Jinyinqingre Oral Liquid alleviates LPS-induced acute lung injury by inhibiting the NF-κB/NLRP3/GSDMD pathway / 中国天然药物

Acute lung injury (ALI) is a prevalent and severe clinical condition characterized by inflammatory damage to the lung endothelial and epithelial barriers, resulting in high incidence and mortality rates. Currently, there is a lack of safe and effective drugs for the treatment of ALI. In a previous clinical study, we observed that Jinyinqingre oral liquid (JYQR), a Traditional Chinese Medicine formulation prepared by the Taihe Hospital, Affiliated Hospital of Hubei University of Medicine, exhibited notable efficacy in treating inflammation-related hepatitis and cholecystitis in clinical settings. However, the potential role of JYQR in ALI/acute respiratory distress syndrome (ARDS) and its anti-inflammatory mechanism remains unexplored. Thus, the present study aimed to investigate the therapeutic effects and underlying molecular mechanisms of JYQR in ALI using a mouse model of lipopolysaccharide (LPS)-induced ALI and an in vitro RAW264.7 cell model. JYQR yielded substantial improvements in LPS-induced histological alterations in lung tissues. Additionally, JYQR administration led to a noteworthy reduction in total protein levels within the BALF, a decrease in MPAP, and attenuation of pleural thickness. These findings collectively highlight the remarkable efficacy of JYQR in mitigating the deleterious effects of LPS-induced ALI. Mechanistic investigations revealed that JYQR pretreatment significantly inhibited NF-κB activation and downregulated the expressions of the downstream proteins, namely NLRP3 and GSDMD, as well as proinflammatory cytokine levels in mice and RAW2647 cells. Consequently, JYQR alleviated LPS-induced ALI by inhibiting the NF-κB/NLRP3/GSDMD pathway. JYQR exerts a protective effect against LPS-induced ALI in mice, and its mechanism of action involves the downregulation of the NF-κB/NLRP3/GSDMD inflammatory pathway.

Establishment of a rat model of cardiopulmonary resuscitation with mechanical chest compression / 中国实验动物学报

Objective To explore the feasibility of mechanical chest compression to establish a rat model of car?diopulmonary resuscitation ( CPR) . Methods 4?month old healthy male Sprague Dawley rats were randomly divided into control group ( n=6 ) and model group ( n=10 ) . After induction of anaesthesia with 10% chloraldurate ( 3 ml/kg, i. p. ) , tracheal intubation and left femoral artery cannulation were performed. Under electrocardiographic and artery blood pressure monitoring, tracheal obstruction ( TO) was performed to rats in model group. At 2 min after the cardiac arrest ( CA) occurred, CPRs were administered to the rats using a self?made animal chest compressor, which provided chest?com?pression at a rate of 200 bpm. Results Shortly after TO, rats in the model group had respiratory arrest, cyanosis and ar?rhythmia. Electrocardiography indicated that CA occurred within 4-5 min, with a decreased artery systolic blood pressure ( <40 mmHg) and a zero pulse pressure. Return of spontaneous circulation ( ROSC) after the CPR was successfully a?chieved in 8 rats (80%), with a transient reperfusion arrhythmia. Finally, 60% of the rats (n=6) recovered to con?sciousness and survived for 24 hrs. The serum biochemical analysis indicated that there were electrolyte disturbances, aci?dosis, impaired renal functions and increased myocardial enzyme spectrum. Pathological examination revealed cardiac rhab? domyolysis, no?reflow phenomenon in renal glomeruli, decrease of neurons and pulmonary congestion in the model group rats. Conclusions Mechanical chest compression can provide minimal cardiac output for the requirement of CPR incardiac arrestin rats. It is feasible to establish rat CPR model with the mechanical chest compression.