Jasminoidin and ursodeoxycholic acid exert synergistic effect against cerebral ischemia-reperfusion injury via Dectin-1-induced NF-κB activation pathway

Hao, Dan-Li; Xie, Ran; Zhong, Yi-Lin; Li, Jiameng; Zhao, Qinghe; Huo, Hai-Ru; Xiong, Xingjiang; Shi, Feng; Wang, Peng-Qian

doi:10.1016/j.phymed.2023.154817

Cited by 3 publications

(3 citation statements)

References 53 publications

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“…In an animal study, it was found that JAS and ursodeoxycholic acid have synergistic effects in treating focal cerebral ischemia/reperfusion injury, it indicated the effect against JAS on the IS (Liu et al, 2012). Moreover, JAS and ursodeoxycholic acid synergistically reduced cerebral infarct volume and alleviated cerebral ischemia-reperfusion injury by inhibiting Dectin-1-induced NF-κB activation (Hao et al, 2023). In addition, JAS is a drug component predicted to be able to target PASK through the Herb database.…”

Section: Introductionmentioning

confidence: 99%

Jasminoidin reduces ischemic stroke injury by regulating microglia polarization via PASK‐EEF1A1 axis

Wu,

Mao,

et al. 2023

Chem Biol Drug Des

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Jasminoidin (JAS) can alleviate ischemic stroke (IS) injury, but its molecular mechanism remains undefined. The polarization of microglia affects IS process. This research is powered to probe whether the molecular mechanism of JAS for IS treatment is coupled with microglia polarization. IS modeling in mice was accomplished by middle cerebral artery occlusion (MCAO) and model mice were injected with 25 and 50 mg/mL JAS, followed by determination of infarct volume, brain water content, and histological changes in mouse brains. The microglia modeling was performed by 1‐h oxygen–glucose deprivation and 24‐h reoxygenation. Oxygen–glucose deprivation/reoxygenation (OGD/R)‐induced microglia were treated with JAS and transfected with Per‐Arnt‐Sim kinase (PASK)‐overexpressing plasmid, subsequent to which cell viability and lactate dehydrogenase (LDH) level were determined. The mRNA or protein expressions of examined genes in microglia and brain tissues were detected by quantitative real‐time polymerase chain reaction or western blot. MCAO‐induced massive infarction, edema, and injury in mouse brain tissues, upregulated interleukin‐1 beta (IL‐1β), FcγRIIB (CD32), tumor necrosis factor alpha (TNF‐α), PASK, p‐eukaryotic elongation factor 1A1 (EEF1A1), and p‐EEF1A1/EEF1A1 levels, but downregulated mannose receptor 1 (CD206), arginase‐1 (Arg‐1) and interleukin‐10 (IL‐10), and EEF1A1 expressions, which was reversed by JAS. OGD/R treatment decreased microglial viability as well as expressions of CD206, Arg‐1, IL‐10, and EEF1A1, yet increased cytotoxicity and levels of IL‐1β, CD32, TNF‐α, PASK, p‐EEF1A1, and p‐EEF1A1/EEF1A1, which was reversed by JAS. PASK overexpression reversed the effects of JAS on microglia. JAS reduces IS injury by regulating microglia polarization via PASK‐EEF1A1 axis.

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Section: Introductionmentioning

confidence: 99%

Jasminoidin reduces ischemic stroke injury by regulating microglia polarization via PASK‐EEF1A1 axis

Wu,

Mao,

et al. 2023

Chem Biol Drug Des

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“…[75,76] Evidence reveals that intertwining autophagy and inflammatory pathways enhances multi-pathway interactions, and combined treatment with Jasminoidin (JA) and ursodeoxycholic (UA) offers synergistic protection against CIRI by diminishing Dectin-1-induced NF-κB activation. [77] The intricate relationship between autophagy and inflammatory pathways awaits further clarification and could be central to CIRI-targeted strategies.…”

Section: Discussionmentioning

confidence: 99%

“…Jasminoidin (JA) and ursodeoxycholic (UA) offers synergistic protection against CIRI by diminishing Dectin-1-induced NF-κB activation. [77] The intricate relationship between autophagy and inflammatory pathways awaits further clarification and could be central to CIRI-targeted strategies.…”

Section: Limitationsmentioning

confidence: 99%

A bibliometric analysis of research foci and trends in cerebral ischemia-reperfusion injury involving autophagy during 2008 to 2022

Shi,

Xu,

et al. 2023

Medicine

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Background: Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process that typically occurs during the treatment of ischemia, with limited therapeutic options. Autophagy plays a vital role during the reperfusion phase and is a potential therapeutic target for preventing and treating cerebral ischemia-reperfusion injury. Methods: We conducted a comprehensive search of the Web of Science Core Collection for publications related to cerebral ischemia-reperfusion injury with autophagy, published between January 1, 2008, and January 1, 2023. We analyzed the selected publications using VOSviewer, CiteSpace, and other bibliometric tools. Results: Our search yielded 877 relevant publications. The field of autophagy in cerebral ischemia-reperfusion injury has grown rapidly since 2016. China has been the leading contributor to publications, followed by the USA and Iran. Chen Zhong and Qin Zhenghong have been influential in this field but have yet to reach all groups. In addition, there has been a shortage of collaboration among authors from different institutions. Our literature and keyword analysis identified Neurovascular protection (#11 Neuroprotective, #13 Neurovascular units, etc) and Inflammation (NLRP3 inflammasome) as popular research directions. Furthermore, the terms “Blood-Brain Barrier,” “Mitophagy,” and “Endoplasmic reticulum stress” have been frequently used and may be hot research topics in the future. Conclusions: The role of autophagy in cerebral ischemia-reperfusion injury remains unclear, and the specific mechanisms of drugs used to treat ischemia-reperfusion injury still need to be explored. This work outlines the changing trends in investigating cerebral ischemia-reperfusion injury involving autophagy and suggests future lines of inquiry.

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Ethanolic extract of Arctium lappa leaves alleviates cerebral ischemia reperfusion-induced inflammatory injury via HDAC9-mediated NF-κB pathway

Wang,

Li,

Ren

et al. 2024

Phytomedicine

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Jasminoidin and ursodeoxycholic acid exert synergistic effect against cerebral ischemia-reperfusion injury via Dectin-1-induced NF-κB activation pathway

Cited by 3 publications

References 53 publications

Jasminoidin reduces ischemic stroke injury by regulating microglia polarization via PASK‐EEF1A1 axis

Jasminoidin reduces ischemic stroke injury by regulating microglia polarization via PASK‐EEF1A1 axis

A bibliometric analysis of research foci and trends in cerebral ischemia-reperfusion injury involving autophagy during 2008 to 2022

Ethanolic extract of Arctium lappa leaves alleviates cerebral ischemia reperfusion-induced inflammatory injury via HDAC9-mediated NF-κB pathway

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