ABSTRACT Objective: To explore the effect of ischemic postconditioning on myocardial ischemia-reperfusion-induced acute lung injury (ALI). Methods: Forty adult male C57BL/6 mice were randomly divided into sham operation group (SO group), myocardial ischemia-reperfusion group (IR group), ischemic preconditioning group (IPRE group) and ischemic postconditioning group (IPOST group) (10 mice in each group). Anterior descending coronary artery was blocked for 60 min and then reperfused for 15 min to induce myocardial IR. For the IPRE group, 3 consecutive cycles of 5 min of occlusion and 5 minutes of reperfusion of the coronary arteries were performed before ischemia. For the IPOST group, 3 consecutive cycles of 5 min reperfusion and 5 minutes of occlusion of the coronary arteries were performed before reperfusion. Pathological changes of lung tissue, lung wet-to-dry (W/D) weight ratio, inflammatory factors, oxidative stress indicators, apoptosis of lung cells and endoplasmic reticulum stress (ERS) protein were used to evaluate lung injury. Results: After myocardial IR, lung injury worsened significantly, manifested by alveolar congestion, hemorrhage, structural destruction of alveolar septal thickening, and interstitial neutrophil infiltration. In addition, lung W/D ratio was increased, plasma inflammatory factors, including interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-17A, were increased, malondialdehyde (MDA) activity of lung tissue was increased, and superoxide dismutase (SOD) activity was decreased after myocardial IR. It was accompanied by the increased protein expression levels of ERS-related protein glucose regulatory protein 78 (GRP78), CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), and caspase-12, and the increased apoptotic indices of lung tissues. Conclusion: IPOST can effectively improve myocardial IR-induced ALI by inhibiting ERS-induced apoptosis of alveolar epithelial cells.

Abstract To study the effect of Jiawei Huangqi Guizhi Decoction on gastrointestinal hormones and TGF-β3 signal pathways in rats with chronic atrophic gastritis (CAG). The model was created by methylnitrosoguanidine (MNNG) comprehensive method. After successful modeling, it was divided into three groups: model group (MC group), frolic acid group (AC group), modified Huangqi Guizhi Decoction high dose group (HH group), modified Huangqi Guizhi Decoction middle dose group (HM group), and modified Huangqi Guizhi Decoction low dose group (HL group). Gastric pathology was observed by HE staining. The levels of gastrin (GAS) and motilin (MTL) in rat serum were detected by ELISA assay. After HE staining, the histopathological sections were analyzed. Inflammatory factors infiltration and disorder of mucosal epithelial cells were found in the model group, which were improved to some extent after administration. According to the pathological chart analysis and score of rats in each group, compared with the model group, the gastric tissue damage of rats in each administration group has been improved in different degrees, among which the pathological scores of HH and HM groups were lower, and the corresponding damage degree was smaller. According to the test results of ELISA, Jiawei Huangqi Guizhi Decoction could reduce the contents of GAS, TGF-β3, and increase MTL abundance in the serum of rats, thus accelerating the apoptosis of tumor cells and inhibiting cancer. Jiawei Huangqi Guizhi Decoction played a positive role in preventing the occurrence of gastric cancer through reducing the concentrations of GAS and TGF-β3 in serum, and increasing the concentration of MLT in serum. This results provided a new treatment idea for CAG.

ABSTRACT Introduction: The objective of this study is to investigate the protective mechanism of dexmedetomidine (Dex) in myocardial ischemia/reperfusion (MIR)-induced acute lung injury (ALI) of diabetic rats by inhibiting hypoxia-inducible factor-1α (HIF-1α). Methods: Initially, healthy male Sprague Dawley rats were treated with streptozocin to induce diabetes. Then, three weeks after the induction, Dex or lentiviral vector (LV)-HIF-1α was injected into the rats 30 minutes prior to the MIR modeling. After four weeks, lung tissues were harvested for pathological changes observation and the wet/dry weight (W/D) ratio determination. Afterwards, oxidative stress indicators and pro-inflammatory factors were measured. In addition, HIF-1α expression was assessed by immunohistochemistry and western blot analysis. Results: Dex could suppress inflammatory cell infiltration, improve lung tissue structure, reduce pathological score and the W/D ratio, and block oxidative stress and inflammatory response in MIR-induced ALI of diabetic rats. Besides, Dex could also inhibit HIF-1α expression. Moreover, Dex + LV-HIF-1α reversed the protective role of Dex on diabetic MIR-induced ALI. Conclusion: Our study has made it clear that Dex inhibited the upregulation of HIF-1α in diabetic MIR-induced ALI, and thus protect lung functions by quenching the accumulation of oxygen radical and reducing lung inflammatory response.

Abstract To evaluate the effects of HIF-1α overexpression on mitochondrial function in aged mice with myocardial ischemia-reperfusion (I/R). Mice were divided into 1) Blank (Sham) group; 2) Ischemia-reperfusion (I/R) group; 3) I/R+2ME2 group (I/R+HIF-1α blocker 2ME2. Compared with Sham group, in I/R group and I/R+2ME2 group, HR slowed down, LVDP and +dp/dtmax decreased, LVEDP, myocardial infarction area, and ROS generation rate was significantly increased; whereas the mitochondrial respiratory function (State3, RCR) and mitochondrial respiratory enzyme activity (NADH-OX, Cytc-OX and SUC-OX) were significantly reduced. Compared with the I/R group, the respiratory function of myocardial mtochondria (State3, RCR) and respiratory enzyme activity of myocardial (NADH-OX, Cytc-OX and SUC-OX) were significantly reduced in the I/R+2ME2 group; and the levels of p-HIF-1α and p-VEGF in the I/R+2ME2 group were significantly decreased. HIF-1α pathway upregulate the respiratory enzyme activity of myocardial and respiratory function of I/R myocardial mitochondria.