Activation of Sirtuin-1 by Pinocembrin Treatment Contributes to Reduced Early Brain Injury after Subarachnoid Hemorrhage

Zeng, Yile; Fang, Zhongning; Lai, Jinqing; Wu, Zhe; Lin, Wei-Jen; Yao, Hao; Hu, Weipeng; Chen, Junyan; Guo, Xieli; Chen, Xiangrong

doi:10.1155/2022/2242833

Cited by 10 publications

(4 citation statements)

References 54 publications

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“…A lower score suggests more severe deficits. To further evaluate the motor deficits after SAH, the beam-balance score test was performed according to previous studies ( 6 ). Behavior functions were recorded in a blinded manner.…”

Section: Methodsmentioning

confidence: 99%

“…SAH involves a variety of pathogenic mechanisms. A considerable number of preclinical and clinical studies have observed that the early robust neuroinflammation might explain the poor outcome after SAH ( 2 – 6 ). Microglia, the primary innate immune cells in the brain, plays a critical role in immune response.…”

Section: Introductionmentioning

confidence: 99%

“…early robust neuroinflammation might explain the poor outcome after SAH (2)(3)(4)(5)(6). Microglia, the primary innate immune cells in the brain, plays a critical role in immune response.…”

mentioning

confidence: 99%

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LDC7559 inhibits microglial activation and GSDMD-dependent pyroptosis after subarachnoid hemorrhage

Cai¹,

Lai

et al. 2023

Front. Immunol.

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Mounting evidence indicates that inhibition of microglial activation and neuronal pyroptosis plays important roles in brain function recovery after subarachnoid hemorrhage (SAH). LDC7559 is a newly discovered gasdermin D (GSDMD) inhibitor. Previous studies have demonstrated that LDC7559 could inhibit microglial proliferation and pyroptosis. However, the beneficial effects of LDC7559 on SAH remain obscure. Based on this background, we investigated the potential role and the mechanism of LDC7559 on SAH-induced brain damage both in vivo and in vitro. The findings revealed that microglial activation and neuronal pyroptosis were evidently increased after SAH, which could be markedly suppressed by LDC7559 both in vivo and in vitro. Meanwhile, LDC7559 treatment reduced neuronal apoptosis and improved behavior function. Mechanistically, LDC7559 decreased the levels of GSDMD and cleaved GSDMD after SAH. In contrast, nod-like receptor pyrin domain-containing 3 (NLRP3) inflammasome activation by nigericin increased GSDMD-mediated pyroptosis and abated the beneficial effects of LDC7559 on SAH-induced brain damage. However, LDC7559 treatment did not significantly affect the expression of NLRP3 after SAH. Taken together, LDC7559 might suppress neuronal pyroptosis and microglial activation after SAH by inhibiting GSDMD, thereby promoting brain functional recovery.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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LDC7559 inhibits microglial activation and GSDMD-dependent pyroptosis after subarachnoid hemorrhage

Cai¹,

Lai

et al. 2023

Front. Immunol.

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“…26 Treatment of pinocembrin (flavanone) regulates early brain injury after subarachnoid hemorrhage by modulation of SIRT1. 27 Interestingly, SIRT1 is found to mediate several important key targets via deacetylation, including p53 and NF-ΚB. 28 SIRT1 represses inflammatory response through deacetylation of p65 subunit and inhibiting NF-kB activity.…”

Section: Dhk Modulated Infantile Pneumonia Via Sirt1/ Nf-κb Pathwaymentioning

confidence: 99%

Dihydrokaempferol attenuates LPS-induced inflammation and apoptosis in WI-38 cells

Wang,

Zhang,

Pang

2023

Allergol Immunopathol

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Background: Globally, pneumonia has been associated as a primary cause of mortality in children aged less than 5 years. Dihydrokaempferol (DHK) has been proposed for being correlated with the process of various diseases. Nevertheless, whether DHK has a role in the progression of infantile pneumonia remains unclear. This study aimed at exploring whether DHK was involved in the progression of infantile pneumonia. Methods: Human fibroblast cells WI-38 were treated with lipopolysaccharide (LPS). The viability of WI-38 cells was measured via Cell counting kit-8. Reverse transcription-quantitative polymerase chain reaction was used to evaluate the levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α). Western blot analysis revealed the protein levels of IL-1β, IL-6, TNF-α, Bax, and cleaved-caspase 3. Flow cytometry was applied for exploring the apoptosis of WI-38 cells. The concentrations of IL-1β, IL-6, and TNF-α were assessed via enzyme-linked-immunosorbent serologic assay. Results: DHK modulated the viability of WI-38 cells in infantile pneumonia. Furthermore, we identified that DHK treatment inversely changed LPS induction-mediated elevation on the levels of inflammation biomarkers. Besides, DHK counteracted LPS-induced production of reactive oxygen species (ROS) in WI-38 cells. DHK also decreased LPS-induced elevation of WI-38 cells apoptosis and mediated the levels of apoptosis-associated indexes. Moreover, modulating sirtuin-1 (SIRT1) protein level was lowered by the induction of LPS, and was reversed by DHK treatment. In addition, DHK counteracted LPS induction-mediated elevation of p-p65 and phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha (p-IκBα) protein levels. Conclusion: DHK alleviated LPS-induced WI-38 cells inflammation injury in infantile pneumonia through SIRT1/NF-κB pathway. The results shed light on the implications of DHK on the prevention and treatment of infantile pneumonia.

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Mechanisms of radiation‐induced tissue damage and response

Zhou,

Zhu,

Liu

et al. 2024

MedComm

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Radiation‐induced tissue injury (RITI) is the most common complication in clinical tumor radiotherapy. Due to the heterogeneity in the response of different tissues to radiation (IR), radiotherapy will cause different types and degrees of RITI, which greatly limits the clinical application of radiotherapy. Efforts are continuously ongoing to elucidate the molecular mechanism of RITI and develop corresponding prevention and treatment drugs for RITI. Single‐cell sequencing (Sc‐seq) has emerged as a powerful tool in uncovering the molecular mechanisms of RITI and for identifying potential prevention targets by enhancing our understanding of the complex intercellular relationships, facilitating the identification of novel cell phenotypes, and allowing for the assessment of cell heterogeneity and spatiotemporal developmental trajectories. Based on a comprehensive review of the molecular mechanisms of RITI, we analyzed the molecular mechanisms and regulatory networks of different types of RITI in combination with Sc‐seq and summarized the targeted intervention pathways and therapeutic drugs for RITI. Deciphering the diverse mechanisms underlying RITI can shed light on its pathogenesis and unveil new therapeutic avenues to potentially facilitate the repair or regeneration of currently irreversible RITI. Furthermore, we discuss how personalized therapeutic strategies based on Sc‐seq offer clinical promise in mitigating RITI.

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Activation of Sirtuin-1 by Pinocembrin Treatment Contributes to Reduced Early Brain Injury after Subarachnoid Hemorrhage

Cited by 10 publications

References 54 publications

LDC7559 inhibits microglial activation and GSDMD-dependent pyroptosis after subarachnoid hemorrhage

LDC7559 inhibits microglial activation and GSDMD-dependent pyroptosis after subarachnoid hemorrhage

Dihydrokaempferol attenuates LPS-induced inflammation and apoptosis in WI-38 cells

Mechanisms of radiation‐induced tissue damage and response

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