Animals ; Endoplasmic Reticulum ; metabolism ; Fatty Liver ; metabolism ; pathology ; Humans ; Mitochondria ; metabolism ; Non-alcoholic Fatty Liver Disease

Apoptosis ; Humans ; Liver Failure, Acute ; metabolism ; pathology ; Mitochondria ; metabolism ; pathology ; Oxidative Stress

Animals ; Endotoxemia ; metabolism ; pathology ; Female ; Liver ; metabolism ; pathology ; Male ; Mitochondria, Liver ; metabolism ; Rats ; Reactive Oxygen Species ; metabolism

OBJECTIVETo investigate the clinicopathological features of infantile cytomegalovirus hepatitis.

METHODLiver biopsies from 30 cases of infantile cytomegalovirus hepatitis were observed under optical microscope and electronic microscope.

RESULTThe main clinical manifestations were jaundice, splenohepatomegaly and hypohepatia. Laboratory test showed dysfunction of liver, high level of CMV DNA, and high titer of anti-CMV antibody. Imaging examination demonstrated hepatomegaly. The histological changes were hepatocellular degeneration, necrosis, apoptosis, and fibrosis. The histological characteristics of cytomegalovirus hepatitis, including intranuclear inclusions in multinucleated giant cells and pseudo-lumens, were also observed under optical microscope. In addition, virion was observed in the nuclei and cytoplasm of hepatocytes under electronic microscope.

CONCLUSIONThe viral DNA and serological tests have limited utility for the diagnosis of infantile cytomegalovirus hepatitis, and the final diagnosis depends on histopathology.

Biopsy, Needle ; Cytomegalovirus Infections ; pathology ; Female ; Hepatitis, Viral, Human ; pathology ; Hepatocytes ; pathology ; ultrastructure ; Humans ; Inclusion Bodies, Viral ; pathology ; Infant ; Infant, Newborn ; Liver ; pathology ; Male ; Mitochondria, Liver ; pathology ; ultrastructure

OBJECTIVE: To observe ultra-structural pathological changes of materiality viscera of rats poisoned by different dose of tetramine and to study the toxic mechanism. METHODS: Acute and subacute tetramine toxicity models were made by oral administration with different dose of tetramine. Brain, heart, liver, spleen and kidney were extracted and observed by electromicroscopic examination. RESULTS: The injuries of brain cells, cardiocytes and liver cells were induced by different dose of tetramine. These were not obviously different of the injuries of the kindy cells and spleen cells of rats poisoned by different dose of tetramine. Ultra-structural pathological changes were abserved including mitochondria slight swelling and neurolemma's array turbulence in the brain cells, mitochondria swelling or abolish and rupture of muscle fiber in the heart cells, mitochondria swelling and the glycogen decreased in the liver cells. CONCLUSION The toxic target organs of tetramine are the heart, brain and liver.
Animals ; Brain/pathology* ; Bridged-Ring Compounds/poisoning* ; Dose-Response Relationship, Drug ; Female ; Liver/pathology* ; Male ; Microscopy, Electron, Transmission ; Mitochondria, Heart/pathology* ; Mitochondria, Liver/pathology* ; Myocardium/pathology* ; Poisoning/pathology* ; Rats ; Rats, Sprague-Dawley

Liver plays a central role in the biogenesis of major metabolites including glucose, fatty acids, and cholesterol. Increased incidence of obesity in the modern society promotes insulin resistance in the peripheral tissues in humans, and could cause severe metabolic disorders by inducing accumulation of lipid in the liver, resulting in the progression of non-alcoholic fatty liver disease (NAFLD). NAFLD, which is characterized by increased fat depots in the liver, could precede more severe diseases such as non-alcoholic steatohepatitis (NASH), cirrhosis, and in some cases hepatocellular carcinoma. Accumulation of lipid in the liver can be traced by increased uptake of free fatty acids into the liver, impaired fatty acid beta oxidation, or the increased incidence of de novo lipogenesis. In this review, I would like to focus on the roles of individual pathways that contribute to the hepatic steatosis as a precursor for the NAFLD.
Acetyl Coenzyme A/metabolism ; Fatty Acids/metabolism ; Fatty Liver/*metabolism/pathology ; Humans ; Lipogenesis ; Mitochondria/metabolism ; Triglycerides/metabolism

OBJECTIVETo investigate the opening of the mitochondrial permeability transition pores of the cultured hepatocytes in a non-alcoholic fatty liver disease model and its relationship with apoptosis of the cells.

METHODSOleic acid was used to induce cultured L02 hepatocyte steatotic in making a model of NAFLD. The steatotic hepatocytes were detected with oil red O staining; the opening of the mitochondrial permeability transition pores was observed under a fluorescence microscope. The apoptosis of the cells was detected with a flow cytometer.

RESULTSAfter adding oleic acid to the cultured hepatocytes, a model of steatosis of human hepatocytes was established after 24 hours. Oleic acid opened the mitochondrial permeability transition pores of the L02 hepatocytes (72.58%+/-2.78%) more than that in the control group (8.28%+/-4.98%) and the difference was statistically significant (P < 0.01). Apoptosis index of the steatotic hepatocytes at 24 hours and 48 hours were 11.09%+/-4.95% and 15.24%+/-2.45%. They were also higher than those of the control group (4.56%+/-1.25%) (P < 0.05, P < 0.01).

CONCLUSIONOpening the mitochondrial permeability transition pores may be the basis of the apoptosis of steatotic hepatocytes in vitro, and it also may be related to the steatosis of NAFLD in human beings.

