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  1. Article: NR0B1 suppresses ferroptosis through upregulation of NRF2/c-JUN-CBS signaling pathway in lung cancer cells.

    Zhang, Xin-Yue / Zhang, Hao / Hu, Si-Jing / Liao, Shun-Yao / Tao, Da-Chang / Tan, Xiao-Lan / Yi, Ming / Leng, Xiang-You / Wang, Zhao-Kun / Shi, Jia-Ying / Xie, Sheng-Yu / Yang, Yuan / Liu, Yun-Qiang

    American journal of cancer research

    2023  Volume 13, Issue 11, Page(s) 5174–5196

    Abstract: Ferroptosis has demonstrated significant potential in treating radiochemotherapy-resistant cancers, but its efficacy can be affected by recently discovered ferroptosis suppressors. In this study, we discovered that NR0B1 protects against erastin- or RSL3- ...

    Abstract Ferroptosis has demonstrated significant potential in treating radiochemotherapy-resistant cancers, but its efficacy can be affected by recently discovered ferroptosis suppressors. In this study, we discovered that NR0B1 protects against erastin- or RSL3-induced ferroptosis in lung cancer cells. Transcriptomic analysis revealed that NR0B1 significantly interfered with the expression of 12 ferroptosis-related genes, and the expression level of NR0B1 positively correlated with that of c-JUN, NRF2, and CBS. We further revealed that NR0B1 suppression of ferroptosis depended on the activities of c-JUN, NRF2, and CBS. NR0B1 directly promoted the expression of NRF2 and c-JUN and indirectly upregulated CBS expression through enhancing NRF2 and/or c-JUN transcription. Moreover, we showed that NR0B1 depletion restrained xenograft tumor growth and facilitated RSL3-induced ferroptosis in the tumors. In conclusion, our findings uncover that NR0B1 suppresses ferroptosis by activating the c-JUN/NRF2-CBS signaling pathway in lung cancer cells, providing new evidence for the involvement of NR0B1 in drug resistance during cancer therapy.
    Language English
    Publishing date 2023-11-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2589522-9
    ISSN 2156-6976
    ISSN 2156-6976
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Inflachromene attenuates seizure severity in mouse epilepsy models via inhibiting HMGB1 translocation.

    Dai, Si-Jie / Shao, Yu-Ying / Zheng, Yang / Sun, Jin-Yi / Li, Zhi-Sheng / Shi, Jia-Ying / Yan, Meng-Qi / Qiu, Xiao-Yun / Xu, Ceng-Lin / Cho, Wan-Sang / Nishibori, Masahiro / Yi, Sihyeong / Park, Seung Bum / Wang, Yi / Chen, Zhong

    Acta pharmacologica Sinica

    2023  Volume 44, Issue 9, Page(s) 1737–1747

    Abstract: Epilepsy is not well controlled by current anti-seizure drugs (ASDs). High mobility group box 1 (HMGB1) is a DNA-binding protein in the nucleus regulating transcriptional activity and maintaining chromatin structure and DNA repair. In epileptic brains, ... ...

    Abstract Epilepsy is not well controlled by current anti-seizure drugs (ASDs). High mobility group box 1 (HMGB1) is a DNA-binding protein in the nucleus regulating transcriptional activity and maintaining chromatin structure and DNA repair. In epileptic brains, HMGB1 is released by activated glia and neurons, interacting with various receptors like Toll-like receptor 4 (TLR4) and downstream glutamatergic NMDA receptor, thus enhancing neural excitability. But there is a lack of small-molecule drugs targeting the HMGB1-related pathways. In this study we evaluated the therapeutic potential of inflachromene (ICM), an HMGB-targeting small-molecule inhibitor, in mouse epilepsy models. Pentylenetetrazol-, kainic acid- and kindling-induced epilepsy models were established in mice. The mice were pre-treated with ICM (3, 10 mg/kg, i.p.). We showed that ICM pretreatment significantly reduced the severity of epileptic seizures in all the three epilepsy models. ICM (10 mg/kg) exerted the most apparent anti-seizure effect in kainic acid-induced epileptic status (SE) model. By immunohistochemical analysis of brain sections from kainic acid-induced SE mice, we found that kainic acid greatly enhanced HMGB1 translocation in the hippocampus, which was attenuated by ICM pretreatment in subregion- and cell type-dependent manners. Notably, in CA1 region, the seizure focus, ICM pretreatment mainly inhibited HMGB1 translocation in microglia. Furthermore, the anti-seizure effect of ICM was related to HMGB1 targeting, as pre-injection of anti-HMGB1 monoclonal antibody (5 mg/kg, i.p.) blocked the seizure-suppressing effect of ICM in kainic acid-induced SE model. In addition, ICM pretreatment significantly alleviated pyramidal neuronal loss and granule cell dispersion in kainic acid-induced SE model. These results demonstrate that ICM is an HMGB-targeting small molecule with anti-seizure potential, which may help develop a potential drug for treating epilepsy.
    MeSH term(s) Mice ; Animals ; Kainic Acid/adverse effects ; Kainic Acid/metabolism ; Epilepsy/chemically induced ; Epilepsy/drug therapy ; Epilepsy/metabolism ; Hippocampus/metabolism ; HMGB Proteins/metabolism ; HMGB Proteins/pharmacology ; HMGB1 Protein/metabolism ; Disease Models, Animal
    Chemical Substances inflachromene ; Kainic Acid (SIV03811UC) ; HMGB Proteins ; HMGB1 Protein
    Language English
    Publishing date 2023-04-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1360774-1
    ISSN 1745-7254 ; 0253-9756 ; 1671-4083
    ISSN (online) 1745-7254
    ISSN 0253-9756 ; 1671-4083
    DOI 10.1038/s41401-023-01087-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1904: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article: Late-onset multiple acyl-CoA dehydrogenase deficiency with cardiac syncope: A case report.

