Gastrodin suppresses pyroptosis and exerts neuroprotective effect in traumatic brain injury model by inhibiting NLRP3 inflammasome signaling pathway

Yang, Fei; Li, Guangzhao; Lin, Bin; Zhang, Kaipeng

doi:10.31083/j.jin2102072

Cited by 21 publications

(13 citation statements)

References 23 publications

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“…Growing evidence has shown that NLRP3 inflammasome‐mediated pyroptosis was involved in the pathogenesis of TBI. Yang et al revealed that Gastrodin suppressed NLRP3 inflammasome signaling pathway, and therefore inhibited pyroptosis, reduced brain tissue injury, and improved functional recovery of injury nerve in TBI rats 31 . Moreover, Yuan et al found that interference of hypoxia‐inducible factor‐1α (HIF‐1α) decreased the expressions of NLRP3, GSDMD‐N and cleaved caspase‐1 in the injured cortex after TBI, suggesting that HIF‐1α aggravated NLRP3 inflammasome‐mediated pyroptosis in TBI 32 .…”

Section: Discussionmentioning

confidence: 99%

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Human umbilical cord mesenchymal stem cell‐derived exosome suppresses programmed cell death in traumatic brain injury via PINK1/Parkin‐mediated mitophagy

et al. 2023

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Aims: Recently, human umbilical cord mesenchymal stem cell (HucMSC)-derived exosome is a new focus of research in neurological diseases. The present study was aimed to investigate the protective effects of HucMSC-derived exosome in both in vivo and in vitro TBI models. Methods:We established both mouse and neuron TBI models in our study. After treatment with HucMSC-derived exosome, the neuroprotection of exosome was investigated by the neurologic severity score (NSS), grip test score, neurological score, brain water content, and cortical lesion volume. Moreover, we determined the biochemical and morphological changes associated with apoptosis, pyroptosis, and ferroptosis after TBI. Results:We revealed that treatment of exosome could improve neurological function, decrease cerebral edema, and attenuate brain lesion after TBI. Furthermore, administration of exosome suppressed TBI-induced cell death, apoptosis, pyroptosis, and ferroptosis. In addition, exosome-activated phosphatase and tensin homolog-induced putative kinase protein 1/Parkinson protein 2 E3 ubiquitin-protein ligase (PINK1/ Parkin) pathway-mediated mitophagy after TBI. However, the neuroprotection of exosome was attenuated when mitophagy was inhibited, and PINK1 was knockdown.Importantly, exosome treatment also decreased neuron cell death, suppressed apoptosis, pyroptosis, and ferroptosis and activated the PINK1/Parkin pathway-mediated mitophagy after TBI in vitro. Conclusion:Our results provided the first evidence that exosome treatment played a key role in neuroprotection after TBI through the PINK1/Parkin pathway-mediated mitophagy.

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Section: Discussionmentioning

confidence: 99%

“…30 suppressed NLRP3 inflammasome signaling pathway, and therefore inhibited pyroptosis, reduced brain tissue injury, and improved functional recovery of injury nerve in TBI rats. 31 Moreover, Yuan et al found that interference of hypoxia-inducible factor-1α…”

Section: Exosome Protected Primary Cultured Neurons From Tbimentioning

confidence: 99%

Human umbilical cord mesenchymal stem cell‐derived exosome suppresses programmed cell death in traumatic brain injury via PINK1/Parkin‐mediated mitophagy

et al. 2023

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“…The GAS content is the most appreciated analytical marker for the quality standardization of P. chinensis (Zhang et al, 2019). The mechanism of GAS action is gradually being understood and recognized Yang et al, 2022). Several reports have shown that the content of GAS in P. chinensis was higher than the content in G. elata, one of the major sources of GAS (Zhang et al, 2019;Wang et al, 2022).…”

