The protective effects of ursodeoxycholic acid on isoniazid plus rifampicin induced liver injury in mice.

Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with isoniazid and rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with isoniazid (75mg/kg) and rifampicin (150mg/kg) for one week.

Melatonin alleviates lipopolysaccharide-induced placental cellular stress response in mice.

Melatonin protects mice from lipopolysaccharide (LPS)-induced fetal death and intra-uterine growth retardation. Nevertheless, its molecular mechanism remains obscure. In the present study, we investigated the effects of melatonin on LPS-induced cellular stress in placenta.

Fenvalerate induces germ cell apoptosis in mouse testes through the Fas/FasL signaling pathway.

Fenvalerate has a potentially adverse effect on male reproduction and spermatogenesis, whereas the precise mechanism remains obscure. The present study investigated the effects of fenvalerate on germ cell apoptosis in testes. Adult male mice were administered with fenvalerate (15 or 60 mg/kg) by gavage for 28 days.

Effects of pubertal fenvalerate exposure on testosterone and estradiol synthesis and the expression of androgen and estrogen receptors in the developing brain.

Fenvalerate is a potential endocrine disruptor. Several studies have demonstrated that fenvalerate disrupts testosterone (T) synthesis in testes. T and estradiol (E(2)) are de novo synthesized in the developing brain.

Acceleration of age-related learning and memory decline in middle-aged CD-1 mice due to maternal exposure to lipopolysaccharide during late pregnancy.

Previous studies have shown that inflammation process involves pathogenesis of Alzheimer's disease (AD). But, the natural AD model of inflammation has not been obtained yet. In the present study, CD-1 mothers intraperitoneally received a 50 μg/kg lipopolysaccharide (LPS) or normal saline daily during gestational days 15-17.

Mitochondrial signaling pathway is also involved in bisphenol A induced germ cell apoptosis in testes.

Bisphenol A (BPA) is a potential endocrine disruptor and testicular toxicant. An earlier study showed that BPA-induced germ cell apoptosis through the Fas/FasL apoptotic pathway. In the present study, we aimed to investigate whether the mitochondrial pathway is also involved in the process of BPA-mediated germ cell apoptosis in testes.

[A comparison of the blind double-lumen plugged telescoping catheter with protected specimen brush for the diagnosis of ventilator-associated pneumonia.].

Objective: To compare the diagnostic value of blind double-lumen plugged telescoping catheter (PTC) and protected specimen brush(PSB) in patients requiring mechanical ventilation (MV) for suspected ventilation-associated pneunonia (VAP).

Methods: Sixty-nine patients with a hospital stay of >/= 48 h who required MV for suspicion of VAP were prospectively enrolled in the study during Jan 2008 and Feb 2009 in the medical intensive care unit. The patients all underwent bronchial samplings: a blind PTC and a fiberoptic PSB were performed successively in each case.

Maternal fenvalerate exposure during pregnancy persistently impairs testicular development and spermatogenesis in male offspring.

Fenvalerate, a widely used pyrethroid insecticide, has been associated with poor semen quality. As yet, little is known about the effects of prenatal fenvalerate exposure on testicular development. The present study investigated the effects of prenatal fenvalerate exposure on testicular development and spermatogenesis.

Maternal cypermethrin exposure during lactation impairs testicular development and spermatogenesis in male mouse offspring.

Within the last decade, numerous epidemiological studies have demonstrated that endocrine disruptors are a possible cause for a decline in semen quality. Cypermethrin is a widely used pyrethroid insecticide, but little is known about its potentially adverse effects on male reproduction. In the present study, we investigated the effects of maternal cypermethrin exposure during lactation on testicular development and spermatogenesis in male offspring.

Pubertal and early adult exposure to fenvalerate disrupts steroidogenesis and spermatogenesis in mice at adulthood.

