Ginsenoside Rb1 (GRb1), a major ingredient of ginseng, has been found to be a potential protective agent in spinal cord injury (SCI) and in activated microglia-induced neuronal injury. This study discovered that GRb1 could facilitate miR-130b-5p expression in SCI rats and Toll-like receptor 4 (TLR4; a crucial player in inflammation) was a potential target of miR-130b-5p. Hence, we further investigated whether GRb1 could relieve SCI by reducing microglia-mediated inflammatory responses and neuronal injury via miR-130b-5p/TLR4 pathways. The results showed that GRb1 alleviated SCI through inhibiting neuronal apoptosis and proinflammatory factor expression via increasing miR-130b-5p.GRb1 weakened the damage of activated microglia to neurons through upregulating miR-130b-5p. miR-130b-5p attenuated activated microglia-induced neuron injury via targeting TLR4. GRb1 inactivated TLR4/nuclear factor-κB (NF-κB) activation and inhibited proinflammatory cytokine secretion by increasing miR-130b-5p in activated microglia. As a conclusion, GRb1 alleviated SCI through reducing activated microglia-induced neuronal injury via miR-130b-5p/TLR4/NF-κB axis, providing a deep insight into the molecular basis of GRb1 in the treatment of SCI.

Download full-text PDF

Source
http://dx.doi.org/10.1002/jcp.30001DOI Listing

Publication Analysis

Top Keywords

activated microglia-induced
12
neuronal injury
12
ginsenoside rb1
8
spinal cord
8
cord injury
8
microglia-induced neuronal
8
sci reducing
8
grb1 alleviated
8
alleviated sci
8
activated microglia
8

Similar Publications

Role of NRF2 in Pathogenesis of Alzheimer's Disease.

Antioxidants (Basel)

December 2024

Department of Biochemistry and Molecular Biology, Tohoku Medical Megabank Organization, Tohoku University, Sendai 980-8573, Japan.

Alzheimer's disease (AD) is a polygenic, multifactorial neurodegenerative disorder and remains the most prevalent form of dementia, globally. Despite decades of research efforts, there is still no effective cure for this debilitating condition. AD research has increasingly focused on transcription factor NRF2 (nuclear factor erythroid 2-related factor 2) as a potential therapeutic target.

View Article and Find Full Text PDF

Purpose: This study aims to explore the neuroprotective effect of propofol in improving traumatic brain injury (TBI) by inhibiting ferroptosis through the modulation of the endothelial nitric oxide (NO) synthase (eNOS)/NO signaling pathway.

Methods: The GSE173975 dataset was used to analyze the differentially expressed genes between TBI and sham surgery control groups in the short and long term. A TBI model was established in 2-month-old male SPF C57BL/6 mice by impact exposure of the exposed dura mater.

View Article and Find Full Text PDF

Microglial Nrf2-mediated lipid and iron metabolism reprogramming promotes remyelination during white matter ischemia.

Redox Biol

December 2024

Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, PR China; Hubei Key Laboratory of Neural Injury and Functional Reconstruction, Huazhong University of Science and Technology, Wuhan, 430030, PR China; Key Laboratory of Vascular Aging, Ministry of Education, Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, PR China. Electronic address:

Background: Oxidative stress and microglial activation are critical pathomechanisms in ischemic white matter injury. Microglia, as resident immune cells in the brain, are the main cells undergoing oxidative stress response. However, the role and molecular mechanism of oxidative stress in microglia have not been clearly elucidated during white matter ischemia.

View Article and Find Full Text PDF

Roles of 4'--Methylalpinum Isoflavone on Activation of Microglia Induced by Oxysterols.

Int J Mol Sci

November 2024

Department of Pharmacology, School of Medicine, Pusan National University, Yangsan 50612, Gyeongnam, Republic of Korea.

Microglia play a crucial role as immune cells responsible for the brain's defense mechanisms. Similar to the actions of macrophages in the body, microglial cells elicit an inflammatory immune response in the brain. Recent papers highlight activated microglial cells as pivotal contributors to inflammatory responses in the brain, leading to damage to nerve tissue and the onset of Alzheimer's disease (AD).

View Article and Find Full Text PDF

Piperine attenuates cancer-associated pain induced by microglial activation via increasing miR-150-50p.

Aging (Albany NY)

November 2024

Institute of Oncology, The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing 210023, Jiangsu, China.

Aim: Severe painful neuropathy often occurs in cancer patients receiving chemotherapy. Emerging evidence has demonstrated that microglia contribute to the occurrence and development of cancer-associated pain. This study aimed to investigate the mechanisms by which piperine influences cancer-associated pain induced by microglia activation.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!