Transplantation of neural stem cells (NSCs) in the injured spinal cord has been shown to improve functional outcome. However, the influence of NSCs transplantation on the sensory function and analgesic behaviors has not been elucidated yet. Here, we investigated whether transplanted NSCs would improve sensory function in rats subjected to complete cord transection (T10) and explore the underlying mechanism. The rats were divided into sham, SCT (spinal cord transection), and NSC implanted groups. NSCs (3 × 10(6)/ml) were implanted into injury site at the day after operation. Mechanical (the hind paw test) and thermal (the tail-flick test) were measured at 5 weeks. Immunohistochemistry and RT-PCR were used to demonstrate that expression of Brain-derived neurotrophic factor (BDNF) in the superficial of the dorsal horn. Consequently, the tail-flick latencies and paw withdrawal thresholds in NSC implanted group exhibit a significant higher than SCT group (P < 0.05). RT-PCR demonstrate that mRNA expression of BDNF was down-regulated remarkably in NSC engrafted rats. The present findings suggest that NSC transplantation inhibits neuropathic pain associated with BDNF down-regulation.
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Mol Cell Probes
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Department of Urology Surgery, Lanzhou University Second Hospital, Lanzhou, 730030, China; Department of Microbiome Laboratory, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, 450003, China. Electronic address:
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Department of Pain Management, Qilu Hospital of Shandong University, 107# West Wenhua Road, Jinan, Shandong 250012, China. Electronic address:
This investigation represents a pioneering effort to examine the therapeutic effects of PCB specifically in the context of CFA-induced mice, as well as to elucidate the underlying mechanisms that facilitate such effects. Our study utilized advanced methodologies, namely high-performance liquid chromatography coupled with mass spectrometry (HPLC-MS)-based metabolomics, alongside comprehensive multivariate data analysis, to identify a distinctive metabolic profile associated with acute inflammation. Through our analyses, we discovered that several potential metabolites were significantly implicated in a variety of critical metabolic pathways.
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Maj Institute of Pharmacology, Polish Academy of Sciences, Department of Neurochemistry, 12 Smetna Str., Krakow 31-343, Poland. Electronic address:
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Department of Medical Neuroscience, Dalhousie University, Halifax, NS B3H 4R2, Canada. Electronic address:
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Department of Physical Therapy, Ibaraki Prefectural University of Health Sciences, Ibaraki, Japan.
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