In order to investigate the therapeutic effect of traditional chinese medicine "Re Du Qing" on silicosis, the cultured and purifiel peritoneal macrophages in five groups obtained from mice were observed dynamically with cytochemical me- thods and scanning electron microscope. The results showed that the survival times of cell cultures were 2-3 weeks, 24-48, 72, 48-72 and 48-72 hr in normal, silica, "Re Du Qing", P204 and joint action group respectively in vitro. The characteristics of cell morphology with a series of cell surface ultrastructural changes in different times of culturd and the stages of various function were different in five groups. The cell surface ultrastructural changes of "Re Du Qing" group were similar to the normal group. The macrophages in the silica group phagocytosed silica dusts rapidly died and broken down much earlier than the cells in "Re Du Qing" group. The cell surface ultrastructural changes in P204 group were less than that of the cells in silica group, whereas the eell surface ultrastructural changes in joint action group were between the cells in "Re Du Qing" and P204 groups. The activities of intracellular acid phosphatase (AcP) and succinic dehydrogenase (SDH) in silica group were also much lower than that of "Re Du Qing" one. This study suggested that traditional chinese medicine "Re Du Qing" is evidently more effective on therapy of experimental silicosis.

AIM: To detect the role of cyclic nucleotides in the alleviation of hypoxic pulmonary vasoconstriction (HPV) in chronic hypoxic animals. METHODS: The intracellular cAMP and cGMP of the cultured porcine pulmonary arterial smooth muscle cells (PASMC) and endothelial cells (PAEC) were assayed by RIA. The length of single PASMC during acute hypoxia was measured by imaging analysis system. RESULTS: The basal levels of cAMP and cGMP in PASMC and cGMP in PAEC of Chronic hypoxic groups decreased remarkably compared with normoxic groups ( P

To investigate whether the change of E-cadherin (ECD) expression plays a role in the injury and repair of airway epithelial cells (AEC) caused by smoking, porcine AECs were cultured by using an enzyme-dispersed method. After exposure of the AECs to cigarette smoke extract(CSE), the ECD expression in the cells was detected by using immunocytochemistry and in situ hybridization. The results showed that ECD was distributed on the plasma membrane at the cell junctions of AECs. After exposure to 20% CSE, the membranous ECD expression was decreased, the cytoplasmic ECD expression was increased (P＜0.01) as the exposure time went on.But the content of ECD mRNA in the AECs did not chang. It suggests that the change of ECD expression is regulated at the posttranslational level and plays a role in the injury and repair of AEC caused by smoking.

To investigate whether the change of E-cadherin (ECD) expression plays a role in the injury and repair of airway epithelial cells (AEC) caused by smoking, porcine AECs were cultured by using an enzyme-dispersed method. After exposure of the AECs to cigarette smoke extract(CSE), the ECD expression in the cells was detected by using immunocytochemistry and in situ hybridization. The results showed that ECD was distributed on the plasma membrane at the cell junctions of AECs. After exposure to 20% CSE, the membranous ECD expression was decreased, the cytoplasmic ECD expression was increased (P＜0.01) as the exposure time went on.But the content of ECD mRNA in the AECs did not chang. It suggests that the change of ECD expression is regulated at the posttranslational level and plays a role in the injury and repair of AEC caused by smoking.

To investigate the effect of lithium on cell cycle progression of airway epithelial cells, primary pig tracheobronchial epithelial cells were incubated with lithium chloride (LiCl) at different concentrations (0, 5 mmol/L, and 10 mmol/L) and time (12 h, 16 h and 24 h). After the treatment, cells were counted, cell cycle profile was measured by BrdU labeling and flow cytometry, and expression of cyclin D1 and cyclin B1 were detected by Western blotting. The results showed that after 24h of 10mmol/L but not 5mmol/L LiCl treatment, proliferation of cells was slowed down as manifested by delayed confluence and cell number accumulation (P<0.05). Lithium did not change the percentage of cells in S phase (P>0.05), but 24 h incubation with 10 mmol/L LiCl induced a G2/M cell cycle arrest. Furthermore, 10mmol/L LiCl elevated cyclin D1 expression after 12h treatment, while expression of cyclin B1 increased more significantly after 24h incubation. These data demonstrate that lithium inhibits proliferation of pig airway epithelial cells by inhibiting cell cycle progression, and suggest that lithium-sensitive molecule(s) such as glycogen synthase kinase 3 may have a role in the regulation of growth of airway epithelial cells.
Animals ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; Cells, Cultured ; Cyclin D1 ; metabolism ; Epithelial Cells ; cytology ; drug effects ; Flow Cytometry ; Glycogen Synthase Kinase 3 ; metabolism ; Lithium Chloride ; pharmacology ; Swine ; Trachea ; cytology

