple sclerosis with emodin, enlarging the scope of clinical application for emodin.
    Language English
    Publishing date 2022-12-26
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.358612
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: FKBP5 Exacerbates Impairments in Cerebral Ischemic Stroke by Inducing Autophagy

    Yu, Shijia / Yu, Mingjun / Bu, Zhongqi / He, Pingping / Feng, Juan

    Frontiers in cellular neuroscience

    2020  Volume 14, Page(s) 193

    Abstract: Cerebral ischemic stroke is regarded as one of the most serious diseases in the human central nervous system. The secondary ischemia and reperfusion (I/R) injury increased the difficulty of treatment. Moreover, the latent molecular regulating mechanism ... ...

    Abstract Cerebral ischemic stroke is regarded as one of the most serious diseases in the human central nervous system. The secondary ischemia and reperfusion (I/R) injury increased the difficulty of treatment. Moreover, the latent molecular regulating mechanism in I/R injury is still unclear. Based on our previous clinical study, we discovered that FK506 binding protein 5 (FKBP5) is significantly upregulated in patients, who suffered acute ischemic stroke (AIS), with high diagnostic value. Levels of FKBP5 were positively correlated with patients' neurological impairments. Furthermore, a transient middle cerebral artery occlusion (tMCAO) model of mice was used to confirm that FKBP5 expression in plasma could reflect its relative level in brain tissue. Thus, we hypothesized that FKBP5 participated in the regulation of cerebral I/R injury. In order to explore the possible roles FKBP5 acted, the oxygen and glucose deprivation and reoxygenation (OGD/R) model was established to mimic I/R injury
    Language English
    Publishing date 2020-07-15
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2452963-1
    ISSN 1662-5102
    ISSN 1662-5102
    DOI 10.3389/fncel.2020.00193
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway.

    Yu, Shi-Jia / Yu, Ming-Jun / Bu, Zhong-Qi / He, Ping-Ping / Feng, Juan

    Neural regeneration research

    2020  Volume 16, Issue 6, Page(s) 1024–1030

    Abstract: Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury. MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury. However, ...

    Abstract Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury. MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury. However, whether miR-670 can regulate cell growth and death in cerebral ischemia/reperfusion and the underlying mechanism are poorly understood. In this study, we established mouse models of transient middle artery occlusion and Neuro 2a cell models of oxygen-glucose deprivation and reoxygenation to investigate the potential molecular mechanism by which miR-670 exhibits its effects during cerebral ischemia/reperfusion injury both in vitro and in vivo. Our results showed that after ischemia/reperfusion injury, miR-670 expression was obviously increased. After miR-670 expression was inhibited with an miR-670 antagomir, cerebral ischemia/reperfusion injury-induced neuronal death was obviously reduced. When miR-670 overexpression was induced by an miR-670 agomir, neuronal apoptosis was increased. In addition, we also found that miR-670 could promote Yap degradation via phosphorylation and worsen neuronal apoptosis and neurological deficits. Inhibition of miR-670 reduced neurological impairments after cerebral ischemia/reperfusion injury. These results suggest that microRNA-670 aggravates cerebral ischemia/reperfusion injury through the Yap pathway, which may be a potential target for treatment of cerebral ischemia/reperfusion injury. The present study was approved by the Institutional Animal Care and Use Committee of China Medical University on February 27, 2017 (IRB No. 2017PS035K).
    Language English
    Publishing date 2020-12-02
    Publishing country India
    Document type Journal Article
    ZDB-ID 2388460-5
    ISSN 1876-7958 ; 1673-5374
    ISSN (online) 1876-7958
    ISSN 1673-5374
    DOI 10.4103/1673-5374.300455
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Emerging Role of Ferroptosis in the Pathogenesis of Ischemic Stroke: A New Therapeutic Target?

    Bu, Zhong-Qi / Yu, Hai-Yang / Wang, Jue / He, Xin / Cui, Yue-Ran / Feng, Jia-Chun / Feng, Juan

    ASN neuro

    2021  Volume 13, Page(s) 17590914211037505

    Abstract: Ischemic stroke is one of the main causes of high morbidity, mortality, and disability worldwide; however, the treatment methods are limited and do not always achieve satisfactory results. The pathogenesis of ischemic stroke is complex, defined by ... ...

    Abstract Ischemic stroke is one of the main causes of high morbidity, mortality, and disability worldwide; however, the treatment methods are limited and do not always achieve satisfactory results. The pathogenesis of ischemic stroke is complex, defined by multiple mechanisms; among them, programmed death of neuronal cells plays a significant role. Ferroptosis is a novel type of regulated cell death characterized by iron redistribution or accumulation and increased lipid peroxidation in the membrane. Ferroptosis is implicated in many pathological conditions, such as cancer, neurodegenerative diseases, and ischemia-reperfusion injury. In this review, we summarize current research findings on ferroptosis, including possible molecular mechanisms and therapeutic applications of ferroptosis regulators, with a focus on the involvement of ferroptosis in the pathogenesis and treatment of ischemic stroke. Understanding the role of ferroptosis in ischemic stroke will throw some light on the development of methods for diagnosis, treatment, and prevention of this devastating disease.
    MeSH term(s) Brain Ischemia/complications ; Brain Ischemia/drug therapy ; Ferroptosis ; Humans ; Ischemic Stroke ; Lipid Peroxidation ; Stroke/drug therapy
    Language English
    Publishing date 2021-08-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2485467-0
    ISSN 1759-0914 ; 1759-0914
    ISSN (online) 1759-0914
    ISSN 1759-0914
    DOI 10.1177/17590914211037505
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: KCNQ1OT1 promotes autophagy by regulating miR-200a/FOXO3/ATG7 pathway in cerebral ischemic stroke.

