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Digestive and Metabolic Actions of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The liver has multiple functions including digestion and detoxification, and it is a key regulator of metabolism via its ability to synthesize proteins and generate and store glycogen. About 70%–85% of the liver volume is occupied by parenchymal hepatocytes. Nonparenchymal cells constitute 40% of the total number of liver cells but only 6.5% of its volume. The liver has sinusoids that are lined with two types of cells—endothelial cells and phagocytic Küpffer cells—while nonparenchymal stellate cells are located in the perisinusoidal space. The liver receives a dual blood supply from the hepatic portal vein and hepatic arteries. The portal vein delivers around 75% of the liver’s blood supply and carries venous blood from the spleen, the GI tract and associated organs. The hepatic arteries supply arterial blood to the liver, accounting for the remaining 25% of its blood flow.
The liver, gallbladder and pancreas
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Dina G. Tiniakos, Alastair D. Burt
Within the parenchyma of the liver there is a complex network of cells. Although the predominant cell type is the hepatocyte, a significant number of other cells, both resident and transitory, are important. Hepatocytes are arranged in plates, lining the blood-filled sinusoids. Sinusoidal endothelial cells are fenestrated, allowing direct access of hepatocytes to constituents of the blood. On the sinusoidal endothelial wall lie phagocytic Kupffer cells and within the perisinusoidal space of Disse are the hepatic stellate cells; these are myofibroblast precursors important in liver fibrosis (Figure 11.3). Liver-specific natural killer (NK) cells are located within the space of Disse and play an important role in the innate immune system response to viral infections. When liver cells are injured, regeneration is rapid and may be complete. Proliferation of hepatocytes can occur anywhere in the acinus, although experimental studies suggest that there is a reserve of hepatic progenitor cells close to the portal tract, within the canal of Hering, the ductular compartment connecting the bile canaliculi to the bile ductules at the limiting plate. The hepatic progenitor cells are capable of differentiating into hepatocytes and/or bile duct cells (cholangiocytes) when toxic injury or extensive hepatic necrosis precludes regeneration of mature hepatocytes.
Structural Organization of the Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
The endothelial cells are flattened and thin, and only their nuclei protrude into the sinusoidal lumen. Their cytoplasm is perforated with numerous fenestrae that are arranged in groups called sieve plates (Figure 27). The number and diameter of the fenestrae may vary according to the animal species (Fraser et al., 1986) and their localization in the hepatic lobule (Vidal-Vanaclocha and Barbera-Guillem, 1985; Wisse et al., 1985). Fenestration are larger in diameter in the periportal than in the centrolobular region, but the number of fenestrations per unit area is greater in the latter. The resulting porosity is greater in the centrolobular than in the periportal regions. The fenestrations are dynamic structures and undergo changes in their size and number in response to hormones and inhibitor of cytoskeletal fibers (Steffan et al., 1987). The neighboring endothelial cells are in contact with each other at their periphery, forming poorly defined cell contacts. As revealed in freeze-fracture preparations, these cell contacts consist of arrays of membrane particles, which remain separated from each other by particle-free intervals. This appearance probably represents an abortive form of tight junction formation, which provides mechanical adhesion without forming a permeability barrier between adjacent endothelial cells. Therefore, the only structurally open communication between the sinusoid and perisinusoidal space is through the fenestrations of endothelial cells (Yee and Revel, 1975).