    Pan, Xue-Qi / Chang, Xue-Li / Zhang, Wei / Meng, Hua-Xing / Zhang, Jing / Shi, Jia-Ying / Guo, Jun-Hong

    World journal of clinical cases

    2020  Volume 8, Issue 5, Page(s) 995–1001

    Abstract: Background: Multiple acyl-CoA dehydrogenase deficiency (MADD) is an uncommon autosomal recessive disorder of mitochondrial fatty acid beta-oxidation. Syncope is a transient loss of consciousness due to acute global cerebral hypoperfusion. Late-onset ... ...

    Abstract Background: Multiple acyl-CoA dehydrogenase deficiency (MADD) is an uncommon autosomal recessive disorder of mitochondrial fatty acid beta-oxidation. Syncope is a transient loss of consciousness due to acute global cerebral hypoperfusion. Late-onset MADD with syncope has not been reported previously.
    Case summary: We report a 17-year-old girl with exercise intolerance and muscle weakness. She felt palpitation and shortness of breath after short bouts of exercise. She also suffered from a transient loss of consciousness many times. Muscle biopsy showed lipid storage. Genetic mutation analysis indicated a compound heterozygous mutation c.250G > A (p.A84T) and c.872T > G (p.V291G) in the
    Conclusion: Late-onset MADD with supraventricular tachycardia can cause cardiac syncope. Carnitine and riboflavin supplement were beneficial for treating the late-onset MADD with cardiac syncope. Attention should be paid to the prevention of cardiac syncope when diagnosing late-onset MADD.
    Language English
    Publishing date 2020-01-05
    Publishing country United States
    Document type Case Reports
    ISSN 2307-8960
    ISSN 2307-8960
    DOI 10.12998/wjcc.v8.i5.995
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Acetazolamide Alleviate Cerebral Edema Induced by Ischemic Stroke Through Inhibiting the Expression of AQP4 mRNA.

    Hao, Jia-Qi / He, Xing-Yue / Yang, Xin / Xiao, You-Chao / Duan, Sheng-Qiang / Wang, Huan / Bai, Hao / Zhang, Yu / Shi, Jia-Ying / Zhu, Xiao-Lin / Wang, Zhuang-Zhuang / Hao, Chun-Yan / Duan, Hu-Bin

    Neurocritical care

    2021  Volume 36, Issue 1, Page(s) 97–105

    Abstract: Objective: We want to investigate the effect of aquaporin-4 (AQP4) on cerebral edema induced by ischemic stroke in rats and explore whether inhibiting the expression of AQP4 through acetazolamide (AZA) could attenuate brain edema and protect cerebral ... ...

    Abstract Objective: We want to investigate the effect of aquaporin-4 (AQP4) on cerebral edema induced by ischemic stroke in rats and explore whether inhibiting the expression of AQP4 through acetazolamide (AZA) could attenuate brain edema and protect cerebral function.
    Methods: The Sprague Dawley (SD) rats were randomly divided into four groups: sham + saline group, sham + AZA group, AZA intervention group, and nonintervention group. Each group was divided into five subgroups according to the time of cerebral ischemia (6 h, 1 day, 3 days, 5 days, and 7 days). The model of cerebral infarction in rats was adopted by means of the bilateral carotid arteries ligation (2-VO) method. The rats in intervention group were given intraperitoneal injection of AZA (35 mg/kg/day). Hematoxylin-eosin staining was performed for pathological analysis of the infarcted area. The brain water content was calculated to evaluate the degree of brain edema. The messenger RNA (mRNA) and protein expressions of AQP4 in the brain were measured by quantitative real-time polymerase chain reaction and immunohistochemistry, respectively.
    Results: Significant cerebral pathological damages were found in ischemic stroke rats. The brain water content, protein, and mRNA expression of AQP4 of the intervention and nonintervention groups were markedly higher than those of the sham groups. By contrast, AZA administration reduced the brain water content, whereas improved cerebral dysfunction was induced by ischemic stroke. Moreover, AZA obviously reduced the protein and mRNA expression of AQP4 after ischemic stroke in rats' brains.
    Conclusions: The expression of AQP4 was closely related to cerebral edema induced by ischemic stroke. Decreasing the expression of AQP4 mRNA by AZA administration can effectively relieve cerebral edema and decrease cerebral pathological damage.
    MeSH term(s) Acetazolamide/pharmacology ; Animals ; Aquaporin 4/metabolism ; Brain Edema/drug therapy ; Brain Edema/etiology ; Brain Edema/metabolism ; Ischemic Stroke ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Aqp4 protein, rat ; Aquaporin 4 ; RNA, Messenger ; Acetazolamide (O3FX965V0I)
    Language English
    Publishing date 2021-07-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2381896-7
    ISSN 1556-0961 ; 1541-6933
    ISSN (online) 1556-0961
    ISSN 1541-6933
    DOI 10.1007/s12028-021-01261-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6538: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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