Objective:To explore the relationship between negative evaluation fear and mobile phone addiction, and the mediating role of balanced time perspective.Methods:In April 2021, totally 1 158 secondary vocational school students were investigated by scales of fear of negative evaluation(FNE), mobile phone addiction index(MPAI)and Zimbardo time perspective inventory(ZTPI). The balanced time perspective was calculated by deviation from the balanced time perspective(DBTP). SPSS 20.0 statistical software was used for descriptive statistical analysis and correlation analysis of the data.Bootstrap method was used to test the mediating effect.Results:(1) Negative evaluation fear(37.87±7.71)was significantly positively correlated with balanced time perspective(4.50±0.75)( r= 0.379, P<0.01) and mobile phone addiction(46.11±11.92)( r=0.437, P<0.01). The balanced time perspective was significantly positively correlated with mobile phone addiction( r=0.475, P<0.01). (2) Negative evaluation fear directly and positively predicted mobile phone addiction( β=0.300, 95% CI=0.248-0.352). The balanced time perspective played a partial mediating role between negative evaluation fear and mobile phone addiction, and the mediating effect value was 0.137, accounted for 31.31%(0.137/0.437) of the total effect. Conclusion:The fear of negative evaluation can directly affect the mobile phone addiction behavior of secondary vocational students, and can also indirectly affect the mobile phone addiction by affecting the balanced time perspective.Good balanced time perspective can reduce the risk caused by the fear of negative evaluation.

AIM:This study aims to explore the impact of Escherichia coli(E.coli)high-pathogenicity island(HPI)on pyroptosis and intestinal inflammation.METHODS:Kunming mice and IPEC-J2 cells(porcine small intesti-nal epithelial cells)were treated with HPI-containing E.coli strain(HPI+),HPI-deleting E.coli strain(ΔHPI),or lipo-polysaccharide(LPS).The intestinal lactate dehydrogenase(LDH)activity,superoxide dismutase(SOD)activity,IgA expression and secretory IgA(SIgA)content were assessed in mice.The expression of key regulatory factors in the nucleo-tide-binding oligomerization domain-like receptor protein 3(NLRP3)/caspase-1 signaling pathway-related proteins in mouse intestinal tract and IPEC-J2 cells was analyzed by RT-qPCR,immunohistochemical staining and Western blot.The levels of interleukin-1β(IL-1β)and IL-18 in mouse serum and IPEC-J2 cell culture supernatants were measured by ELISA.The pivotal role of NLRP3 in HPI+infection was confirmed by silencing NLRP3 in IPEC-J2 cells using siRNA.RE-SULTS:The HPI+infection markedly decreased SOD activity,increased IgA+B cell count,and induced the LDH release and SIgA secretion in the mouse intestine compared with ΔHPI infection.The results of ELISA,HE staining and TUNEL staining indicated that E.coli HPI triggered DNA damage,tissue injury and inflammation in mouse intestinal epithelial cells.Western blot revealed an increase in intestinal gasdermin D N-terminal fragment(GSDMD-N)protein level with HPI+infection compared with ΔHPI infection.E.coli HPI significantly up-regulated mRNA and protein expression of NLRP3,apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),caspase-1,GSDMD,IL-1β and IL-18 in mouse intestinal tissues and IPEC-J2 cells,accompanied by the elevated secretion of IL-1β and IL-18.The confo-cal microscopy demonstrated an enhanced assembly of the NLRP3 inflammasome with HPI+infection compared with ΔHPI infection,leading to colocalization of NLRP3 and caspase-1.Furthermore,NLRP3 silencing in IPEC-J2 cells attenuated E.coli HPI-induced cell inflammation,damage,and NLRP3/caspase-1 signaling pathway activation.CONCLUSION:The presence of HPI enhances the virulence of E.coli and exacerbates intestinal inflammation.Moreover,pyroptosis,regu-lated by the NLRP3/caspase-1 signaling pathway,plays a pivotal role in the intestinal injury induced by E.coli HPI.