    Yu, Shijia / Yu, Mingjun / He, Xin / Wen, Lulu / Bu, Zhongqi / Feng, Juan

    Aging cell

    2019  Volume 18, Issue 3, Page(s) e12940

    Abstract: Dysregulation of long noncoding RNAs (lncRNAs) is associated with abnormal development and pathophysiology in the brain. Increasing evidence has indicated that ischemic stroke is becoming the most common cerebral disease in aging populations. The ... ...

    Abstract Dysregulation of long noncoding RNAs (lncRNAs) is associated with abnormal development and pathophysiology in the brain. Increasing evidence has indicated that ischemic stroke is becoming the most common cerebral disease in aging populations. The treatment of ischemic stroke is challenging, due in part to ischemia and reperfusion (I/R) injury. In this study, we revealed that potassium voltage-gated channel subfamily Q member 1 opposite strand 1 (KCNQ1OT1) was significantly upregulated in ischemic stroke. Knockdown of KCNQ1OT1 remarkably reduced the infarct volume and neurological impairments in transient middle cerebral artery occlusion (tMCAO) mice. Mechanistically, KCNQ1OT1 acted as a competing endogenous RNA of miR-200a to regulate downstream forkhead box O3 (FOXO3) expression, which is a transcriptional regulator of ATG7. Knockdown of KCNQ1OT1 might inhibit I/R-induced autophagy and increase cell viability via the miR-200a/FOXO3/ATG7 pathway. This finding offers a potential novel strategy for ischemic stroke therapy.
    MeSH term(s) Aged ; Animals ; Autophagosomes/metabolism ; Autophagosomes/ultrastructure ; Autophagy/genetics ; Autophagy-Related Protein 7/genetics ; Autophagy-Related Protein 7/metabolism ; Brain Ischemia/genetics ; Brain Ischemia/metabolism ; Brain Ischemia/pathology ; Cell Line, Tumor ; Cell Survival/genetics ; Female ; Forkhead Box Protein O3/genetics ; Forkhead Box Protein O3/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Middle Aged ; Potassium Channels, Voltage-Gated/genetics ; Potassium Channels, Voltage-Gated/metabolism ; RNA, Long Noncoding/metabolism ; Reperfusion Injury/genetics ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Signal Transduction/genetics ; Stroke/genetics ; Stroke/metabolism ; Stroke/pathology ; Vacuoles/genetics ; Vacuoles/metabolism ; Vacuoles/ultrastructure
    Chemical Substances Atg7 protein, mouse ; Forkhead Box Protein O3 ; FoxO3 protein, mouse ; KCNQ1OT1 long non-coding RNA, human ; MicroRNAs ; Mirn200 microRNA, mouse ; Potassium Channels, Voltage-Gated ; RNA, Long Noncoding ; Autophagy-Related Protein 7 (EC 6.2.1.45)
    Language English
    Publishing date 2019-04-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2113083-8
    ISSN 1474-9726 ; 1474-9718
    ISSN (online) 1474-9726
    ISSN 1474-9718
    DOI 10.1111/acel.12940
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Potential Roles of Exosomes in Parkinson's Disease: From Pathogenesis, Diagnosis, and Treatment to Prognosis.

    Yu, Haiyang / Sun, Tong / An, Jing / Wen, Lulu / Liu, Fei / Bu, Zhongqi / Cui, Yueran / Feng, Juan

    Frontiers in cell and developmental biology

    2020  Volume 8, Page(s) 86

    Abstract: Parkinson's disease (PD) is the second most prevalent neurodegenerative disease in the world, after Alzheimer's disease (AD), affecting approximately 1% of people over 65 years of age. Exosomes were once considered to be cellular waste and functionless. ... ...

    Abstract Parkinson's disease (PD) is the second most prevalent neurodegenerative disease in the world, after Alzheimer's disease (AD), affecting approximately 1% of people over 65 years of age. Exosomes were once considered to be cellular waste and functionless. However, our understanding about exosome function has increased, and exosomes have been found to carry specific proteins, lipids, functional messenger RNAs (mRNAs), high amounts of non-coding RNAs (including microRNAs, lncRNAs, and circRNAs) and other bioactive substances. Exosomes have been shown to be involved in many physiological processes
    Language English
    Publishing date 2020-02-21
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2020.00086
    Database MEDical Literature Analysis and Retrieval System OnLINE

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