Regulatory effects of Trichinella spiralis and a serine protease inhibitor on the endoplasmic reticulum stress response of intestinal epithelial cells.

The accumulation of unfolded or misfolded proteins in the endoplasmic reticulum can cause an endoplasmic reticulum stress (ERS) response. If ERS continues or cannot be alleviated, it will cause the production of proapoptotic factors and eventually lead to apoptosis. Therefore, this study mainly explored whether Trichinella spiralis Kazal-type serine protease inhibitor (TsKaSPI) contributed to the invasion of intestinal epithelial cells during the infectious stage of T. spiralis by regulating ERS. First, in the T. spiralis infection model, H&E staining was used to analyse the damage to jejunum tissue, a TUNEL assay was used to examine cell apoptosis, and the expression of ERS-related and apoptosis-related molecules was also measured. The results showed that ERS occurred during the intestinal phase of T. spiralis infection, while remission began during the cyclic phase. Then, we selected TsKaSPI, one of the important components of T. spiralis ES antigens, for in vitro experiments. The results showed that TsKaSPI could induce apoptosis in a porcine small intestinal epithelial cell line (IPEC cells) by activating ERS and promote activation of the NF-κB signalling pathway. Inhibition experiments confirmed that the occurrence of ERS was accompanied by the activation of NF-κB, and the two processes regulated each other. Finally, we conducted in vivo experiments and administered TsKaSPI to mice. The results confirmed that TsKaSPI could activate ERS and lead to apoptosis in intestinal epithelial cells. In conclusion, T. spiralis infection and TsKaSPI can promote cell apoptosis by activating the ERS response in intestinal epithelial cells and activate the NF-κB signalling pathway to promote the occurrence and development of inflammation.

Characterization of a Bioresorbable Magnesium-Reinforced PLA-Integrated GTR/GBR Membrane as Dental Applications.

Inferior mechanical properties have always been a limitation of the bioresorbable membranes in GBR/GTR. This study is aimed at fabricating a bioresorbable magnesium-reinforced polylactic acid- (PLA-) integrated membrane and investigating its mechanical properties, degradation rate, and biocompatibility. The uncoated and fluoride-coated magnesium alloys, AZ91, were made into strips. Then, magnesium-reinforced PLA-integrated membrane was made through integration. PLA strips were used in the control group instead of magnesium strips. Specimens were cut into rectangular shape and immersed in Hank's Balanced Salt Solution (HBSS) at 37°C for 4, 8, and 12 d. The weight loss of the AZ91 strips was measured. Three-point bending tests were conducted before and after the immersion to determine the maximum load on specimens. Potentiodynamic polarization (PDP), electrochemical impedance spectroscopy (EIS), scanning electron microscopy (SEM), and energy-dispersive spectroscopy (EDS) were conducted on coated and uncoated AZ91 plates to examine corrosion resistance. Murine fibroblast and osteoblast cells were cultured on circular specimens and titanium disks for 1, 3, and 5 d. Thereafter, WST test was performed to examine cell proliferation. As a result, the coated and uncoated groups showed higher maximum loads than the control group at all time points. The weight loss of AZ91 strips used in the coated group was lower than that in the uncoated group. PDP, EIS, SEM, and EDS showed that the coated AZ91 had a better corrosion resistance than the uncoated AZ91. The cell proliferation test showed that the addition of AZ91 did not have an adverse effect on osteoblast cells. Conclusively, the magnesium-reinforced PLA-integrated membrane has excellent load capacity, corrosion resistance, cell affinity, and proper degradation rate. Moreover, it has great potential as a bioresorbable membrane in the GBR/GTR application.