Figure - available from: Applied Biochemistry and Biotechnology
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Representative light microphotographs (40 ×) of corpus striatum region of brain stained with H&E of a control, b NAC-treated, c MCP-treated and d NAC + MCP-treated. The figure shows neurodegeneration with pyknotic nuclei and degeneration associated with gliosis (arrowhead), neuropil vacuolation (asterisk) and distorted and darkly stained neurons (arrow)
Source publication
Monocrotophos (MCP) is systemic organophosphate insecticide used against crop pests. It is reported to cause mammalian toxicity through both acute and chronic exposure. In the present study, we have shown the protective role of N-acetylcysteine (NAC) against MCP-induced oxidative stress in frontal cortex, corpus striatum and hippocampus brain regio...
Citations
... N-acetylcysteine (NAC); a thiol amino acid, was reported to act as a free radicals scavenger, to replenish brain tissue glutathione (GSH) content and to inhibit neuronal lipid peroxidation (Samuni et al., 2013;Dhillon et al., 2022). Moreover, NAC is reported to possess neurovascular-protective effects that have a positive effect in neurological disorders treatment via the NAC-induced downregulation of oxidative stress and inflammatory cascades (Bavarsad-Shahripour et al., 2014;Bhatti et al., 2018) in experimental cisplatin-induced neurotoxicity (Abdel-Wahab & Moussa, 2019). ...
Neonatal hypoxic-ischemic brain damage (HIBD) is a prominent contributor to both immediate mortality and long-term impairment in newborns. The elusive nature of the underlying mechanisms responsible for neonatal HIBD presents a significant obstacle in the effective clinical application of numerous pharmaceutical interventions. This comprehensive review aims to concentrate on the potential neuroprotective agents that have demonstrated efficacy in addressing various pathogenic factors associated with neonatal HIBD, encompassing oxidative stress, calcium overload, mitochondrial dysfunction, endoplasmic reticulum stress, inflammatory response, and apoptosis. In this review, we conducted an analysis of the precise molecular pathways by which these drugs elicit neuroprotective effects in animal models of neonatal hypoxic-ischemic brain injury (HIBD). Our objective was to provide a comprehensive overview of potential neuroprotective agents for the treatment of neonatal HIBD in animal experiments, with the ultimate goal of enhancing the feasibility of clinical translation and establishing a solid theoretical foundation for the clinical management of neonatal HIBD.
