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LIVER PATHOLOGY PDF

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Recall normal liver anatomy and histology. • 2. Understand basic terminology/ definitions. • Apoptosis, cholestasis, limiting plate, interface. Fundamental Liver Pathology. Part 2 .. myavr.info results_merged/myavr.info hepatocellular. Pathology of Liver Diseases is a rapid reference consultation tool that uses both book and online material to present a whole range of liver.


Liver Pathology Pdf

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Pathology of The Liver - Practice Natural History of Chronic Liver Diseases ( general features) . myavr.info . caused by chronic infection with the liver fluke, Opisthorchis. Viverrini histology. Multicentric HCCs are associated with a high rate of tumour recurrence , even. Since , liver pathology activities in the UK have been developed and coordinated by a subcommittee of the BSG Pathology Section.

Pages General Processes. Developmental Abnormalities. Metabolic Liver Disease. Fatty Liver Disease. Viral Liver Disease.

Nonviral Infectious Liver Disease. Drug-Induced Liver Injury.

Autoimmune Hepatitis. Biliary Disease. Vascular Disorders. Premalignant Lesions.

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Neoplasm-like Liver Lesions. Epithelial Liver Neoplasms. Nonepithelial Liver Neoplasms. Obstetric Liver Disease. Transplantation Pathology. Back Matter Pages Abstract Alcoholic liver disease ALD is caused by heavy alcohol consumption over a long period. Acetaldehyde-mediated toxicity, oxidative stress, and imbalance of lipid metabolism are generally considered involved in the initiation of ALD. There is an increasing requirement for alternative and natural medicine to treat ALD.

Recently, aldose reductase AR has been reported to be involved in the development of ALD by affecting inflammatory cytokines, oxidative stress, and lipid metabolism.

And we conclude that AR inhibitors of plant origin may enhance antioxidant capacity, inhibit lipid peroxidation and inflammatory cytokines expression, and activate AMP-activated protein kinase thereby subsequently suppressing alcohol-induced lipid synthesis in liver to achieve ALD protection. Introduction Alcoholic liver disease ALD is caused by heavy alcohol consumption over a long period. Metabolism of alcohol in the body produces harmful substances, which lead to liver damage and a series of pathological changes in the liver.

The incidence of ALD is relatively high among liver diseases. ASH exhibits symptoms similar to those of chronic hepatitis, such as mild malaise through the entire body, fatigue, exhaustion, upper abdominal discomfort, nausea and vomiting, loss of appetite, and abdominal distension.

Moreover, the severe ASH may lead to alcoholic hepatitis AH , which is an acute clinical presentation of ALD and requires an effective drug treatment strategy. ASH and AH are terms often used interchangeably in scientific literature [ 2 ]. Alcohol abstinence is still the best treatment for all stages of ALD.

Drug options for AH include corticosteroids as a first choice and pentoxifylline, an inhibitor of phosphodiesterase, as a second line therapy. In the case of advanced disease such as cirrhosis or HCC, liver transplantation may be required [ 1 , 2 ]. Thus, there is an increasing requirement for alternative and natural medicine to treat ALD. Acetaldehyde-mediated toxicity, oxidative stress, and imbalance of lipid metabolism are generally considered involved in the initiation of ALD [ 6 — 9 ].

Alcohol, acting as the first hit, increases the concentration of reactive oxides by promoting oxidative stress, which induces fat accumulation in the liver; oxidative stress-related lipid peroxidation and inflammatory cytokines act as the second hit on the hepatocytes in fatty liver, causing inflammation, necrosis, and fibrosis [ 10 ].

Many studies have suggested that alcohol-induced imbalance in lipid metabolism may be caused by alcohol-induced abnormal expression of genes involved in lipid metabolism, e. It plays a key role in regulating lipid transport and fatty-acid oxidative degradation in the liver, so it can prevent the development of fatty liver to some extent [ 11 , 12 ]. AMPK plays an important role in increasing fatty acid oxidation, enhancing insulin sensitivity, and reducing oxidative stress.

