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Danshenol B alleviates central post-stroke pain by regulating PIK3CG/NLRP3 signaling pathway

ABSTRACT: Danshenol B alleviates central post-stroke pain by regulating PIK3CG/NLRP3 signaling pathway

PROVIDER: PRJNA1181879 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR31221191_1.fastq.gz	Fastqsanger.gz
	SRR31221191_2.fastq.gz	Fastqsanger.gz
	SRR31221195_1.fastq.gz	Fastqsanger.gz
	SRR31221195_2.fastq.gz	Fastqsanger.gz

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Danshenol B alleviates central post-stroke pain by regulating PIK3CG/NLRP3 signaling pathway

Project description:Background: Central post-stroke pain (CPSP) severely impairs quality of life and is challenging to manage, potentially leading to self-harm or suicide. Although Compound Salvia miltiorrhiza (Danshen) is effective against neuropathic pain, its specific active components and mechanisms remain unclear. Study design and methods: We established a CPSP mouse model and performed RNA sequencing on the ipsilateral Ventral posterolateral thalamic nucleus and Ventral posteromedial thalamic nucleus (VPL/VPM) to identify differentially expressed genes (DEGs). DEGs were analyzed through network pharmacology and molecular docking to assess interactions with 42 Danshen components. We evaluated the effects of varying Danshenol B concentrations, administered daily into the VPL/VPM, on CPSP. Changes in PIK3CG and NLRP3 were monitored to determine Danshenol B’s analgesic effects. Additionally, we overexpressed and knocked down PIK3CG to examine its role in CPSP and assessed NLRP3 to explore if it acts downstream of PIK3CG. Results: In the CPSP model, 409 DEGs were identified in the VPL/VPM, involved in pathways like signal transduction and NOD-like receptor signaling. Network pharmacology linked 21 Danshen components to 11 DEGs. Molecular docking showed strong binding affinities (≤ −7.00 kcal/mol) between four Danshen components—tanshinaldehyde, sclareol, MOL007155, and Danshenol B—and proteins including BTK, CASP1, MMP9, and PIK3CG. Danshenol B (0.5 μM) significantly alleviated CPSP and reduced PIK3CG and NLRP3 protein. PIK3CG overexpression increased NLRP3 and counteracted Danshenol B’s effects, while its knockdown induced CPSP and reduced NLRP3 expression. Conclusion: Danshenol B alleviates CPSP by suppressing the PIK3CG/NLRP3 signaling pathway, clarifying its therapeutic mechanism, and highlighting its potential in analgesic drug development.

2025-06-25 | GSE281041 | GEO

TMAO promotes NLRP3 inflammasome activation of microglia aggravating neurological injury in stroke through FTO/IGF2BP2

Project description:Stroke is a kind of cerebrovascular disease with high mortality. TMAO has been shown to aggravate stroke outcomes, but its mechanism remains unclear. Mice were treated with TMAO in normal saline by oral gavage for 14 consecutive days. Then, mice were made into MCAO models. Neurological score, infarct volume, neuronal damage and markers associated with inflammation were assessed. Since microglia played a crucial role in stroke, microglia of MCAO mice were isolated for high-throughput sequencing to identify the most differentially expressed gene following TMAO treatment. Afterward, the downstream pathways of TMAO were investigated using primary microglia. Our results demonstrated that TMAO promoted the release of inflammatory cytokines in the brain of MCAO mice and promoted the activation of OGD/R microglial inflammasome, thereby exacerbating stroke outcomes. FTO/IGF2BP2 inhibited NLRP3 inflammasome activation in OGD/R microglia by downregulating the m6A level of NLRP3, TMAO can inhibit the expression of FTO and IGF2BP2, thus promoting the activation of NLRP3 inflammasome in OGD/R microglia. In conclusion, these results demonstrated that TMAO promotes NLRP3 inflammasome activation of microglia aggravating neurological injury in stroke through FTO/IGF2BP2.

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Therapeutic Interrupting C/EBPβ-Clec7a Cross-talk-mediated NLRP3 Inflammasome-dependent Pyroptosis for Relieving Neuropathic Pain

Project description:Neuropathic pain (NP) is a complex chronic pain due to the nervous system damage or diseases.During NP development and progression, the neuroinflammation has been observed along the pain pathways from the spinal cord to the thalamus and the parietal cortex. It may be caused by the activation of glial cells, especially microglia, with production of cytokines and other inflammatory mediators within the central nervous system (CNS), especially in spinal cord. In this study, we used high-throughput RNA-seq technology to detect the global gene expression in spinal cord of rats in sham group and CCI model group(an animal model of neuropathic pain), and the differentially expressed genes between diseases and control group were obtained.Significant differentially expressed genes (DEGs) of the Sham vs. CCI groups were identified using the criteria of a fold change>1.5 and P value <0.05. Finally, we focused on C/EBPβ-Clec7a Cross-talk-mediated NLRP3 Inflammasome-dependent Pyroptosis pathway and further studied its role in neuropathic pain.

2021-10-28 | GSE186237 | GEO

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Normalization of cholesterol metabolism in spinal microglia alleviates neuropathic pain

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Effective control of neuropathic pain by interrupting C/EBPβ-CLEC7A cross-talk-mediated NLRP3 inflammasome-dependent pyroptosis

2021-10-05 | GSE185278 | GEO

Morphine alleviates pain after heart cryonjury in zebrafish without impeding regeneration

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Central nervous system-associated macrophages modulate the immune response following stroke in aged mice

Project description:To study the differential role of central nervous system-associated macrophages (CAMs) in neuroinflammation after stroke between young and aged mice, we FACS sorted CD3-CD11b+CD45+CD206+ CAMs from brains of C57BL/6 mice aged 2 months (young) and 18 months (old)

2024-05-22 | GSE267623 | GEO

Genome-wide CRISPR/Cas9 knockout screen for novel regulators of mechanical stress on NLRP3 inflammasome activation

Project description:Immune cells sense the microenvironment to fine-tune their inflammatory responses. Patients with cryopyrin associated periodic syndrome (CAPS), caused by mutations in the NLRP3 gene, present auto-inflammation and its manifestation is largely dependent on environmental cues. However, the underlying mechanisms are poorly understood. Here, we uncover that KCNN4, a calcium-activated potassium channel, links PIEZO-mediated mechanotransduction to NLRP3 inflammasome activation. Yoda1, a PIEZO1 agonist, lowers the threshold for NLRP3 inflammasome activation. PIEZO-mediated sensing of stiffness and shear stress increases NLRP3-dependent inflammation. Myeloid-specific deletion of PIEZO1/2 protects mice from gouty arthritis. Activation of PIEZO1 triggers calcium influx, which activates KCNN4 to evoke potassium efflux promoting NLRP3 inflammasome activation. Activation of PIEZO signaling is sufficient to activate the inflammasome in cells expressing CAPS-causing NLRP3 mutants via KCNN4. Finally, pharmacologic inhibition of KCNN4 alleviates auto-inflammation in CAPS patient cells and in CAPS-mimicking mice. Thus, PIEZO-dependent mechanical inputs augment inflammation in NLRP3-dependent diseases including CAPS.

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Macrophage depletion alleviates pain-related behaviors in osteoarthritic mice

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2024-09-13 | GSE246252 | GEO

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