Publications by authors named "Qiu-Li He"
Microglia-mediated neuroinflammation has been shown to exert an important effect on the progression of a growing number of neurodegenerative disorders. Prolonged exposure to detrimental stimuli leads to a state of progressive activation and aging-related features in microglia (also termed as senescent microglia). However, the mechanisms by which senescent microglia contribute to neuroinflammation-induced cognitive dysfunction remain to be elucidated.
View Article and Find Full Text PDFNeuroinflammation is one of crucial pathogenic mechanisms underlying Alzheimer's disease, sepsis-associated encephalopathy, and postoperative cognitive dysfunction. These diseases or conditions are often accompanied by typical clinical manifestations of cognitive impairments, including impaired learning and memory but underlying mechanisms are unknown. Hence, effective treatments are not available.
View Article and Find Full Text PDFSleep is pivotal to memory consolidation, and sleep deprivation (SD) after learning can impede this process, leading to memory disorders. In the present study, we aimed to explore the effects of acute sleep deprivation (ASD) on memory disorders and the underlying mechanisms. ASD model was induced by subjecting the mice to 6 h of SD following fear conditioning training.
View Article and Find Full Text PDFArticle Synopsis
- Neuroinflammation involves activating glial cells and significantly influences cognitive impairment in central nervous system disorders, although the details of these mechanisms are not fully understood.
- The study investigated the role of perineuronal nets (PNNs) and the ApoE gene in this process, using a model of neuroinflammation induced by lipopolysaccharides (LPS) while assessing cognitive function through various tests.
- Results indicated that LPS treatment led to cognitive deficits due to reduced PNNs and altered neural oscillations, highlighting that microglial phagocytosis of PNNs, influenced by ApoE, is crucial to understanding neuroinflammation-related cognitive decline.
Article Synopsis
- Bone cancer pain (BCP) is a significant medical issue with limited research on its underlying mechanisms, particularly regarding the role of the Nrf2 protein.
- This study hypothesizes that BCP causes Nrf2 to move from the cytoplasm to the nucleus, promoting the expression of heme oxygenase-1 (HO-1) and inhibiting the inflammatory NF-κB pathway.
- The results indicate that increased nuclear Nrf2 expression reduces pain sensitivity and neuroinflammation through the activation of HO-1 and suppression of NF-κB, suggesting a potential therapeutic target for BCP management.
Phosphoproteomic profiling of oxycodone‑treated spinal cord of rats with cancer‑induced bone pain.
Mol Med Rep
November 2019
Treatment of cancer‑induced bone pain (CIBP) is challenging in clinical settings. Oxycodone (OXY) is used to treat CIBP; however, a lack of understanding of the mechanisms underlying CIBP limits the application of OXY. In the present study, all rats were randomly divided into three groups: The sham group, the CIBP group, and the OXY group.
View Article and Find Full Text PDFArticle Synopsis
- The study focuses on the complex mechanisms behind cancer-induced bone pain (CIBP), specifically highlighting the role of glutamate receptors and the protein SAP102.
- SAP102 helps anchor glutamate receptors in neurons, but its exact impact on pain sensitivity (hyperalgesia) in CIBP had not been previously understood.
- Experimental results show that reducing SAP102 levels in spinal neurons can significantly decrease abnormal pain responses in rats with CIBP, suggesting SAP102's crucial involvement in pain mechanisms related to bone cancer.