Lung macrophages are involved in lung injury secondary to repetitive diving / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

This study aimed to establish an animal model of decompression-induced lung injury (DILI) secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentration hydrogen (HCH) on DILI. Mice were divided into three groups: control group, DILI group, and HCH group. Mice were exposed to hyperbaric air at 600 kPa for 60 min once daily for consecutive 3 d and then experienced decompression. In HCH group, mice were administered with HCH (66.7% hydrogen and 33.3% oxygen) for 60 min after each hyperbaric exposure. Pulmonary function tests were done 6 h after decompression; the blood was harvested for cell counting; the lung tissues were harvested for the detection of inflammatory cytokines, hematoxylin and eosin (HE) staining, and immunohistochemistry; western blotting and polymerase chain reaction (PCR) were done for the detection of markers for M1 and M2 macrophages. Our results showed that bubbles formed after decompression and repeated hyperbaric exposures significantly reduced the total lung volume and functional residual volume. Moreover, repetitive diving dramatically increased proinflammatory factors and increased the markers of both M1 and M2 macrophages. HCH inhalation improved lung function to a certain extent, and significantly reduced the pro-inflammatory factors. These effects were related to the reduction of M1 macrophages as well as the increase in M2 macrophages. This study indicates that repetitive diving damages lung function and activates lung macrophages, resulting in lung inflammation. HCH inhalation after each diving may be a promising strategy for the prevention of DILI.

Neuroprotective effects of kukoamine A against rotenone-induced neurotoxicity in PC12 cells / 中草药

Objective: To investigate the neuroprotective effects of kukoamine A (KuA) on rotenone-induced PC12 cells damage and to preliminary verify its potential action mechanisms. The present study may lay the foundation for finding leading compounds with anti-Parkinson's disease (PD) effects. Methods: A PD model induced by rotenone was established in vitro, and MTT, LDH, and Hoechst33342 staining were used for preliminary confirmation of KuA resistance to rotenone-induced PC12 cell injury in vitro. The effects of KuA on superoxide dismutase (SOD) activity, malondialdehyde (MDA) and reactive oxygen species (ROS) content, and mitochondrial membrane potential (MMP) were investigated by colorimetric method and fluorescence staining, respectively. Western blotting was applied to explore the underlying mechanisms of protective effects of KuA against rotenone-induced PC12 cells damage. Results: The PC12 cell viability was significantly decreased after exposure to 0.5 μmol/L rotenone, whereas pretreatment with different concentrations of KuA could attenuate the cell injury induced by rotenone. Compared with the rotenone-treated group, KuA could decrease the ROS production and MDA level, while increase the SOD activity. In addition, KuA could effectively increase the MMP, decrease the cytochrome c release and the Bax/Bcl-2 ratio as well as inhibit caspase-3, caspase-9, and α-synuclein protein expressions. Conclusion: KuA showed neuroprotective ability on rotenone-induced PC12 cells PD model and the potential protective mechanisms of KuA can be related with inhibition of ROS generation, protection of MMP, regulation of protein expressions involved in the mitochondrial apoptosis pathway and reduction of α-synuclein expression.

Chemical constituents of coumarins compounds from Notopterygium incisum and their anti-oxidant activity / 中草药

Objective: To investigate the coumarin compounds from Notopterygium incisum and their anti-oxidant activities. Methods The coumarin compounds and their analogues were separated and purified by recrystallization, silica gel column chromatography, Sephadex LH-20 column chromatography, and preparative HPLC. The structure was identified by modern spectroscopy. The isolated compound was tested for anti-oxidant activity by DPPH and ABTS assay. Results Ten compounds were isolated from the dichloromethane extraction layer of 70% ethanol extract, which were identified as bergaptol (1), d-laserpitin (2), falcarindiol (3), phenethyl ferulate (4), selinidin (5), archangelicin (6), notoptol (7), nodakenetin (8), (+)-cis-khellactone (9), and oxypeucedanin hydrate (10). The anti-oxidant activity of these compounds was tested by DPPH and ABTS methods. Conclusion Compounds 2 and 6 are isolated from this plant for the first time. Compounds 1 and 7 have shown the strongest anti-oxidant activity. The structure-activity relationship (SAR) studies revealed the -OH and unsaturated double bond on C-5′ in the aromatic ring significantly improved the anti-oxidant activity than other coumarin compounds.

Necroptosis Signaling Pathways in Stroke: From Mechanisms to Therapies.

It has been confirmed that apoptosis, autophagy and necrosis are the three major modes of cell death. For a long time, necrosis is regarded as a deranged or accidental cell demise. In recent years, there is evidence showing that necrotic cell death can be a well regulated and orchestrated event, which is also known as programmed cell death or "necroptosis". Necroptosis can be triggered by a variety of external stimuli and regulated by a caspase-independent pathway. It plays a key role in the pathogenesis of some diseases including neurological diseases. In the past two decades, a variety of studies have revealed that the necroptosis related pathway is activated in stroke, and plays a crucial role in the pathogenesis of stroke. Moreover, necroptosis may serve as a potential target in the therapy of stroke because genetic or pharmacological inhibition of necroptosis has been shown to be neuroprotective in stroke in vitro and in vivo. In this review, we briefly summarize recent advances in necroptosis, introduce the mechanism and strategies targeting necroptosis in stroke, and finally propose some issues in the treatment of stroke by targeting necroptosis.

Treatment of pretreated coking wastewater by flocculation, alkali out, air stripping, and three-dimensional electrocatalytic oxidation with parallel plate electrodes.

The coking wastewater generally comprises highly concentrated, recalcitrant, and toxic organic pollutants, so its treatment has been of great importance to prevent living beings and their environment from these hazardous contaminations. The treatment of pretreated coking wastewater by flocculation-coagulation, alkali out, air stripping, and three-dimensional (3-D) electrocatalytic oxidation was performed (gap between the used ß-PbO2/Ti anode and titanium cathode, 12 mm; mass ratio of Cu-Mn/granular activated carbon (GAC) to effluent, 1:4; cell voltage, 7 V). The results showed that the pH adjusting from 3.7 to 6.1 was necessary for coagulants; alkali out played an important role because it brought up precipitation containing higher fatty acids as well as other contaminants to decrease the chemical oxygen demand (COD) in the effluent, and it had also forced the reduction of ammonia nitrogen (NH3-N) by incorporating with air stripping; for 3-D electrocatalytic oxidation with a bleaching liquid assisting, the initial pH 8.5 of effluent was suitable for Cu-Mn/GAC; moreover, it was considered that its Cu component was dedicated to the decrease of COD and NH3-N, while the Mn component specialized in the decay of NH3-N. The residual COD and NH3-N values in the final effluent with pH 6.5 were 95.8 and 8.8 mg/L, respectively, demonstrating that the whole processes applied were feasible and low in cost.

Mitochondrial nitric oxide synthase: Biological function / 第二军医大学学报

Increasing evidences have shown the existance of a mitochondrial nitric oxide synthase (mtNOS), which binds to the matrix face of the mitochondrial inner membrane and produces nitric oxide (NO) through a Ca2+ sensitive pathway. Under physiological condition, the NO catalyzed by mtNOS regulates mitochondrial oxygen consumption and transmembrane potential via reversible competition with cytochrome C oxidase. The reaction of NO with superoxide anion, which was produced by mitochondrial respiratory chain, yields peroxynitrite. Peroxynitrite irreversibly modifies susceptible targets in mitochondria and induces oxidative and/or nitrative stress. In addition, NO has also been implicated in the programmed cell death. This article reviews the current understanding of mtNOS's role in the regulation of mitochondrial functions.