Résumé
Aim To investigate the possible mechanism of paeonol inhibiting the inflammatory response of fibroblast synovial cells (RA-FLSS) in rheumatoid arthritis. Methods CCK-8 assay was used to detect Paeonol's inhibitory level on the abnormal proliferation of arthritis human fibroblast synovial cells (RA-FLSs). The levels of endoplasmic reticulum stress-related proteins MANF and ATF6 were detected by Western blot. Cell localization of transcription factor p65 and Mesencephalic Astrocyte Derived Neurotrophic Factor (MANF) was detected by immunofluorescence. RT-qPCR detected the changes of p65 target genes. Results Paeonol could significantly inhibit the abnormal proliferation of RA-FLSS cells. Paeonol activates ATF6 and increases the expression of MANF. Paeonol promoted the nuclear transfer of MANF protein and inhibited the transcriptional activity of p65. Conclusion Paeonol promotes the expression of MANF and nuclear transfer through the endoplasmic reticulum stress pathway and affects the progression of RA by inhibiting the transcriptional activity of p65.
Résumé
Aim To investigate the protective effect of cardiopulmonary resuscitation (CPR) on hippocampal brain tissues of rats after cardiac arrest and its mechanism. Methods Forty SD rats were randomly divided into control group, ischemia group, cardiopulmonary resuscitation group and Edaravone treatment group. The rats in ischemia group were subjected to cardiac arrest by suffocation for 10 min. In resuscitation group, cardiac arrest/cardiopulmonary resuscitation (CA/CPR) was performed, after 3 min of cardiac arrest, cardiopulmonary resuscitation was performed for 7 min. After 10 min, the rats in each group were sacrificed, venous blood was taken to detect oxidative stress indicators, and the pathology of rat hippocampal brain tissues were examined by HE staining and electron microscopy, and the expressions of Nrf2 and Keapl gene and proteins were detected by real-time fluorescent quantitative PCR and Western blot. Results Compared with control group, the serum oxidative stress level of the ischemic model group rats increased, the Nissl body of the hippocampal nerve cells decreased significantly, the mitochondrial cristae were destroyed significantly, and the expressions of Nrf2 and Keapl genes and proteins in the hippocampal tissues increased. Compared with ischemic group, the serum oxidative stress level of resuscitation group rats decreased. Compared with ischemic group, the serum oxidative stress level of the rats in cardiopulmonary resuscitation group decreased, the neuronal cells in the hippocampus increased, the mitochondrial cristae damage was alleviated, and the expressions of Nrf2 and Keapl genes and proteins in the hippocampus decreased. Conclusions CPR has protective effect on hippocampal tissues of rats, and its mechanism is related to the alleviation of Nrf2/Keapl pathway of oxidative stress injury.