Objective:To analyze the clinical efficacy of Seretide combined with noninvasive positive pressure ventilation (NIPPV) in the treatment of chronic obstructive pulmonary disease (COPD) complicated with type 2 respiratory failure (RF).Methods:120 patients of COPD complicated with type 2 RF were randomly divided into the observation group and the control group.All patients were treated with routine,symptomatic and supportive treatment,based on that NIPPV was used in the control group,and the observation group was treated with Seretide on the basis of NIPPV.The levels of arterial blood gas,inflammatory factors,pulmonary function and CAPS score before and after treatment were compared and analyzed.Results:After treatment,the pH,PaO2 and SaO2 of both groups were significantly increased,PaCO2 levels weresignificantly decreased,serum IL-33,TNF-oα and sICAM-1 levels were significantly decreased,FVC,PEFR,FEV1％ and FEV1/FVC were significantly decreased,and the CAPS scores were significantly decreased;the changes of all the index mentioned above in the observation group were more statistically significant (P＜0.05).Conclusion:Seretide com bined with NIPPV could more effectively decrease the levels of inflammatory factors and improve the blood gas and lung function in the patients of COPD with type 2 respiratory failure.

Objective To investigate the function of burdock leaf extract NBY-4 in protecting vascular endothelial cells from oxidative damage.Methods The oxidative damage model of vascular endothelial cells was established with hydrogen peroxide(H2O2).ROS,LDH,SOD,apoptosis rate and the expression of apoptosis were measured;Further test the nuclear transcription factor-κB(NF-κB).Results In the model group,H2O2 increased the apoptosis rate of endothelial cells,increased the ratio of Bax/Bcl-2 and the expression of Caspase-3,promoted the production of ROS and LDH in endothelial cells,and inhibited the level of SOD,resulting in oxidative damage to endothelial cells(P<0.05).NBY-4 could slow down the process of these effects;At the same time,NBY-4 can reduce NF-κB in endothelial cells.Conclusion NBY-4 can inhibit endothelial cell apoptosis and antioxidant damage by NF-κB signaling pathway.

As an effective anticancer drug, the clinical limitation of doxorubicin (Dox) is the time- and dose-dependent cardiotoxicity. Yes-associated protein 1 (YAP1) interacts with transcription factor TEA domain 1 (TEAD1) and plays an important role in cell proliferation and survival. However, the role of YAP1 in Dox-induced cardiomyopathy has not been reported. In this study, the expression of YAP1 was reduced in clinical human failing hearts with dilated cardiomyopathy and Dox-induced

The clinical application of doxorubicin (DOX) in cancer chemotherapy is limited by its life-threatening cardiotoxic effects. Chrysophanol (CHR), an anthraquinone compound isolated from the rhizome of L., is considered to play a broad role in a variety of biological processes. However, the effects of CHR׳s cardioprotection in DOX-induced cardiomyopathy is poorly understood. In this study, we found that the cardiac apoptosis, mitochondrial injury and cellular PARylation levels were significantly increased in H9C2 cells treated by Dox, while these effects were suppressed by CHR. Similar results were observed when PARP1 activity was suppressed by its inhibitors 3-aminobenzamide (3AB) and ABT888. Ectopic expression of PARP1 effectively blocked this CHR׳s cardioprotection against DOX-induced cardiomyocyte injury in H9C2 cells. Furthermore, pre-administration with both CHR and 3AB relieved DOX-induced cardiac apoptosis, mitochondrial impairment and heart dysfunction in Sprague-Dawley rat model. These results revealed that CHR protects against DOX-induced cardiotoxicity by suppressing cellular PARylation and provided critical evidence that PARylation may be a novel target for DOX-induced cardiomyopathy.

The clinical utilization of doxorubicin (Dox) in various malignancies is restrained by its major adverse effect: irreversible cardiomyopathy. Extensive studies have been done to explore the prevention of Dox cardiomyopathy. Currently, ferroptosis has been shown to participate in the incidence and development of Dox cardiomyopathy. Sorting Nexin 3 (SNX3), the retromer-associated cargo binding protein with important physiological functions, was identified as a potent therapeutic target for cardiac hypertrophy in our previous study. However, few study has shown whether SNX3 plays a critical role in Dox-induced cardiomyopathy. In this study, a decreased level of SNX3 in Dox-induced cardiomyopathy was observed. Cardiac-specific Snx3 knockout (Snx3-cKO) significantly alleviated cardiomyopathy by downregulating Dox-induced ferroptosis significantly. SNX3 was further demonstrated to exacerbate Dox-induced cardiomyopathy via induction of ferroptosis in vivo and in vitro, and cardiac-specific Snx3 transgenic (Snx3-cTg) mice were more susceptible to Dox-induced ferroptosis and cardiomyopathy. Mechanistically, SNX3 facilitated the recycling of transferrin 1 receptor (TFRC) via direct interaction, disrupting iron homeostasis, increasing the accumulation of iron, triggering ferroptosis, and eventually exacerbating Dox-induced cardiomyopathy. Overall, these findings established a direct SNX3-TFRC-ferroptosis positive regulatory axis in Dox-induced cardiomyopathy and suggested that targeting SNX3 provided a new effective therapeutic strategy for Dox-induced cardiomyopathy through TFRC-dependent ferroptosis.

Prostate cancer (PCa) patients who progress to metastatic castration-resistant PCa (mCRPC) mostly have poor outcomes due to the lack of effective therapies. Our recent study established the orphan nuclear receptor ROR