Objective·To investigate the role of caspase recruitment domain-containing protein 9(CARD9)in regulating macrophage polarization in a rat model of severe acute pancreatitis(SAP).Methods·SD rats were divided into 4 groups:Control group,SAP group,SAP+CARD9 shRNA group,and SAP+Control shRNA group with six rats in each group.The SAP rats transfected with CARD9 shRNA were established by injecting CARD9 shRNA adenovirus 48 hours before the SAP model was induced.The pancreatic tissues,peripheral blood,and peritoneal macrophages were collected 12 hours after the model was established.The expressions of CARD9 gene and CARD9 protein in peritoneal macrophages and pancreatic tissues were measured by real-time PCR and Western blotting.The expressions of TNF-α,IL-6,IL-10 and Arg-1 mRNA were detected by real-time PCR and the polarization types of peritoneal macrophages were detected by flow cytometry.Results·The expressions of CARD9 gene and CARD9 protein in peritoneal macrophages in CARD9 shRNA rats were significantly lower than those in SAP rats and interference control rats,which confirmed the success of CARD9 interference model.Compared with SAP rats,CARD9 shRNA rats had significantly reduced degree of inflammation and pathological scores;the mRNA levels of TNF-α,and IL-6 in peritoneal macrophages were significantly decreased;meanwhile,the mRNA levels of IL-10 and Arg-1 were increased,and the changes in TNF-α and IL-6 were significantly higher than those of IL-10 and Arg-1.The proportion of M1 macrophages was significantly reduced,and the ratio of M1/M2 was significantly decreased.The expression level of CARD9 mRNA in peritoneal macrophages was positively correlated with the proportion of M1 macrophages and the mRNA levels of TNF-α and IL-6.Conclusion·CARD9 is involved in regulating macrophage polarization in SAP rats,and it mainly regulates M1 polarization.Inhibition of CARD9 expression can reduce M1 macrophage polarization and reduce the inflammatory response in SAP rats.

Objective·To investigate the role of caspase recruitment domain-containing protein 9(CARD9)in regulating macrophage polarization in a rat model of severe acute pancreatitis(SAP).Methods·SD rats were divided into 4 groups:Control group,SAP group,SAP+CARD9 shRNA group,and SAP+Control shRNA group with six rats in each group.The SAP rats transfected with CARD9 shRNA were established by injecting CARD9 shRNA adenovirus 48 hours before the SAP model was induced.The pancreatic tissues,peripheral blood,and peritoneal macrophages were collected 12 hours after the model was established.The expressions of CARD9 gene and CARD9 protein in peritoneal macrophages and pancreatic tissues were measured by real-time PCR and Western blotting.The expressions of TNF-α,IL-6,IL-10 and Arg-1 mRNA were detected by real-time PCR and the polarization types of peritoneal macrophages were detected by flow cytometry.Results·The expressions of CARD9 gene and CARD9 protein in peritoneal macrophages in CARD9 shRNA rats were significantly lower than those in SAP rats and interference control rats,which confirmed the success of CARD9 interference model.Compared with SAP rats,CARD9 shRNA rats had significantly reduced degree of inflammation and pathological scores;the mRNA levels of TNF-α,and IL-6 in peritoneal macrophages were significantly decreased;meanwhile,the mRNA levels of IL-10 and Arg-1 were increased,and the changes in TNF-α and IL-6 were significantly higher than those of IL-10 and Arg-1.The proportion of M1 macrophages was significantly reduced,and the ratio of M1/M2 was significantly decreased.The expression level of CARD9 mRNA in peritoneal macrophages was positively correlated with the proportion of M1 macrophages and the mRNA levels of TNF-α and IL-6.Conclusion·CARD9 is involved in regulating macrophage polarization in SAP rats,and it mainly regulates M1 polarization.Inhibition of CARD9 expression can reduce M1 macrophage polarization and reduce the inflammatory response in SAP rats.

Objective To explore the effect of back Tuina on motor behavior,oxidative stress and in-flammation in rats with chronic fatigue syndrome(CFS).Methods Twenty-four Sprague-Dawley rats were randomly divided into a blank group,a model group and a Tuina group,each of 8,according to a random number table.The CFS rat model was prepared by means of forced weight-bearing swimming combined with chronic stress stimulation in 21 days.After modeling,the Tuina group was given daily 20-minute Tuina for 14 days.The general condition semi-quantitative score,exhaustion swimming time and open field experiment(OFE)distance of all groups were recorded.After the experiment,sam-ples were collected,and the histopathological changes of the vertical spine muscles were observed by hematoxylin and eosin(HE)staining.The cross-sectional area and diameter of muscle fibers were calcu-lated using Image Pro Plus software,and the frequency distribution diagram of cross-sectional area of muscle fibers was processed by using the Origin software.The contents of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px)and peroxisome proliferator-activated receptor γ-coactivator 1α(PGC-1α)and tumor necrosis factor(TNF)-α,interleukin(IL)-1β,IL-6 in the serum of rats were mea-sured.Results After the intervention,the general condition semi-quantitative score of the Tuina group was significantly lower than the model group(P<0.01),while the exhaustion swimming time and OFE distance were significantly higher than the latter group(P<0.05,P<0.01).(2)HE staining showed that the significant atrophy of erector spinal muscle cells in the model group,was significantly relieved in the Tuina group.(3)Compared with the blank group,the contents of SOD,GSH-Px and PGC-1α in erectus muscles decreased significantly(P<0.01),while those of TNF-α,IL-1β and IL-6 in the se-rum of the model group increased significantly(P<0.01).However,compared with model group,the contents of SOD,GSH-Px and PGC-1α in erectus muscle increased significantly(P<0.05,P<0.01),while those of TNF-α,IL-1β and IL-6 of the Tuina group decreased significantly(P<0.05,P<0.01).Conclusion Tuina in the back can regulate the oxidative stress response,reliever the inflammatory re-sponse and improve the motor behavior of CFS rats.