It is also closely related to the pathogenesis of ALD [ 15 ]. The oxidative stress that forms during ethanol metabolism is also an important cause of ALD. In addition, oxidative stress caused by alcohol metabolism induces lipid peroxidation, resulting in further damage to hepatocytes.

The lipid peroxidation caused by oxidative stress induces damage to biological membranes, which reduces the concentration of unsaturated fatty acids in the membrane and causes imbalance in the ratio of unsaturated fatty acids to proteins [ 6 , 9 ].

During alcohol metabolism, some antioxidant pathways become activated and so interfere with oxidative stress damage in the human body. For example, the endogenous antioxidant superoxide dismutase SOD can interfere with alcohol-induced damage in the liver.

Antioxidants such as SOD and catalase in the liver and vitamin C in food can eliminate a large proportion of ROS produced after alcohol intake. Long-term heavy consumption of alcohol can cause gastrointestinal dysfunction and reduce the absorption of antioxidants from food sources.

Further, the process of alcohol metabolism also consumes large quantities of antioxidants, causing ROS to accumulate in the body [ 6 , 7 ]. It is multifunctional and acts as a rate-limiting enzyme of the polyol pathway in sugar metabolism. Through the regulation of cytokines, growth factors, oxidative stress, and other mediated intracellular signal transduction pathways, AR participates in a variety of disease pathological processes [ 48 ].

AR is widespread in organs and tissues that are related to diabetic complications, such as the kidney, blood vessels, lens of the eye, retina, and heart. It catalytically converts glucose to sorbitol, which cannot easily pass through the cell membrane, resulting in swelling, degeneration, and necrosis of the cells [ 49 ].

The roles of AR in the complications of diabetes have been reported extensively in the literature [ 50 , 51 ]. In addition to being highly expressed in organs and tissues that are relative to diabetic complications, AR expression is also induced in the livers of ALD patients [ 52 ] and alcohol-stimulated mice [ 5 ]. In another previous study, we also showed that AR inhibitor reduced Cytochrome P 2E1- CYP2E1- mediated oxidative stress and inflammatory cytokine expression, and activated AMPK to improve alcohol-induced hepatic steatosis in mice [ 5 ].

Our metabolomics study further demonstrated that AR inhibitor improved alcohol-induced hepatic steatosis in mice by suppressing the biosynthesis of saturated fatty acids [ 3 ].

Nitric oxide plays an important role in maintaining the physiological functions of vascular endothelium and nerve tissues. Consumption of large amounts of NADPH causes significant reductions in the amount of nitric oxide synthesized, which ultimately disrupts the reduction-oxidation redox system and damages tissue. Ethanol intake causes damage to the intracellular redox system and a decrease in antioxidant levels, resulting in intracellular oxidative stress and long-term accumulation of fat, thereby leading to ALD [ 7 ].

AR inhibitors may be a suitable resource for the development of drugs for the prevention and treatment of ALD with broad application prospects. Role of Plant-Derived AR Inhibitors in the Prevention and Treatment of ALD AR inhibitors are generally divided into three categories according to the sources: natural AR inhibitors of plant origin, natural AR inhibitors of microbial origin, and synthetic AR inhibitors such as carboxylic acids, hydantoins, and phenylpyrrolidone compounds.

Among the three categories of AR inhibitors, plant AR inhibitors, which mainly include flavonoids, polyphenols, terpenoids, and alkaloids, have seen widespread use because of their wide range of sources and low rate of adverse reactions. Plant-derived compounds with AR inhibitory effect have been extensively reviewed by Veeresham et al. Among these compounds, currently only some commercially available ones have been tested for hepatoprotection activity in rodents with ethanol-induced liver injury and are summarized in Table 1 in this review.

