====== Experimental spinal cord injury treatment ======

Cui et al. from the Department of Neurosurgery Department of Pathology, Baoding First Central Hospital, [[Baoding]], Hebei Province, China evaluated the neuroprotective [[efficacy]] of [[fisetin]] against the [[experimental model of spinal cord injury]] (SCI).

SCI was induced in male [[Sprague Dawley rat]]s by placing an aneurysm [[clip]] [[extradural]]. [[Rat]]s were treated either with vehicle or fisetin for 28 days after SCI.

Treatment with fisetin significantly attenuated SCI-induced alternations in mechano-tactile and thermal allodynia, hyperalgesia, and nerve conduction velocities. SCI-induced upregulated [[TNFα]], [[interleukin]]s, inducible [[nitric oxide synthase]], [[cox-2]], [[Bcl-2]]-associated X protein and [[caspase 3]] mRNA expressions in the spinal cord and these were markedly reduced by fisetin. Spinal [[nuclear factor kappa]] B and nuclear factor of kappa light polypeptide gene enhancer in [[B-cell]]s inhibitor-alpha protein levels were also significantly downregulated by fisetin. Hematoxylin and eosin staining of the [[spinal cord]] suggested that fisetin significantly ameliorated histological aberrations such as neuronal degeneration, necrosis, and inflammatory infiltration induced in it.

Fisetin exerts [[neuroprotection]] via modulation of nuclear factor kappa B/nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha pathway by inhibiting release of inflammatory mediators (inducible nitric oxide synthase and cyclooxygenase-II), proinflammatory cytokines (tumor necrosis factor-alpha and interleukins), apoptotic mediators (Bcl-2-associated X protein and caspase-3)
((Cui J, Fan J, Li H, Zhang J, Tong J. Neuroprotective potential of fisetin in an experimental model of spinal cord injury: via modulation of NF-κB/IκBα pathway. Neuroreport. 2021 Jan 18. doi: 10.1097/WNR.0000000000001596. Epub ahead of print. PMID: 33470764.)).