An optimal medicinal and edible Chinese herbal formula attenuates particulate matter-induced lung injury through its anti-oxidative, anti-inflammatory and anti-apoptosis activities / 中草药·英文版

OBJECTIVE@#Identifying novel strategies to prevent particulate matter (PM)-induced lung injury is crucial for the reduction of the morbidity of chronic respiratory diseases. The combined intervention represented by herbal formulae for simultaneously targeting multiple pathological processes can provide a more beneficial effect than the single intervention. The aim of this paper is therefore to design a safe and effective medicinal and edible Chinese herbs (MECHs) formula against PM-induced lung injury.@*METHODS@#PM-induced oxidative stress, inflammatory response and apoptosis A549 cell model were used to screen anti-oxidant, anti-inflammatory and anti-apoptotic MECHs, respectively. A network pharmacology method was utilized to rationally design a novel herbal formula. Ultra performance liquid chromatography-mass spectrometer was utilized to assess the quality control of MECHs formula. The excretion of magnetic iron oxide nanospheres of the MECHs formula was estimated in zebrafish. The MECH formula against PM-induced lung injury was investigated with mice experiments.@*RESULTS@#Five selected herbs were rationally designed to form a new MECH formula, including Citri Exocarpium Rubrum (Juhong), Lablab Semen Album (Baibiandou), Atractylodis Macrocephalae Rhizoma (Baizhu), Mori Folium (Sangye) and Polygonati Odorati Rhizoma (Yuzhu). The formula effectively promoted the magnetic iron oxide nanospheres excretion in zebrafish. The mid/high dose formula significantly prevented PM-induced lung damage in mice by enhancing the activity of SOD and GSH-Px, reducing the MDA and ROS level and attenuating the upregulation of pro-inflammatory cytokine (IL-6, IL-8, IL-1β and TNF-α), down regulating the protein expression of NF-κB, STAT3 and Caspase-3.@*CONCLUSION@#Our findings suggest that the effective MECHs formula will become a novel strategy for preventing PM-induced lung injury and provide a paradigm for the development of functional foods using MECHs.

Mitophagy induced by classical swine fever virus nonstructural protein 5A promotes viral replication.

The classical swine fever virus (CSFV) is one of the most harmful pathogens of swine and causes considerable economic loss. Mitophagy is a selective form of autophagy that degrades damaged mitochondria by combining with lysosomes. Previous studies have been reported that CSFV infection can induce mitophagy, but which effector protein is responsible for this process remains unclear. Herein, we revealed here that the CSFV nonstructural protein 5A (NS5A) plays a critical role in inducing cellular mitophagy. Specifically, the expression of CSFV NS5A in the PK-15 cells induces membrane potential loss and mitochondrial fission, and the quantities of mitophagosomes, the expression of Parkin and PINK1 were significantly increased compared with mock cells. Intriguingly, we found that Parkin-overexpression promotes CSFV propagation. Furthermore, the expression level of reactive oxygen species (ROS) was increased by CSFV NS5A protein, while NS5A-induced mitophagy correlated with the quantity of ROS production. In summary, our results reveal a new function of NS5A in inducing cellular mitophagy and broaden our understanding of the mechanism of CSFV-induced mitophagy, which may provide a new way to develop an antiviral strategy.

CSFV protein NS5A activates the unfolded protein response to promote viral replication.

Classical swine fever is a world organization for animal health listed disease and is caused by classical swine fever virus (CSFV). CSFV can induced unfolded protein response (UPR) and whether NS5A protein plays a role in this process remains unknown. Here, we demonstrate that CSFV induced all the three signal pathways ATF6, IRE1 and PERK of UPR. Furthermore, this phenomenon may be mediated by the NS5A protein since expression of NS5A alone can achieve the same effect. In the current study, we show that NS5A can interact with GRP78 as measured by using the CO-IP and GST pulldown assays. This interaction plays a positive role in the promotion of CSFV replication. Overexpression or knockdown of GRP78 mediated by lentivirus can enhance or decrease viral replication, respectively. Our findings provide the evidence that CSFV infection can activate the cellular UPRs, in which NS5A and GRP78 play key roles in the process.

Intraclot microbubble combined with urokinase mediated ultrasound thrombolysis: Experiment in vitro / 中国介入影像与治疗学

Objective To investigate the efficiency of intraclot microbubbles (MB) combined with urokinase (UK) mediated ultrasound (US) thrombolysis.Metho ds Fifty clots prepared by bovine whole blood were equally divided into 5 groups and were treated in a circulation system with collateral circulation tube.The clots were treated by US,MB and UK in group 1,by US and MBingroup 2,by US and UK in group 3 and by UK in group 4.The group5 was the control group without any treatment.The thrombolysis rate of each group was measured and compared.Residual clots were histologically observed with hematoxylin-eosin staining and immunofluorescence.Results The thrombolysis rate of group 1 ([73.64±14.16]％) was significantly higher than group 2 ([47.97± 11.66]％),group 3 ([57.33±8.65]％),group 4 ([50.85±9.63]％),and group 5 ([29.76±18.06] ％,all P＜0.05).Histological examination of the clots in group 1 showed multiple thrombolysis foci with clots collapse,and the degradation of fibrin network was further confirmed by immunofluorescence.Conclusion The intraclot MB mediated US thrombolysis combined with UK can enhance the rate of thrombolysis in vitro experiment.