Toxoplasma gondii Induces Apoptosis via Endoplasmic Reticulum Stress-Derived Mitochondrial Pathway in Human Small Intestinal Epithelial Cell-Line

Toxoplasma gondii, an intracellular protozoan parasite that infects one-third of the world’s population, has been reported to hijack host cell apoptotic machinery and promote either an anti- or proapoptotic program depending on the parasite virulence and load and the host cell type. However, little is known about the regulation of human FHs 74 small intestinal epithelial cell viability in response to T. gondii infection. Here we show that T. gondii RH strain tachyzoite infection or ESP treatment of FHs 74 Int cells induced apoptosis, mitochondrial dysfunction and ER stress in host cells. Pretreatment with 4-PBA inhibited the expression or activation of key molecules involved in ER stress. In addition, both T. gondii and ESP challenge-induced mitochondrial dysfunction and cell death were dramatically suppressed in 4-PBA pretreated cells. Our study indicates that T. gondii infection induced ER stress in FHs 74 Int cells, which induced mitochondrial dysfunction followed by apoptosis. This may constitute a potential molecular mechanism responsible for the foodborne parasitic disease caused by T. gondii.

Adenosine A3 Receptor Mediates ERK1/2- and JNK-Dependent TNF-α Production in Toxoplasma gondii-Infected HTR8/SVneo Human Extravillous Trophoblast Cells

Toxoplasma gondii is an intracellular parasite that causes severe disease when the infection occurs during pregnancy. Adenosine is a purine nucleoside involved in numerous physiological processes; however, the role of adenosine receptors in T. gondii-induced trophoblast cell function has not been investigated until now. The goal of the present study was to evaluate the intracellular signaling pathways regulated by adenosine receptors using a HTR-8/SVneo trophoblast cell model of T. gondii infection. HTR8/SVneo human extravillous trophoblast cells were infected with or without T. gondii and then evaluated for cell morphology, intracellular proliferation of the parasite, adenosine receptor expression, TNF-α production and mitogen-activated protein (MAP) kinase signaling pathways triggered by adenosine A3 receptor (A3AR). HTR8/SVneo cells infected with T. gondii exhibited an altered cytoskeletal changes, an increased infection rate and reduced viability in an infection time-dependent manner. T. gondii significantly promoted increased TNF-α production, A3AR protein levels and p38, ERK1/2 and JNK phosphorylation compared to those observed in uninfected control cells. Moreover, the inhibition of A3AR by A3AR siRNA transfection apparently suppressed the T. gondii infection-mediated upregulation of TNF-α, A3AR production and MAPK activation. In addition, T. gondii-promoted TNF-α secretion was dramatically attenuated by pretreatment with PD098059 or SP600125. These results indicate that A3AR-mediated activation of ERK1/2 and JNK positively regulates TNF-α secretion in T. gondii-infected HTR8/SVneo cells.

Study on Mechanism of Compound Biejiaruangan Troche in Inhibiting Alcohol Hepatic Fibrosis in Rats / 中国中医药信息杂志

Objective To probe into the inhibiting action of Compound Biejiarangan Troche on alcohol hepatic fibrosis in rats. Methods Forty Wistar male rats were divided into control, model, Compound Biejiarangan Troche and Anfate treatment groups. Alcohol hepatic fibrosis model was established by intragastrical perfusion with mixture of "alcohol-Pyrazole-coil oil" and high-fat diet for sixteen weeks. After four weeks’ intervention, changes of hepatic fibrosis index, liver tissue pathology and expression of TGF-?1 in liver tissue were observed. Results The hepatic function of model rats were changed and abnormal, with obvious fibrosis in hepatic histopathology. After intervention for four weeks, HA decreased (P

Study on Influence Factors of TCM Syndrome Characteristics Distribution of Alcoholic Hepatic Fibrosis / 中国中医药信息杂志

Objective To explore the influence factors of TCM syndrome characteristics distribution of alcoholic hepatic fibrosis. Methods The study overall collected and discussed the influence factors of TCM syndrome characteristics distribution of alcoholic hepatic fibrosis patients by adopting the principles and methods of clinical epidemiology based on the previous research of TCM syndrome characteristics. Results The important influence factors of TCM syndrome characteristics distribution of alcoholic hepatic fibrosis were total alcohol intakes and the total alcohol intakes under family alcoholism history condition. Conclusion The degree of viscera damage by alcohol is closely related to the distribution of TCM syndrome characteristics of alcoholic hepatic fibrosis and its pathogenesis evolution. The genetic constitution is one of the important influence factors of TCM syndrome characteristics distribution of alcoholic hepatic fibrosis.

Empirical study on protective effect of preparations from Tiaogan Lipi prescription on mouse with hepatic injury induced by ethanol / 中华中医药杂志

Objective: To compare the protective effect of various preparations from Tiaogan Lipi prescription on mouse ethanol hepatic injury.Methods:The hepatic injury model of mice was replicated with ethanol.Comparing with Fufang Biejia Ruan’gan prescription,three preparations from Tiaogan Lipi prescription were administrated for protecting the hepatic injury.The contents of AST,ALT,CHOL and TG in serum and the MDA and SOD in liver tissue were tested.The pathological changes of the liver had been evaluated.Results:Three preparations from Tiaogan Lipi reduces the level of ASTALTCHOL TG,lowers the content of MDA(P