New insights into Nod-like receptors (NLRs) in liver diseases.

Activation of inflammatory signaling pathways is of central importance in the pathogenesis of alcoholic liver disease (ALD) and nonalcoholic steatohepatitis (NASH). Nod-like receptors (NLRs) are intracellular innate immune sensors of microbes and danger signals that control multiple aspects of inflammatory responses. Recent studies demonstrated that NLRs are expressed and activated in innate immune cells as well as in parenchymal cells in the liver.

Effects of Contrast-Enhanced Ultrasonography in Monitoring Hepatic Microcirculation After Rat Liver Ischemia-Reperfusion Injury.

Objectives: Our objective was to evaluate the effects of contrast-enhanced ultrasonography in monitoring microcirculation after rat liver ischemia-reperfusion injury.

Materials And Methods: Male Wistar rats (n = 36) were divided into sham-operated and ischemia-reperfusion groups. Rats in the ischemia-reperfusion groups underwent normothermic liver ischemia for 15 minutes followed by 1, 6, or 24 hours of reperfusion.

Calcitonin gene-related peptide enhances CREB phosphorylation and attenuates tau protein phosphorylation in rat brain during focal cerebral ischemia/reperfusion.

Calcitonin gene-related peptide (CGRP) is a potent vasodilator and immune cell modulator. Exogenous CGRP could increase the cerebral blood flow significantly and protect the ischemic neurons, but its mechanism is not entirely clear. The effect of CGRP on the expressions of CREB and tau in the ipsilateral parietal cortex were detected in focal cerebral ischemia/reperfusion model.

Cyclic-AMP response element binding protein and tau are involved in the neuroprotective mechanisms of nerve growth factor during focal cerebral ischemia/reperfusion in rats.

Nerve growth factor (NGF) has protective and therapeutic effects after cerebral ischemic injury. However, its mechanism of action is not clear. We explored the protective mechanism of exogenous NGF on rat hippocampal neurons after focal cerebral ischemia/reperfusion.

Effect of adrenomedullin on neuron apoptosis, infarction volume and expression of Egr-1 mRNA after focal ischemia-reperfusion in rats.

Objective To observe the influence of adrenomedullin (ADM) on neuron apoptosis, infarction volume of brain, and the expression of early growth response 1 (Egr-1) mRNA in ischemia-reperfusion rats. Methods The arteria cerebri media was tied for 2 h to construct the ischemia model. Infarction volume was detected by triphenltetrazolium chloride (TTC) staining, neuronal apoptosis and necrosis was detected with terminal deoxynucleotidyl transferase nick labeling (TUNEL) method, and the Egr-1 mRNA expression was examined by in situ hybridization (ISH).

[Effect of adrenomedullin on neuron apoptosis and early growth response gene-1 after focal ischemia/ reperfusion in rats].

Objective: To explore the influence of adrenomedullin (ADM) on apoptosis of neuron, volume of infarction and the expression of early growth response gene-1 (Egr-1) mRNA in the rat with focal ischemia/reperfusion (I/R) injury.

Methods: Fifty-four SD rats were randomly divided into sham operation group, ADM femoral vein group, internal carotid artery group and lateral cerebral ventricle group. The model was reproduced by ligating the middle cerebral artery (MCA) with a ligature for 2 hours followed by injection of ADM through femoral artery, internal carotid artery and lateral cerebral ventricle before reperfusion for 22 hours.

[The expression of protein kinase C and the regulatory effect of nerve growth factor in the lung and the visceral sensory afferent system of asthmatic guinea pigs].

Objective: To explore the expression of protein kinase C (PKC) and the regulatory effect of nerve growth factor (NGF) in the lung and the visceral sensory afferent system (C(7)-T(5) spinal ganglia and the corresponding posterior horn of the spinal cord) of asthmatic guinea pigs.

Methods: Forty guinea pigs were divided to four groups, a saline control group (group A, n = 8), a provocation alone control group (group B, n = 8), an asthmatic group (group C, n = 12) and an anti-NGF group (group D, n = 12). The alterations of PKC immunoreactivity were investigated by means of immunohistochemistry in the C(7)-T(5) spinal ganglia and the corresponding posterior horn of the spinal cord of all groups.