Emodin alleviates sepsis-mediated lung injury via inhibition and reduction of NF-kB and HMGB1 pathways mediated by SIRT1.

Inflammation plays an important role during sepsis, and excessive inflammation can result in organ damage, chronic inflammation, fibrosis, and scarring. The study aimed to investigate the specific mechanism of emodin by constructing in vivo and in vitro septic lung injury models via inhibition and reduction of NF-kB and high mobility group box 1 (HMGB1) pathways. A cecal ligation and puncture (CLP) model was built for adult male Sprague-Dawley rats. Concentrations of TNF-α, IL-1ß, and IL-6 in bronchoalveolar lavage fluid were determined using commercially available ELISA kits. Hematoxylin and eosin staining was used for the right lung inferior lobes. Myeloperoxidase (MPO) activity of the lung tissue was detected by using the MPO kit. Murine alveolar epithelial cell line (MLE-12) cells were used for flow cytometry and Western blot to analyze the apoptosis rate and protein expression. Emodin significantly decreased CLP-induced cell apoptosis, upregulated expression of sirtuin 1 (SIRT1), and inhibited p-p65/p65 and HMGB1. In lipopolysaccharide (LPS) treated cell model, emodin treatment markedly decreased LPS-induced release of IL-1, IL-6, and tumor necrosis factor (TNF)-α, inhibited LPS-induced cell apoptosis and suppressed protein levels of P-P65/P65 and HMGB1. However, science of SIRT1 reversed the above effects by treatment of emodin. In summarize, this study found that emodin can alleviate sepsis-induced lung injury in vivo and in vitro through regulation of SIRT1.

Multi-slice computed tomography for diagnosis of combined thoracoabdominal injury / 中华创伤杂志(英文版)

<p><b>PURPOSE</b>To investigate the diagnostic value of multi-slice computed tomography (MSCT) for combined thoracoabdominal injury.</p><p><b>METHODS</b>A retrospective study was conducted to analyze the clinical data and MSCT images of 68 patients who sustained a combined thoracoabdominal injury associated with diaphragm rupture, and 18 patients without diaphragm rupture. All the patients were admitted and treated in the Chongqing Emergency Medical Center (a level I trauma center) between July 2005 and February 2014. There were 71 males and 15 females with a mean age of 39.1 years (range 13e88 years). Among the 86 patients, 40 patients suffered a penetrating injury, 46 suffered a blunt injury as a result of road traffic accident in 21 cases, fall from a height in 16, and crushing injury in 9. The MSCT images were retrospectively reviewed by two radiologists. The results of CT diagnosis were compared with surgical findings and/or follow-up results.</p><p><b>RESULTS</b>Among the 86 cases, diaphragm discontinuity was found in 29 cases, segmental nonrecognition of the diaphragm in 14, diaphragmatic hernia in 21, collar sign in 14, dependent viscera sign in 18, elevated abdominal organs in 21, bowel wall thickening and/or hematoma in 6, and pneumoperitoneum in 8. CT diagnostic accuracy for diaphragm rupture was 88.4% in the right side and 90.7% in the left side. CT diagnostic accuracy for hemopneumothorax, pulmonary contusion, mediastinal hemorrhage, kidney and adrenal gland injuries was 100%, while for liver, spleen and pancreas injuries was 96.5%, 96.5%, 94.2% respectively.</p><p><b>CONCLUSION</b>To reach an early diagnosis of combined thoracoabdominal injury, surgeons and radiologists should be familiar with all kinds of images which might show signs of diaphragm rupture, such as diaphragm discontinuity, segmental nonrecognition of the diaphragm, dangling diaphragm sign, diaphragm herniation, collar sign, dependent viscera sign, and elevated abdominal organs.</p>

Mechanisms underlying low Ca(2+)(o)-induced increased excitability of hippocampal neurons / 神经科学通报·英文版

<p><b>OBJECTIVE</b>Concentration of extracellular calcium ([Ca(2+)](o)) in the central nervous system decreases substantially in different conditions. It results in facilitating neuronal excitability. The goal of this study is to examine the mechanisms of enhanced neuronal excitation in low [Ca(2+)](o) in order to provide new clues to treat the hyperexcitability diseases in clinic.</p><p><b>METHODS</b>Whole-cell patch-clamp technique and neuron culture were used in the study.</p><p><b>RESULTS</b>The firing threshold of cultured hippocampal neurons decreased markedly in low [Ca(2+)](o) saline. Unexpectedly, apamine and isoprenaline, antagonists of medium afterhyperpolarization (mAHP) and slow AHP (sAHP) respectively, had no statistic significant effect on excitability of neurons. TTX at a low concentration was sufficient to inhibit I(NaP), which blocked the increase of firing frequency in low [Ca(2+)](o). It also reduced the number of spikes in normal [Ca(2+)](o).</p><p><b>CONCLUSION</b>These results suggest that in cultured hippocampal neurons, modulation of spiking threshold but not AHP may cause the increased excitability in low [Ca(2+)](o).</p>

Effects and mechanisms of morphine on synaptic transmission of hippocampal neurons of rat / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of morphine on synaptic transmission of neurons of central nervous system and reveal the mechanism underlying it.</p><p><b>METHODS</b>New born wistar rats were used for primary culture of hippocampus neurons. Using whole-cell patch-clamp technique, we observed the excitatory and spontaneous inhibitory postsynaptic current (EPSC, sIPSC) and glutamate-induced current before and after morphine treatment.</p><p><b>RESULTS</b>(1) sEPSC of hippocampal neurons was markedly increased after morphine application. The effect of morphine was blocked by opioid antagonist naloxone (n=18, P < 0.01). (2) The frequency of mEPSC and the amplitude of glutamate-induced current of hippocampal neurons had no significant changes after morphine treatment (P > 0.05). (3) Morphine inhibited sIPSC of hippocampal neurons markedly and naloxone could block this effect (n=13, P < 0.01).</p><p><b>CONCLUSION</b>The results suggest that the exciting effect of morphine on hippocampal neurons are not due to direct influence of morphine on glutamate synapses transmission, but may result from the inhibition on interneurons, that is "disinhibition" way.</p>