Objective To evaluate the relationship between the expression of Nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) in nerve tissues and mitochondrial function during mechanical stretch-induced damage to mouse alveolar epithelial cells.Methods Alveolar epithelial type Ⅱ cell line MLE-12 cells were divided into 3 groups (n=13 each) using a random number table:control group (group C),cyclic stretch group (group CS) and cyclic stretch plus NLRP3 inhibitor TAK-242 group (group CS+T).MLE-12 cells underwent 20％ cyclic stretch at a frequency of 0.5 Hz (stretch ∶ intermittence =1 ∶ 1) for 4 h in group CS.In group CS+T,after being incubated for 1 h with 1 μ mol/L TAK-242,MLE-12 cells underwent 20％ cyclic stretch for 4 h,and the parameters were similar to those previously described in group CS.The reactive oxygen species (ROS) content and mitochondrial membrane potential (△ΨM) were measured using chemiluminescence assay.Enzyme-linked immunosorbent assay was used to determine the concentration of interleukin-1 beta (IL-1β) in the supernatant.The expression of NLRP3 in MLE-12 cells was detected using Western blot.Results Compared with group C,the △ΨM of cells was significantly decreased,the ROS content and IL-1β concentration were increased,and the expression of NLRP3 was up-regulated in group CS,and the △ΨM of cells was significantly decreased,the ROS content was increased,and the expression of NLRP3 was up-regulated in group CS+T (P＜0.05).Compared with group CS,the △ΨM of cells was significantly increased,the ROS content and IL-1β concentration were decreased,and the expression of NLRP3 was down-regulated in group CS+T (P＜ 0.05).Conclusion Mechanical stretch induces damage to mitochondria through up-regulating the expression of NLRP3,thus leading to damage to mouse alveolar epithelial cells.

Objective To evaluate the effect of recombinant human annexin A5 on the expression of phosphorylated protein kinase C alpha (p-PKCα) and p120-catenin during endotoxin-induced damage to cardiomyocytes.Methods H9c2 cells cultured in vitro were randomly divided into 3 groups (n=18 each) using a random number table:control group (group C),endotoxin group (group L),and recombinant human annexin A5 group (group A).Recombinant human annexin A5 (final concentration 5 ng/ml) was added,and the cells were incubated for 2 h in group A,and then lipopolysaccharide (final concentration 1 μg/ml) was added,and the cells were incubated for 4 h in L and A groups.At 4 h of incubation,cell apoptosis was detected using the cell apoptosis detection kit,the intercellular space was measured using the confocal microscopy,and the expression of p-PKCα and p120-catenin was determined by Western blot.The apoptosis rate was calculated.Results Compared with group C,the apoptosis rate was significantly increased,the intercellular space was significantly widened,the expression of p120-catenin was significantly down-regulated,and the expression of p-PKCα was significantly up-regulated in group L (P＜0.05).Compared with group L,the apoptosis rate and intercellular space were significantly decreased,the expression of p120-catenin was significantly up-regulated,and the expression of p-PKCα was significantly down-regulated in group A (P＜0.05).Conclusion Recombinant human annexin A5 can inhibit phosphorylation of PKCα and up-regulate the expression of p120-catenin,thus attenuating endotoxin-induced damage to cardiomyocytes.