The AR inhibitory activities of these compounds have been well documented. However, some commercially available flavonoids, including luteolin, quercetin, apigenin, fisetin, and myricitrin, were also found to have strong AR inhibitory activities with IC50 values of 0. In another study, a phenolics, ellagic acid, isolated from Chrysanthemum morifolium exhibited inhibitory activity with an IC50 of 0. These studies demonstrate that luteolin, quercetin, apigenin, rhamnetin, fisetin, myricitrin, and ellagic acid are potent AR inhibitors.

Moreover, silybin, puerarin, and baicalin were found to exhibit markedly inhibitory effects on AR comparable to sorbinil, another commercial synthetic aldose reductase inhibitor [ 57 ]. In addition, genistein, puerarin and baicalin were reported to inhibit rat lens AR with IC50 values of 4. Chlorogenic acid, another phenolic compound, was also reported to inhibit rat AR with an IC50 of 0.

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The chemical structures of these compounds are depicted in Figure 1. Figure 1: Chemical structure of some potent AR inhibitors of plant origin. The same mechanisms whereby zopolrestat improves lipid accumulation were also demonstrated in ethanol-intoxicated mouse AML12 liver cells [ 5 ] and human hepatoma HepG2 cells [ 4 ].

Of note, among the plant-derived AR inhibitors which were found to exert hepatoprotection effect in rodents, all of them were at least in part through potential antioxidant and anti-inflammatory mechanisms. A recent work reported that chlorogenic acid ameliorated ethanol-induced reactive oxygen species and subsequently reduced hepatic steatosis in mice [ 47 ].

Besides these in vivo studies, some in vitro studies also demonstrated that AR inhibitors from nature, including myricitrin [ 62 ], puerarin [ 63 ], and isoliquiritigenin [ 64 ], protected ethanol-intoxicated hepatocytes by regulating the AMPK signaling pathway. In addition, phenolic acid and flavonoid rich ethyl acetate fraction of S. Interestingly, p-coumaric acid and rutin, myricetin were the predominant phenolic acid and flavonoid in SQEA, and they are all AR inhibitors.

Seminars in Liver Disease

These studies together demonstrate that AR inhibitors from plant protect against alcohol-induced liver injury through the similar mechanisms with those of chemical synthesized AR inhibitor and indicate that AR inhibitors from nature may be a promising source for developing anti-ALD drugs. Conclusion In summary, as depicted in Figure 2 , AR participates in the development of ALD by affecting inflammatory cytokines, oxidative stress, and lipid metabolism in liver while natural AR inhibitors may reduce inflammation, enhance antioxidant activation, inhibit lipid peroxidation, and suppress alcohol-induced lipid synthesis through activating AMPK in liver to achieve ALD protection.

This review provides a theoretical basis for the use of natural AR inhibitors in the prevention and treatment of ALD. Figure 2: Schematic showing the mechanisms by which aldose reductase inhibitors prevent ALD. Conflicts of Interest The authors declare no conflict of interest. References H. Seitz, R. Bataller, H. Cortez-Pinto et al. Guo, L. Chen, J. Huang et al. Qiu, C. Cai, X. Zhao, Y. Fang, W. Tang, and C. Shi, Y. Wang, J.

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Back Matter Pages Forgot password? Zhou, Z. Several primary liver diseases, such as hepatitis C and Wilson disease, hepatocellular adenoma and carcinoma, and certain drugs and toxins, such as steroids and alcohol, commonly show these forms of steatosis Figure 1a. It catalytically converts glucose to sorbitol, which cannot easily pass through the cell membrane, resulting in swelling, degeneration, and necrosis of the cells [ 49 ]. CiteULike About this book Pathology of Liver Diseases is a rapid reference consultation tool that uses both book and online material to present a whole range of liver disorders.

The following chapters are dedicated to developmental, metabolic, infectious, drug related, autoimmune, biliary, vascular and neoplastic disorders.

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