Prenatal exposure to opioids such as morphine poses significant risks to fetal neurodevelopment, particularly in brain regions critical for cognition, such as the hippocampus. Despite the prescription Show more
Prenatal exposure to opioids such as morphine poses significant risks to fetal neurodevelopment, particularly in brain regions critical for cognition, such as the hippocampus. Despite the prescription and use of opioids during pregnancy, the molecular and histological consequences of such exposure remain insufficiently explored. To evaluate the effects of short-term prenatal morphine exposure on the expression of key neurodevelopmental genes and the structural integrity of the hippocampus in neonatal rats. Pregnant Sprague Dawley rats were administered intraperitoneal injections of morphine sulfate (10 mg/kg) on gestational days 15 and 16. On postnatal day 12, offspring (n = 6 per group) were euthanized, and their hippocampal tissues were collected. Quantitative real-time PCR was performed to assess the expression levels of neurodevelopmental genes, including MDH2, Neurog1, and BDNF. Histological evaluations were conducted using hematoxylin and eosin and cresyl violet staining to assess cellular architecture and neuronal viability. Immunohistochemical staining for GFAP, S100, and synaptophysin was used to evaluate astrocytic integrity and synaptic density. The morphine-exposed group showed significant up-reglation of MDH2, Neurog1, and BDNF ( Prenatal morphine exposure leads to marked molecular and histopathological changes in the developing hippocampus, suggesting long-term risks for neurocognitive dysfunction. These findings emphasize the importance of limiting opioid use during pregnancy and identifying molecular targets for future therapeutic interventions. Show less
The aim of this study was to consider the expression of farnesoid X receptor (Fxr), liver X receptor (LXRα) and sirtuin 1 (Sirt1), oxidative stress, inflammation, apoptosis, and the protective role of Show more
The aim of this study was to consider the expression of farnesoid X receptor (Fxr), liver X receptor (LXRα) and sirtuin 1 (Sirt1), oxidative stress, inflammation, apoptosis, and the protective role of N-acetylcysteine (NAC) in the liver of rats treated with cadmium (Cd). 30 Wistar rats were divided into 5 groups: G1 (control), G2 (single dose of Cd), G3 (continuous dose of Cd), G4 (single dose of Cd + continuous dose of NAC), and G5 (continuous dose of Cd + continuous dose of NAC). The apoptosis of hepatic cells was measured using the TUNEL assay. Levels of malondialdehyde (MDA), IL-10, TNF-α, and total antioxidant capacity (TAC) were measured by specific kits. The expression of Fxr, LXRα, and Sirt1 genes and ratio of Bax/Bcl2 was considered using RT-PCR. While NAC treatment improved TAC and IL-10 values, it decreased MDA and TNF-α levels in the liver of rats exposed to Cd (P < 0.001). NAC decreased Bax/Bcl2 in the liver of G4 and G5 groups (P < 0.001). Exposure to a continuous dose of Cd decreased Fxr, LXRα, and Sirt1 expression by 36.65- (P < 0.001), 12.52- (P < 0.001) and 11.34-fold (P < 0.001) compared to control, respectively. NAC increased Fxr, LXRα, and Sirt1 expression (P < 0.01) and decreased Cd concentrations in both serum and tissue samples in G4 and G5 groups. Our results suggested that NAC protects liver tissue against Cd toxicity by elevating antioxidant capacity, mitigating oxidative stress, inflammation, apoptosis and up-regulation of FXR, LXR, and SIRT1 genes. Show less