Objective:To investigate whether sivelestat sodium (SV) mitigates paraquat (PQ)-induced acute lung injury (ALI)/acute respiratory distress syndrome (ARDS)-associated pulmonary fibrosis in mice by suppressing the NLRP3 inflammasome signaling pathway.Methods:Male C57BL/6J mice were randomly divided into four groups ( n=8 per group): Control group, PQ group, PQ+SV group, and SV group. The PQ and PQ+SV groups received an intraperitoneal injection of PQ solution (20 mg/kg) to establish a PQ poisoning model, while the Control and SV groups received an equivalent volume of saline. One hour later, the PQ+SV and SV groups were administered SV solution (100 mg/kg) intraperitoneally, whereas the Control and PQ groups received saline. After 48 hours, the mice were euthanized, and lung tissues were collected. Pathological changes were assessed via hematoxylin-eosin (HE) and Masson staining, followed by Smith and Ashcroft scoring. Immunohistochemistry was performed to evaluate the expression of NLRP3 inflammasome, caspase-1, α-smooth muscle actin (α-SMA), and collagen I. Western blotting was used to measure NLRP3 protein levels. Intergroup comparisons were conducted using one-way ANOVA with LSD post-hoc correction. Results:The Control and SV groups exhibited normal lung morphology, whereas the PQ+SV group showed reduced hemorrhage, congestion, and edema compared to the PQ group. Both PQ and PQ+SV groups exhibited significant weight loss post-intervention compared to the Control group (both P<0.001). HE and Masson staining revealed thickened alveolar septa, congestive and edematous alveolar walls, extensive inflammatory cell infiltration, and collagen deposition in the PQ group. In contrast, the PQ+SV group demonstrated alleviated alveolar wall congestion, reduced inflammatory infiltration, and decreased collagen deposition, with significantly lower Smith and Ashcroft scores [(5.92±1.34) vs. (10.88±1.88), P<0.001; (3.42±1.35) vs. (5.75±0.79), P<0.001]. Immunohistochemistry indicated reduced expression percentages of NLRP3 and caspase-1 in the PQ+SV group compared to the PQ group [(12.79%±0.43%) vs. (16.59%±0.40%), P<0.001; (17.71%±0.92%) vs. (19.84%±0.71%), P<0.001]. Similarly, α-SMA and collagen I expression in lung interstitium was significantly lower in the PQ+SV group [(11.79%±0.58%) vs. (16.14%±0.74%), P<0.001; (16.43%±0.56%) vs. (18.86%±0.60%), P<0.001]. Western blotting confirmed decreased NLRP3 protein expression in the PQ+SV group [(0.54±0.12) vs. (0.81±0.24), P<0.05]. Conclusions:SV attenuates PQ-induced ALI/ARDS-associated pulmonary fibrosis progression by inhibiting the NLRP3 inflammasome, suggesting that NLRP3 may be a key therapeutic target for early intervention in PQ-induced pulmonary fibrosis.

Objective: To explore the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection who received entecavir alone or in combination with anluohuaxianwan for 78 weeks. Methods: Patients with chronic HBV infection were randomly treated with entecavir alone or in combination with anluohuaxian for 78 weeks. Ishak fibrosis score was used for blind interpretation of liver biopsy specimens. The improvement in liver fibrosis condition before and after the treatment was compared. Student's t test and non-parametric test (Mann-Whitney U-Test and Kruskal-Wallis test) were used to analyze the measurement data. The categorical variables were analyzed by Chi-square test method and Spearman’s rank correlation coefficient was used to test bivariate associations. Results: Liver fibrosis improvement rate after 78 weeks of treatment was 36.53% (80/219) and the progression rate was 23.29% (51/219). The improvement of liver fibrosis was associated to the degree of baseline fibrosis and treatment methods (P < 0.05). The improvement rate of hepatic fibrosis in patients treated with anluohuaxianwan combined with entecavir at baseline F < 3 (54.74%, 52/95) was significantly higher than that in patients treated only with entecavir (33.33%, 16/48), P = 0.016 and the progression rate of hepatic fibrosis (13.68%, 13/95) was lower than that in patients treated alone (18.75%, 9/48), P = 0.466. In patients with baseline F < 3, the proportion of patients with improved and stable liver fibrosis in the combined treatment group (68.1%, 32/47) was higher than that in the treatment group alone (51.7%, 15/29). Conclusion Combined anluohuaxianwan and entecavir treatment can significantly improve the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection. Furthermore, it has the tendency to improve the stability rate and reduce the rate of progression of liver fibrosis.

Objective To study the protective effect of trimetazidine pretreatment on myocardial I/R in a rat I/R model and its mechanism.Methods One hundred and twenty SD rats were divided into control group,I/R group,HSP70 inhibitor group,trimetazidine treatment group and combined treatment group (24 in each group).The rats in each group were further divided into 30 min reperfusion group,4 h reperfusion group and 8 h reperfusion group (8 in each group).Their HSP70-positive myocardial cells were calculated,their serum CK,CK-MB,MDA,SOD levels and their myocardial infarction size were measured.Results The serum CK and CK-MB levels were significantly higher in I/R group,HSP70 inhibitor group,trimetazidine treatment group and combined treatment group than in control group and were significantly lower in trimetazidine treatment group than in combined treatment group and I/R group after reperfusion for 4 and 8 h (P＜0.01).The serum levels of HSP70 and SOD were significantly higher,the MDA levels were significantly lower in trimetazidine treatment group than in combined treatment group and I/R group after reperfusion for 30 min,4 and 8 h (P＜0.01).The infraction size was significantly smaller in trimetazidine treatment group than in combined treatment group and I/R group after reperfusion for 4 and 8 h (P＜0.05).Conclusion Trimetazidine can increase the serum HSP70 level in myocardial cells,reduce the infarction size,and protect the myocardium against I/R in rats.

Objective To investigate the relationship between the plasma NT-proBNP level and the severity of acute asthmatic attack,and to provide a reference for the assessment of the severity of asthma and the prognosis of patients with acute asthmatic attack. Methods A total of 103 adult patients with mild,moderate,severe,and very severe acute asthmatic attack were enrolled in this study. The difference of plasma NT-proBNP level among groups,and the correlation between plasma NT-proBNP level and APACHE II score(Acute Physiology and Chron-ic Health Evaluation)were investigated.The correlation between plasma NT-proBNP level and Peak Expiratory Flow (PEF)was also studied in each group. Results There was significant difference in plasma NT-proBNP among groups(P < 0.05). Plasma NT-proBNP and APACHE II score was positive correlated(R = 0.767 1,P < 0.05). However,plasma NT-proBNP was negatively correlated with PEF(R =-0.709 7,P < 0.05). Conclusion NT-proBNP can be used as one of the indexes to evaluate the severity of acute asthmatic attack.