Search

Rocket Force is an important strategic branch of our army, but rocket force medicine, as an independent new discipline of military medicine, is still in its infancy. This paper briefly introduces the establishment background, discipline connotation, construction achievements and development prospect of the new discipline of rocket force medicine.

Objective To evaluate the effects of IR-61 on the development of pulmonary fibrosis and on the proliferation and migration of lung fibroblasts in rats. Methods Forty male SD rats (6 to 8 weeks old) were randomized equally into normal control group, IR-61 group, bleomycin group and bleomycin+IR-61 group. In the latter 2 groups, rat models of pulmonary fibrosis were established by intratracheal infusion of bleomycin (2.5 mg/kg). In the 2 groups with IR-61 treatment, IR-61 was intraperitoneally injected at the dose of 2.0 mg/kg 30 min following intratracheal bleomycin infusion and was then administered twice a week. At 10 d after bleomycin treatment, 3 rats from each group were selected for IR-61 injection (2 mg/kg) via the tail vein to observe the accumulation of IR-61 in each organ at 24 h using near infrared fluorescence imaging (NIR). After 28 d of treatment, the rats were euthanized and the lung tissue was collected for HE and Masson staining. RT-PCR and Western blotting were performed to detect the changes of the expression of the genes related with lung fibroblast transdifferentiation and proliferation (including Collagen-1, Collagen-3, α-SMA, fibronectin, FOXM1, CCNB1, CDC25b and AURKB) in human lung fibroblasts (HFL1) and primary rat lung fibroblasts in response to IR-61 and transforming growth factor-β1 (TGF-β1) treatments; the migration of the cells was assessed using cell scratch test. Results NIR imaging showed that IR-61 could target the injured lung tissue induced by bleomycin. Morphological observation showed that compared with bleomycin-treated rats, the rats with IR-61 treatment presented with better structural integrity of the lungs with less obvious lung collapse, fewer fibrotic nodules and a significantly milder of pulmonary fibrosis (0.103 3±0.014 53 vs 0.460 0±0.037 86, P < 0.05). In HFL1 cells and primary rat lung fibroblasts, IR-61 pretreatment prior to TGF-β1 stimulation resulted in significantly lowered mRNA and protein expression of collagen-1, collagen-3, α-SMA, and fibronectin as well as the proliferation-specific genes FOXM1, CCNB1, CDC25b and AURKB (P < 0.05). Cell scratch test showed that TGF-β1 treatment significantly increased the cell migration activity, which was effectively suppressed by IR-61 treatment. Conclusion IR-61 ameliorates bleomycin-induced pulmonary fibrosis in rats by targeting the injured lung tissue and inhibiting the transdifferentiation, proliferation and migration of lung fibroblasts

To rescue ischemic myocardium from progressing to myocardial infarction, timely identification of the infarct size and reperfusion is crucial. However, fast and accurate identification, as well as the targeted protection of injured cardiomyocytes following ischemia/reperfusion (I/R) injury, remain significantly challenging. Here, a near infrared heptamethine dye IR‐780 is shown that has the potential to quickly monitor the area at risk following I/R injury by selectively entering the cardiomyocytes of the at‐risk heart tissues. Preconditioning with IR‐780 or timely IR‐780 administration before reperfusion significantly protects the heart from ischemia and oxidative stress‐induced cell death, myocardial remodeling, and heart failure in both rat and pig models. Furthermore, IR‐780 can directly bind to F0F1‐ATP synthase of cardiomyocytes, rapidly decrease the mitochondrial membrane potential, and subsequently slow down the mitochondrial energy metabolism, which induces the mitochondria into a "quiescent state" and results in mitochondrial permeability transition pore inhibition by preventing mitochondrial calcium overload. Collectively, the findings show the feasibility of IR‐780‐based imaging and protection strategy for I/R injury in a preclinical context and indicate that moderate mitochondrial function depression is a mode of action that can be targeted in the development of cardioprotective reagents. [ABSTRACT FROM AUTHOR]