Apoptosis ; Cell Line ; Fatty Liver ; metabolism ; pathology ; Hepatocytes ; metabolism ; Humans ; Mitochondria, Liver ; metabolism ; Mitochondrial Membrane Transport Proteins ; metabolism

Non-alcoholic fatty liver disease(NAFLD), as a metabolic stress liver injury disease, is one of the most common chronic liver diseases, which seriously threatens people's health. The pathogenesis of NAFLD is very complex. A large number of studies show that the hepatic mitochondrial dysfunction leads to the disorder of hepatic glucose and lipid metabolism, oxidative stress, and inflammation, thus inducing hepatocyte apoptosis, which plays an important role in the progression of NAFLD. In recent years, researchers have begun to focus on developing drugs that slowed the progression of NAFLD by regulating the hepatic mitochondrial function. Chinese medicine has a good curative effect on the treatment of NAFLD, with the advantages of high safety and few side effects. Various studies have shown that Chinese medicine prevented and treated NAFLD by regulating the mitochondrial function. Therefore, this paper summarized the relationship between NAFLD and mitochondria, and the mechanism of Chinese medicine(single Chinese medicine, Chinese medicine monomer, and Chinese medicine compound prescription) in the prevention and treatment of NAFLD by regulating mitochondrial function. This paper is expected to provide references for clinical application of traditional Chinese medicine in the treatment of NAFLD by regulating mitochondrial function.
Humans ; Non-alcoholic Fatty Liver Disease/metabolism* ; Medicine, Chinese Traditional/adverse effects* ; Liver ; Mitochondria/pathology* ; Lipid Metabolism

OBJECTIVESTo explore the clinical and pathological features and the pathogenesis of primary biliary cirrhosis (PBC) in Chinese Mainland.

METHODS30 PBC patients were divided into the early group (Scheuer stage I and II, 19 patients) and the late group (Scheuer stage III and IV, 11 patients). The data of clinics and serology were analyzed, and the pathological features of the liver tissues were characterized. The changes of dendritic cells (DCs) and hepatic stellate cells (HSCs) were studied by immunohistochemistry.

RESULTSIn all the PBC patients, the rate of the male to the female was 1 to 5, and the average age was 40.6 years. The mean levels of TBiL, ALP and GGT in the sera were (95.9+-88.5) micromol/L, (537.2+-339.2) U/L, and (582.0+-351.2) U/L, respectively. 73.3% patients showed AMA positive, and the level of GGT was positively correlated with the AMA level according to the result of statistical analysis (r=0.778, P=0.000). The symptoms of jaundice and hepatomegaly were presented more commonly in the late group than those in the early group (chi2=5.182, P<0.05; chi2=13.659, P<0.01, respectively). The main changes of morphology of PBC located in portal tracts. The liver tissues in the early stage of PBC showed the damage of bile ducts and obvious proliferation of small bile ducts. The granulomas, the lymphoid follicles and the foamy cells were found in the liver tissues of PBC (2/19 patients, 12/19 patients, and 10/19 patients in the early stage respectively, while 0/11 patients, 4/11 patients, and 3/11 patients in the late stage respectively). There was significant difference between the early stage and the late stage in presence of the lymphoid follicles and the foamy cells (t=4.489, P<0.05; t=4.019, P<0.05, respectively). The biliary pigmentary particles were mainly accumulated in the liver cells around the portal tracts in 90.0% PBC patients, and the accumulation of copper and iron increased, compared with that in normal specimens. The DCs and HSCs located mainly in the portal tracts, especially around the damaged bile ducts.

CONCLUSIONSThere are some clinical and pathological characteristics in the patients with PBC. The level of AMA has no direct relationship with the level of transaminase or bilirubin. The proliferated bile ductules may express the antigens which maybe the target of immune attack. As an antigen-presenting cell, DCs may play an important role in the pathogenesis of PBC.

Adolescent ; Adult ; Antibodies, Antinuclear ; blood ; Antigen-Presenting Cells ; immunology ; pathology ; Dendritic Cells ; pathology ; Female ; Humans ; Liver ; pathology ; Liver Cirrhosis, Biliary ; etiology ; immunology ; pathology ; Male ; Middle Aged ; Mitochondria ; immunology

OBJECTIVE: To study the pathological change and the toxic mechanism of Dioscorea bulbifera L in mice. METHODS: Sixty ICR mice were randomly assigned to four groups poisoned respectively with 200% Dioscorea bulbifera L of 1/4 LD50, 1/10LD50, 1/30LD50 and a control group treated with distilled water by oral administration. All animals were pathologically examined with LM and some of them were examined with TEM when the mice died during the experiment or the survival mice were sacrificed after thirty days. RESULTS: The pathological changes showed fatty change and the increasing glycogen of liver cells; degeneration and necrosis of the epithelia of uriniferous tubules. The serum BUN and ALT of the experimental groups mice were higher than that of control group. Enzyme histochemical staining showed the decreasing activity of G-6-P and SDH in the liver cells in the experimental groups. CONCLUSION The experiment suggests that the target organs were liver and kidney. The toxic mechanism of Dioscorea bublifera L was the damage of the mitochondrional and endoplasmic reticulum membrane directly. As a result, the activity of the SDH and G-6-P decreased, the metabolism was affected.
Animals ; Chemical and Drug Induced Liver Injury/pathology* ; Dioscorea/toxicity* ; Endoplasmic Reticulum/pathology* ; Female ; Forensic Medicine ; Kidney/pathology* ; Male ; Mice ; Mice, Inbred ICR ; Mitochondria, Liver/pathology* ; Random Allocation