Section: Discussionmentioning

confidence: 99%

The gastrodin biosynthetic pathway in Pholidota chinensis Lindl. revealed by transcriptome and metabolome profiling

et al. 2022

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Pholidota chinensis Lindl. is an epiphytic or lithophytic perennial herb of Orchidaceae family used as a garden flower or medicinal plant to treat high blood pressure, dizziness and headache in traditional Chinese medicine. Gastrodin (GAS) is considered as a main bioactive ingredient of this herb but the biosynthetic pathway remains unclear in P. chinensis. To elucidate the GAS biosynthesis and identify the related genes in P. chinensis, a comprehensive analysis of transcriptome and metabolome of roots, rhizomes, pseudobulbs and leaves were performed by using PacBio SMART, Illumina Hiseq and Ultra Performance Liquid Chromatography Tandem Mass Spectrometry (UPLC-MS/MS). A total of 1,156 metabolites were identified by UPLC-MS/MS, of which 345 differential metabolites were mainly enriched in phenylpropanoid/phenylalanine, flavone and flavonol biosynthesis. The pseudobulbs make up nearly half of the fresh weight of the whole plant, and the GAS content in the pseudobulbs was also the highest in four tissues. Up to 23,105 Unigenes were obtained and 22,029 transcripts were annotated in the transcriptome analysis. Compared to roots, 7,787, 8,376 and 9,146 differentially expressed genes (DEGs) were identified in rhizomes, pseudobulbs and leaves, respectively. And in total, 80 Unigenes encoding eight key enzymes for GAS biosynthesis, were identified. Particularly, glycosyltransferase, the key enzyme of the last step in the GAS biosynthetic pathway had 39 Unigenes candidates, of which, transcript28360/f2p0/1592, was putatively identified as the most likely candidate based on analysis of co-expression, phylogenetic analysis, and homologous searching. The metabolomics and transcriptomics of pseudobulbs versus roots showed that 8,376 DEGs and 345 DEMs had a substantial association based on the Pearson’s correlation. This study notably enriched the metabolomic and transcriptomic data of P. chinensis, and it provides valuable information for GAS biosynthesis in the plant.

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“…TBI induces activation of the NLRP3 inflammasome in neurons, astrocytes, and microglia in the cortex, and activated caspase-1 promotes cleavage of pro-interleukin (IL)-1β, pro-IL-18, and the amino terminus of gasdermin-D (GSDMD) ( 31 ). Cleaved IL-1β, IL-18, and GSDMD ultimately cause cell pyroptosis, which is accompanied by the release of pro-inflammatory cytokines ( 32 , 33 ). Numerous studies have demonstrated that knockout or pharmacologic inhibition of the NLRP3 inflammasome can alleviate neuroinflammation and improve neurological outcomes after brain injury ( 34 – 36 ).…”

Section: Traumatic Brain Injury and Neuroinflammationmentioning

confidence: 99%

Neuroinflammation of traumatic brain injury: Roles of extracellular vesicles

Liu

Zhang²,

Cao³

et al. 2023

Front. Immunol.

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Traumatic brain injury (TBI) is a major cause of neurological disorder or death, with a heavy burden on individuals and families. While sustained primary insult leads to damage, subsequent secondary events are considered key pathophysiological characteristics post-TBI, and the inflammatory response is a prominent contributor to the secondary cascade. Neuroinflammation is a multifaceted physiological response and exerts both positive and negative effects on TBI. Extracellular vesicles (EVs), as messengers for intercellular communication, are involved in biological and pathological processes in central nervous system (CNS) diseases and injuries. The number and characteristics of EVs and their cargo in the CNS and peripheral circulation undergo tremendous changes in response to TBI, and these EVs regulate neuroinflammatory reactions by activating prominent receptors on receptor cells or delivering pro- or anti-inflammatory cargo to receptor cells. The purpose of this review is to discuss the possible neuroinflammatory mechanisms of EVs and loading in the context of TBI. Furthermore, we summarize the potential role of diverse types of cell-derived EVs in inflammation following TBI.

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Gastrodin suppresses pyroptosis and exerts neuroprotective effect in traumatic brain injury model by inhibiting NLRP3 inflammasome signaling pathway

Cited by 21 publications

References 23 publications

Human umbilical cord mesenchymal stem cell‐derived exosome suppresses programmed cell death in traumatic brain injury via PINK1/Parkin‐mediated mitophagy

Human umbilical cord mesenchymal stem cell‐derived exosome suppresses programmed cell death in traumatic brain injury via PINK1/Parkin‐mediated mitophagy

The gastrodin biosynthetic pathway in Pholidota chinensis Lindl. revealed by transcriptome and metabolome profiling

Neuroinflammation of traumatic brain injury: Roles of extracellular vesicles

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