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. Objective ischemiareperfusioninduced ischemia induced ALI. . (ALI) Methods C57BL6 CBL C57BL 6 C BL C57BL/ SO , ischemiareperfusion IR 10 (1 group. 1 wettodry wet dry WD W D (W/D factors indicators ERS (ERS Results significantly congestion hemorrhage thickening infiltration addition IL6, IL6 IL 6, (IL)-6 TNFα, TNFα TNF α, α (TNF)-α IL17A, IL17A ILA 17A, 17A A IL-17A MDA (MDA SOD (SOD ERSrelated related 7 GRP78, GRP78 GRP (GRP78) CCAAT/enhancerbinding CCAATenhancerbinding CCAAT/enhancer binding CCAAT enhancer C/EBP CEBP EBP (C/EBP CHOP, CHOP (CHOP) caspase12, caspase12 caspase 12, 12 caspase-12 tissues Conclusion IRinduced ERSinduced (ALI ( (IL)- GRP7 (GRP78 enhancerbinding CCAATenhancer (CHOP caspase1 caspase-1 (IL) (GRP7 caspase- (IL (GRP

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.

The plant growth-promoting rhizobacterial strain Pseudomonas putida Rs-198 was isolated from salinized soils from Xinjiang Province. We optimized the composition of the low-cost medium of P. putida Rs-198 based on its bacterial concentration, as well as its phosphate-dissolving and indole acetic acid (IAA)-producing capabilities using the response surface methodology (RSM), and a mathematical model was developed to show the effect of each medium component and its interactions on phosphate dissolution and IAA production. The model predicted a maximum phosphate concentration in medium containing 63.23 mg/L inorganic phosphate with 49.22 g/L corn flour, 14.63 g/L soybean meal, 2.03 g/L K2HPO4, 0.19 g/L MnSO4 and 5.00 g/L NaCl. The maximum IAA concentration (18.73 mg/L) was predicted in medium containing 52.41 g/L corn flour, 15.82 g/L soybean meal, 2.40 g/L K2HPO4, 0.17 g/L MnSO4 and 5.00 g/L NaCl. These predicted values were also verified through experiments, with a cell density of 10(13) cfu/mL, phosphate dissolution of 64.33 mg/L, and IAA concentration of 18.08 mg/L. The excellent correlation between predicted and measured values of each model justifies the validity of both the response models. The study aims to provide a basis for industrialized fermentation using P. putida Rs-198.