Protective effect of dendropanoxide against cadmium-induced hepatotoxicity via anti-inflammatory activities in Sprague-Dawley rats
Published in Toxicology Mechanisms and Methods, 2023
Sreevarsha Gali, Swati Sharma, Amit Kundu, Eunah Lee, Joo Hee Han, Joo Kyung Shin, Ji Soo Choi, So Young Kyung, Jae-Sung Kim, Hyung Sik Kim
In our study, in over two weeks of body weight monitoring, the CdCl2-exposed group showed moderate body weight loss, and the control group showed no significant change. Rats treated with CdCl2 lost body weight due to suppressed hypothalamic stimulation or damage to multiple organs (Alshehri et al. 2021). In rats with CdCl2-induced hepatotoxicity, body weight was restored after treatment with DPx and silymarin. According to our data, CdCl2 accumulation in the liver adversely affected the relative weight of the liver, which increased; administration of DPx or silymarin restored the organ weight. A previous study showed that CdCl2 affects liver weight relatively more than other organs like the kidney, testes, and spleen (Haouem and El Hani 2013). Histopathological analysis of the liver revealed severe vacuolation in the cytoplasm, hepatocellular degeneration, and sinusoidal dilation in the CdCl2-treated group (Ismail and Aziz 2017). The sections from the control group demonstrated normal histopathology, showing hepatocytes with clear boundaries, diverging away from the central vein, and forming strips, perisinusoidal space and hepatic sinusoids separating the hepatocytes strips. DPx and silymarin improved the hepatocyte architecture by alleviating hepatocellular degeneration; however, the effect of DPx was comparatively lesser.
ARRDC3 inhibits liver fibrosis and epithelial-to-mesenchymal transition via the ITGB4/PI3K/Akt signaling pathway
Published in Immunopharmacology and Immunotoxicology, 2023
Bingling Zhang, Feng Wu, Pingping Li, Haiding Li
The collagen family, as a class of substances in the ECM, performs various functions, such as supporting the structure of tissue and forming the basement organ membrane [30]. Collagen I, collagen III, and fibronectin are closely correlated with fibrosis [31]. In normal liver, collagen I and III are located mainly between the HSCs and hepatic parenchymal cells, and collagen IV is located mainly between the HSCs and hepatic blood sinusoidal endothelial cells [32]. The expression of collagen I and III is increased in liver fibrosis [32]. In the fibrotic liver, the normal ECM in the perisinusoidal space is replaced by abundant type I and type III collagen, leading to the loss of hepatocyte microvilli structures and hepatic blood sinusoidal endothelial cell sieve plates, contributing to a progressive loss of normal liver function [32]. In our study, type I and type III collagen were significantly reduced after elevating the expression of ARRDC3 in hepatocytes. It is suggested that increasing ARRDC3 expression can significantly reduce collagen deposition in tissues and cells undergoing liver fibrosis. It has been found that HSCs are activated and transformed into myofibroblast-like cells, and the expression level of α-SMA is up-regulated, which could be used as an indicator of HSC activation [7]. Our findings indicate that overexpressed ARRDC3 reduced the expression of α-SMA, suggesting that the activation of HSCs could be restricted by increasing the expression of ARRDC3.
Histomorphological changes and molecular mechanisms underlying the ameliorative effect of resveratrol on the liver of silver nanoparticles-exposed rats
Published in Ultrastructural Pathology, 2022
Shaimaa A. Abdelrahman, Abeer A. Mahmoud, Abeer A. Abdelrahman, Walaa Samy, Ebtehal Zaid Hassen Saleh
When AgNPs-exposed rats were left for another 28 days for recovery, they showed some apoptotic hepatocytes with dark acidophilic cytoplasm and pyknotic nuclei, some cells were vacuolated, and others showed karyolysis. The portal area showed dilated portal vein, bile duct proliferation, with extensive lymphocytic and eosinophilic infiltration (Figure 2e,f). Semithin sections showed observable infiltration of brown to black- stained AgNPs in cytoplasm of kupffer cells. Blood sinusoids were also dilated and congested (Figure 3d). electron microscope-examined ultrathin sections of the same group showed hepatocytes having heterochromatic nuclei. The perisinusoidal space showed many collagen fibers and kupffer cell with many lysosomes (Figure 4f). Recovery group showed moderate amount of collagen fibers around central vein and portal area (Figure 5g,h), which is represented by the significant decrease in the area percent of collagen fibers blue staining compared to AgNPs-exposed group but still revealed a significant difference from both control and RSV-treated groups (P < .05), as shown in Figure 5i).