Novel, small molecule induced GABA-hATSCs for targeting of neuropathic pain.
Jee M., Im Y., Choi JI., Kang SK.
Laboratory Study on Spinal Cord Injury, published in Hum Gene Ther (2013) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Hum Gene Ther (2013)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 23473301
- DOI
- 10.1089/hum.2012.097
Abstract (original English)
Recent study showed that ROS has a crucial function during neuropathic pain development and maintenance. In this study, we suggest that a small, novel molecule, CMB-1078, can effectively induce GABAergic neuronal differentiation from human adipose tissue-derived stromal cells (hATSCs; GABA-hATSCs), which play a key role in ameliorating neuropathic pain caused by spinal cord injury. Compared to control hATSCs, the engraftment of GABA-hATSCs into animals with neuropathic pain significantly reduced secondary injury, including inflammation, GABAergic neuronal degeneration, and the circulation or propagation of proinflammatory factors cyclooxygenase2 (COX2), interlukin-1 β (IL-1β), NADPH oxidase 2 (NOX 2), NADPH oxidase 4 (NOX 4) and tumor necrosis factor α (TNFα) into the lesion. At the protein level, we also demonstrated that GABA-hATSCs engrafted into animals with neuropathic pain increased glutamic acid decarboxylase 65 (GAD65) and glutamic acid decarboxylase 67 (GAD67) expression levels. In addition, we evaluated functional pain behavior in the GABA-hATSCs- or control hATSCs-engrafted animal group, the pain in the PBS-infused animal group, and healthy animals by measuring mechanical and heat sensitivity. The pain plus GABA-hATSCs-engrafted animal groups showed paw withdrawal thresholds (PWTs) that gradually improved. In contrast, the mice with neuropathic pain did not show impr
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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