4/6/2023 0 Comments Actdec pdf plus 150The objective of this study was to identify brain damage caused by uremic toxicity and determine the protective effects of ω-3 PUFA against uremic toxin. Additionally, omega-3 polyunsaturated fatty acid (ω-3 PUFA) plays an important role in maintaining normal nerve function, but its protective effects against uremic toxin is unclear. We also provide suggestions on how to modulate the inflammation and discuss key therapeutic approaches leading to better functional outcome after SCI.Īlthough the cause of neurological disease in patients with chronic kidney disease (CKD) has not been completely identified yet, recent papers have identified accumulated uremic toxin as its main cause. Finally, the review highlights the time-dependent transformation of reactive microglia and astrocytes into their neuroprotective phenotypes (M2a, M2c and A2) which are crucial for spontaneous post-SCI locomotor recovery. In addition, temporal correlation in progressive degeneration of neurons and astrocytes and their functional interactions after SCI are discussed. anti-inflammatory) in individual cell phenotypes (microglia, astrocytes, blood inflammatory cells) in acute and subacute SCI stages, and how they contribute to delayed neuronal death in the surrounding spinal cord tissue which is spared and functional but reactive. Here we review current information about the release of diverse signaling molecules (pro-inflammatory vs. Conversely, astrocytes have the potency to trigger microglial activation and control their cellular functions. Recently published data indicate that microglia induces astrocyte activation and determines the fate of astrocytes. It is driven by the immediate response of macrophages and microglia, which triggers activation of genes responsible for the dysregulated microenvironment within the lesion site and in the spinal cord parenchyma immediately adjacent to the lesion. Traumatic spinal cord injury (SCI) elicits an acute inflammatory response which comprises numerous cell populations. Taken together, our results suggested that omega-3 fatty acid supplementation reduced oxidative stress, apoptosis, and the levels of inflammatory markers in ischemia-reperfusion-induced rats. Omega-3 fatty acid supplementation decreased caspase-3 and p53 protein expression by >30%. Omega-3 fatty acid supplementation decreased p53, caspase-3, bax, and pro-NGF mRNA expression by >40%, while the level of bcl-2 mRNA expression was increased by 286.9%. Caspase-3, p53, bax, and pro-NGF mRNA expression levels were increased by 1.3-, 1.4-, 1.2-, and 0.9-fold, respectively, whereas bcl-2 mRNA expression was decreased by 0.77-fold in control rats. TNF-α and IL-6 mRNA expression were reduced. Omega-3 fatty acid supplementation decreased tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels by >50%. The levels of oxidative, apoptotic, and inflammatory markers were examined in each of these groups.Īltered lipid peroxidation, reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (Gpx), and catalase were normalized. The rats were classified into sham, control, spinal cord injury plus 50 mg/kg Omega-3 fatty acids and spinal cord injury plus 100 mg/kg Omega-3 fatty acids. In this study, the effects of omega-3 fatty acids were examined in a rat model of spinal cord injury.
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