Plasmacytoid Dendritic Cells Mediate Myocardial Ischemia/Reperfusion Injury by Secreting Type I Interferons.

Background We previously demonstrated that ischemically injured cardiomyocytes release cell-free DNA and HMGB1 (high mobility group box 1 protein) into circulation during reperfusion, activating proinflammatory responses and ultimately exacerbating reperfusion injury. We hypothesize that cell-free DNA and HMGB1 mediate myocardial ischemia-reperfusion injury by stimulating plasmacytoid dendritic cells (pDCs) to secrete type I interferon (IFN-I). Methods and Results C57BL/6 and interferon alpha receptor-1 knockout mice underwent 40 minutes of left coronary artery occlusion followed by 60 minutes of reperfusion (40'/60' IR) before infarct size was evaluated by 2,3,5-Triphenyltetrazolium chloride-Blue staining.

Role of endoplasmic reticulum oxidase 1α in H9C2 cardiomyocytes following hypoxia/reoxygenation injury.

Endoplasmic reticulum (ER) oxidase 1α (ERO1α) is a glycosylated flavoenzyme that is located on the luminal side of the ER membrane, which serves an important role in catalyzing the formation of protein disulfide bonds and ER redox homeostasis. However, the role of ERO1α in myocardial hypoxia/reoxygenation (H/R) injury remains largely unknown. In the present study, ERO1α expression levels in H9C2 cardiomyocytes increased following H/R, reaching their highest levels following 3 h of hypoxia and 6 h of reoxygenation.

Lazaroid U83836E protects the heart against ischemia reperfusion injury via inhibition of oxidative stress and activation of PKC.

Oxidative stress has been demonstrated to be important during myocardial ischemia/reperfusion injury (MIRI). The lazaroid U83836E, which combines the amino functionalities of the 21‑aminosteroids with the antioxidant ring portion of vitamin E, is a reactive oxygen species scavenger. The aim of the current study was to investigate the effect of U83836E on MIRI and its mechanisms of action.

Effect of artesunate supplementation on bacterial translocation and dysbiosis of gut microbiota in rats with liver cirrhosis.

Aim: To evaluate the effect of artesunate (AS) supplementation on bacterial translocation (BT) and gut microbiota in a rat model of liver cirrhosis.

Methods: Fifty-four male Sprague-Dawley rats were randomly divided into a normal control group (N), a liver cirrhosis group (M) and a liver cirrhosis group intervened with AS (MA). Each group was sampled at 4, 6 and 8 wk.

Artesunate alleviates hepatic fibrosis induced by multiple pathogenic factors and inflammation through the inhibition of LPS/TLR4/NF-κB signaling pathway in rats.

The current study was performed in order to explore the effect of artesunate (Art) on experimental hepatic fibrosis and the potential mechanism involved. Art, a water-soluble hemisuccinate derivative of artemisinin extracted from the Chinese herb Artemisia Annua, is a safe and effective antimalarial drug. Hepatic fibrosis was induced in SD rats by multiple pathogenic factors.

Electrochemical sensors using gold submicron particles modified electrodes based on calcium complexes formed with alizarin red S for determination of Ca(2+) in isolated rat heart mitochondria.

A simple glassy carbon electrode (GCE) modified with gold submicron particles (AuSPs), characterized by a mean diameter of about0.15-0.20μm has been developed.

Study on the interaction between ligustrazine and 12-tungstophosphoric acid using resonance Rayleigh scattering and resonance nonlinear scattering spectra, and its analytical applications.

In an HCl medium (pH 1.5), ligustrazine (2,3,5,6-tetramethylpyrazine, TMP) reacted with 12-tungstophosphoric acid (TP) to form a 3 : 1 ion-association complex. As a result, the intensities of resonance Rayleigh scattering (RRS), second-order scattering (SOS) and frequency doubling scattering (FDS) were greatly enhanced and new scattering spectra appeared.

[Protective effect of tanshinol on the hepatopulmonary syndrome in rat].

Objective: To explore the mechanism of tanshinol on alleviate the inflammatory injury of lung tissue in rat hepatopulmonary syndrome (HPS).

Methods: SD rats were randomly divided into normal control group (n = 8), hepatopulmonary syndrome (HPS) group (n = 11) and tanshinol intervention group (n = 9). HE staining was used to observe the histopathology changes of pulmonary and hepatic tissues, and to count the number of macrophages in lung tissues.

[A method for primary culture of pulmonary microvascular endothelial cells].

Objective: To explore a simple and practical method of primarily culturing rat pulmonary microvascular endothelial cells (PMECs) in vitro, and observe the cell growth status and identify the PMECs.

Methods: Wistar rats (n=40, aged 4-5 weeks) were sacrificed to take the lung tissue. After removal of pleura, the peripheral lung tissues were cut into pieces (1 mm(3)) in aseptic condition.

Glucose-regulated protein 78 may play a crucial role in promoting the pulmonary microvascular remodeling in a rat model of hepatopulmonary syndrome.

Objective: This study is to investigate the role of glucose-regulated protein 78 (GRP78) in the pulmonary microvascular remodeling during hepatopulmonary syndrome (HPS) development.

Methods: The rat models with liver cirrhosis and HPS were induced by multiple pathogenic factors for 4 to 8 wk. The concentrations of alanine transferase (ALT) and endotoxin in plasma were detected in the models, followed by the detection of GRP78 expression.

Expression of the 78 kD glucose-regulated protein is induced by endoplasmic reticulum stress in the development of hepatopulmonary syndrome.

Objective: This study is to explore the role of 78 kD glucose-regulated protein (GRP78) in the development of hepatopulmonary syndrome (HPS) in rats.

Methods: The rat model of liver cirrhosis and HPS were induced with multiple pathogenic factors. Hematoxylin and eosin (H & E) staining was performed to detect the pathological changes of the lung and liver tissues.

Surface display and bioactivity of Bombyx mori acetylcholinesterase on Pichia pastoris.

A Pichia pastoris (P. pastoris) cell surface display system of Bombyx mori acetylcholinesterase (BmAChE) was constructed and its bioactivity was studied. The modified Bombyx mori acetylcholinesterase gene (bmace) was fused with the anchor protein (AGα1) from Saccharomyces cerevisiae and transformed into P.