investigation effect of ethanol on the structure of Kupffer cells in the liver of male pups of rats during pregnancy and lactation

Alcohol consumed by the mother can pass through the placenta without delay and may affect the fetus immediately and spread rapidly to any body water chamber such as neurons or lipid membranes, and the baby genotype is most likely related to the baby's alcohol consumption. It is after birth. Like other organs, the liver is exposed to intrauterine ethanol. However, little is known about the effect of maternal ethanol exposure on the developing liver. Previous studies have shown that ethanol exposure during pregnancy leads to liver fibrosis and fat degradation by testing abnormal liver function in children with FASD. Blood alcohol concentrations in the fetus are comparable to those in the mother. Alcohol metabolism in pregnant mice increases fetal alcohol and fetal toxicity. Kupffer cells (KCs) are hepatic macrophages that reside in the sinusoids and make up 15% of the hepatocytes and 50% of the macrophages that reside in the body. KC originates in fetal yolk sac precursors and their self-development depends on GM-CSF and M-CSF. Some data suggest that Kupffer cells or their lineage may play a role in erythrocyte maturation during fetal liver hematopoiesis. Have . Deficiency of Kupffer cells in rats after partial hepatectomy (PH) leads to delayed liver regeneration. In the absence of Kupffer cells, there is a decrease in the secretion of TNF-α and IL-6 compared to normal liver and the delay in liver regeneration is attributed to the inactivation of NF-κB. During chronic injury, Wnt ligands are released, KC during phagocytosis can lead bipolar ancestors to liver fate. In addition, KCs play an important role in liver regeneration by affecting the aggressive behavior of liver progenitor cells.

Ethanol, liver, Kupffer cells, pregnancy,, rats