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The patient with acute gastrointestinal problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Rebecca Maindonald, Adrian Jugdoyal
The liver is dark reddish-brown in colour and is divided into two main lobes (the larger right and the smaller left) which are further subdivided into approximately 100,000 small lobes, or lobules. About 60% of the liver is made up of liver cells called hepatocytes, which absorb nutrients and detoxify and remove harmful substances from the blood. A hepatocyte has an average lifespan of 150 days. There are approximately 202,000 hepatocytes in every milligram of liver tissue. The liver receives its blood supply via the hepatic artery and portal vein. Instead of capillaries, the liver has large endothelium lined spaces (sinusoids) through which blood passes. The sinusoids also contain fixed phagocytes called stellate reticuloendothelial (Kupffer) cells which perform several functions, including the breakdown of worn out red blood cells, bacteria and other foreign matter which can then pass into the venous circulation.
Functions of the Liver
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The hepatocytes contain a large variety of organelles. The endoplasmic reticulum is a complex of intracellular membranes comprising high-density fatty acid complexes forming a large surface area. The smooth endoplasmic reticulum is associated with drug biotransformation. The rough endoplasmic reticulum is characterized by the presence of aggregates of ribosomes (RNA) on tubules and is responsible for protein synthesis. In addition, peroxisomes are contiguous with both types of endoplasmic reticulum and are sites of β-oxidation of fatty acids and storage of catalase.
Biological Perspectives of Cytokine and Hormone Networks
Published in Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, Acute Phase Proteins, 2020
Aleksander Koj, Jack Gauldie, Heinz Baumann
Liver regeneration is a highly complex process triggered by hepatocyte growth factors (HGFs) which also appear to be potent mitogens for some epidermal and epithelial cells, but which inhibit proliferation of hepatomas (for references, see References 100 and 101). We observed that human recombinant HGF stimulates the synthesis of α2-macroglobulin in primary cultures of rat hepatocytes.102 Its effects on the synthesis of AP proteins are broader in Hep G2 cells, where HGF inhibits the synthesis of albumin, but increases the basal production of fibrinogen, α1-antichymotrypsin, and α1-proteinase inhibitor (Figure 3). However, in cells stimulated by high concentrations of IL-6, HGF decreases the maximum response of haptoglobin, fibrinogen, and α1-antichymotrypsin. A similar phenomenon was observed with insulin (Figure 3). On the other hand, TGFβ increased the production of α1 antichymotrypsin and al-proteinase inhibitor in Hep G2 cells, even at high concentrations of IL-6. These results emphasize again the existence of intricate networks of cytokines and cellular growth factors in the regulation of the liver AP response.
Evening primrose oil attenuates oxidative stress, inflammation, fibrosis, apoptosis, and ultrastructural alterations induced by metanil yellow in the liver of rat: a histological, immunohistochemical, and biochemical study
Published in Ultrastructural Pathology, 2023
Amany Mohamed Shalaby, Rania H. Shalaby, Mohamed Ali Alabiad, Doaa I. Abdelrahman, Mohammed Alorini, Fatima A. Jaber, Shaimaa Mohamed Abdelfattah Hassan
The current work found that chronic Myl intake caused histological changes in the rats’ liver, including dilatation and congestion of portal and central veins, cellular infiltrations, and hepatocyte vacuolation. These findings agreed with the previous work of Sharma et al.,1 who discovered comparable alterations in the livers of rats given Myl. Myl is a food dye that reaches the liver after being absorbed from the digestive tract together with other dietary components. Hepatocytes are damaged by oxidative stress as a result of their accumulation in the liver. The liver’s function is compromised as a result of hepatic cell structural damage. The oxidative breakdown of lipids, mainly membrane lipids, is known as lipid peroxidation. Free radicals start a chain reaction that degrades the membranes of cells and organelles, causing cell damage.28
Microanatomy of the metabolic associated fatty liver disease (MAFLD) by single-cell transcriptomics
Published in Journal of Drug Targeting, 2023
Lijun Wang, Kebing Zhou, Qing Wu, Lingping Zhu, Yang Hu, Xuefeng Yang, Duo Li
Metabolic-associated fatty liver disease remains a prominent risk factor for many chronic diseases, including obesity, diabetes, cardiovascular disease, and cancer [16]. Moreover, MAFLD can progress to steatohepatitis or cirrhosis. However, there is no definite target and therapeutic mechanism for MAFLD. Single-cell sequencing has guiding significance for screening potential therapeutic targets and molecular mechanisms of MAFLD. In the present study, we conducted transcriptome profiling of 30,038 single cells, including hepatocytes and non-hepatocytes, from normal and steatosis adult mouse livers. Comparative analysis of hepatocytes and non-hepatocytes revealed significant heterogeneity, and non-hepatocytes acted as major cell communication hubs. Systematic analysis of cellular compositions and cell-cell interaction networks showed that hepatocyte metabolism was significantly correlated with changes in liver function. We also uncovered the active involvement of non-hepatocyte cells in regulating the behaviour of hepatocytes, exemplified by Kupffer cells, which could preserve liver function after steatosis.
Gastrodin ameliorates Concanavalin A-induced acute hepatitis via the IL6/JAK2/STAT3 pathway
Published in Immunopharmacology and Immunotoxicology, 2022
Yingqun Zhou, Jiaojiao Chen, Zhilu Yao, Xuezhen Gu
Hepatocyte injury and death are prominent features in various liver diseases. ConA stimulation leads to hepatocyte apoptosis and autophagy [12]. Apoptosis, a highly organized and genetically controlled form of cell death [13], is essential to regulate cell survival and the homeostasis of organisms. Apoptosis is strictly controlled by the Bcl-2 family, which is composed of pro-apoptotic factors (Bax, Bak, Bid) and antiapoptotic factors (BCL-2, Bcl-XL) [14,15]. Autophagy occurs as a cellular self-protection mechanism to protect cells from metabolic stress and oxidative damage and to maintain intracellular homeostasis. Various autophagy-related proteins regulate and control the autophagy process [16]. Inhibition of apoptosis and autophagy processes can, to some extent, influence the regression of liver disease and may provide new therapeutic directions.