Fenvalerate, a pyrethroid insecticide used worldwide, has been shown to have a potentially adverse effect on male reproduction. Our earlier study showed that maternal fenvalerate exposure during lactation impaired testicular development in male offspring. In this study, we investigated the effects of pubertal and early adult exposure to fenvalerate on steroidogenesis and spermatogenesis in mice.

Pubertal cadmium exposure impairs testicular development and spermatogenesis via disrupting testicular testosterone synthesis in adult mice.

Cadmium (Cd) is a well-known testicular toxicant. However, the effects of pubertal Cd exposure on testicular development and spermatogenesis remained to be elucidated. The present study investigated the effects of pubertal Cd exposure on testicular development and spermatogenesis.

Age- and gender-dependent impairments of neurobehaviors in mice whose mothers were exposed to lipopolysaccharide during pregnancy.

Lipopolysaccharide (LPS)-induced intrauterine infection has been associated with neurodevelopmental injury in rodents. The purpose of the present study was to analyze the dynamic changes of neurobehaviors in mice whose mothers were exposed to LPS during pregnancy. The pregnant mice were intraperitoneally (i.

Cypermethrin exposure during puberty disrupts testosterone synthesis via downregulating StAR in mouse testes.

Cypermethrin is a widely used synthetic pyrethroid insecticide. Previous studies showed that cypermethrin significantly decreased the fertility and reduced the number of implantation sites and viable fetuses in females impregnated by males exposed to cypermethrin. As yet, little is known about the mechanism of cypermethrin-induced reproductive toxicity.

Lactational fenvalerate exposure permanently impairs testicular development and spermatogenesis in mice.

Fenvalerate, a widely used synthetic pyrethroid insecticide, has been associated with poor semen quality in human being. However, little is known about the effects of lactational fenvalerate exposure on testicular development and spermatogenesis. The purpose of the present study was to investigate the effects of maternal fenvalerate exposure during lactation on testicular development and spermatogenesis in male offspring.

Altered integrity and decreased expression of hepatocyte tight junctions in rifampicin-induced cholestasis in mice.

Rifampicin is a well-known hepatotoxicant, but little is known about the mechanism of rifampicin-induced hepatotoxicity. The aim of this study was to characterize the expression and localization of hepatocyte tight junctions in rifampicin-induced cholestasis in mice. Cholestasis was induced by administration of rifampicin (200 mg/kg) for 7 consecutive days or treatment with a single dose of rifampicin (200 mg/kg) by gastric intubation.

Melatonin pretreatment attenuates 2-bromopropane-induced testicular toxicity in rats.

2-Bromopropane (2-BP) was used as an alternative for ozone-depleting solvents, which caused reproductive disorders in male workers and laboratory animals. A recent study indicated that 2-BP impaired antioxidant cellular defences and enhanced lipid peroxidation (LPO). Melatonin is a powerful endogenous antioxidant.

Tumor necrosis factor alpha partially contributes to lipopolysaccharide-induced downregulation of CYP3A in fetal liver: its repression by a low dose LPS pretreatment.

With embryonic development, fetal hepatocytes gradually express various types of cytochromes P450 (CYPs) that play a key role in the detoxification of xenobiotics. In the present study, we showed that maternal lipopolysaccharide (LPS) exposure downregulated cyp3a11 mRNA and CYP3A protein in fetal liver. The increased level of TNF-alpha protein in fetal liver, transferred from either the maternal circulation or amniotic fluid, seems to be associated with LPS-induced downregulation of cyp3a11 mRNA and CYP3A protein in fetal liver.

Reactive oxygen species contribute to lipopolysaccharide-induced teratogenesis in mice.

Lipopolysaccharide (LPS) has been associated with adverse developmental outcome, including embryonic resorption, fetal death and growth retardation, and preterm delivery. In the present study, we showed that an ip injection with LPS daily from gestational day (gd) 8 to gd 12 resulted in the incidence of external malformations. The highest incidence of malformed fetuses was observed in fetuses from dams exposed to 20 microg/kg LPS, in which 34.

Maternally administered lipopolysaccharide (LPS) upregulates the expression of heme oxygenase-1 in fetal liver: the role of reactive oxygen species.

Heme oxygenase-1 (HO-1) is an inducible enzyme that catalyzes the rate-limiting step in the degradation of heme to biliverdin, carbon monoxide and iron. Previous studies have demonstrated that lipopolysaccharide (LPS) upregulates the expression of HO-1 in adult mouse liver. The present study aimed to investigate the effects of maternal LPS exposure on the expression of HO-1 in fetal liver.

Differential effects of pyrrolidine dithiocarbamate on TNF-alpha-mediated liver injury in two different models of fulminant hepatitis.

Background/aims: Pyrrolidine dithiocarbamate (PDTC) is an inhibitor of nuclear factor kappa B (NF-kappaB) activation. The present study aimed to investigate the effects of PDTC on lipopolysaccharide (LPS)-induced liver injury in two different models of fulminant hepatitis.

Methods: Mice infected with Bacillus Calmette Guerin (BCG) were challenged with LPS (0.

Maternally-administered lipopolysaccharide (LPS) increases tumor necrosis factor alpha in fetal liver and fetal brain: its suppression by low-dose LPS pretreatment.

Lipopolysaccharide (LPS) has been associated with adverse developmental outcome, including intra-uterine fetal death (IUFD), intra-uterine growth retardation (IUGR) and neurological injury. In the LPS model, tumor necrosis factor alpha (TNF-alpha) is the major mediator leading to IUFD, IUGR and neurological injury. In the present study, we investigated the effect of maternally-administered LPS on TNF-alpha in maternal serum, amniotic fluid, fetal liver and fetal brain.

N-acetylcysteine attenuates lipopolysaccharide-induced apoptotic liver damage in D-galactosamine-sensitized mice.

Aim: To investigate the effects of N-acetylcysteine on D-galactosamine (GalN)/ lipopolysaccharide (LPS)-induced apoptotic liver injury in mice.

Methods: When given together with a low dose of LPS, GalN highly sensitizes animals to produce apoptotic liver injury with severe hepatic congestion, resulting in rapid death. In the GalN/LPS model, TNF-alpha is the major mediator leading to apoptotic liver injury.

Maternally administered melatonin differentially regulates lipopolysaccharide-induced proinflammatory and anti-inflammatory cytokines in maternal serum, amniotic fluid, fetal liver, and fetal brain.

Lipopolysaccharide (LPS) has been associated with adverse developmental outcome, including intra-uterine fetal death and intra-uterine growth retardation. In the LPS model, tumor necrosis factor alpha (TNF-alpha) is the major mediator leading to intra-uterine fetal death and intra-uterine growth retardation. Interleukin (IL)-10 protects rodents against LPS-induced intra-uterine fetal death and intra-uterine growth retardation.

Melatonin attenuates lipopolysaccharide (LPS)-induced apoptotic liver damage in D-galactosamine-sensitized mice.

D-Galactosamine (GalN) depletes UTP primarily in liver, resulting in decreased RNA synthesis in hepatocytes. When given together with a sublethal dose of lipopolysaccharide (LPS), GalN highly sensitizes animals to produce apoptotic liver injury with severe hepatic congestion, resulting in rapid death. Melatonin is a cytokine modulator, antioxidant and anti-apoptotic agent.

Effects of low-dose lipopolysaccharide (LPS) pretreatment on LPS-induced intra-uterine fetal death and preterm labor.

Lipopolysaccharide (LPS) has been associated with adverse developmental outcome, including embryonic resorption, intra-uterine fetal death (IUFD), intra-uterine growth retardation (IUGR) and preterm delivery in rodents. The purpose of the present study was to investigate whether administration of a low-dose LPS to the pregnant mice induce a reduced sensitivity to subsequent high-dose LPS-induced IUFD and preterm labor. We found that LPS-induced IUFD was obviously attenuated when the pregnant mice were pretreated with low-dose LPS (10 microg/kg, i.