This study investigated the therapeutic effects and mechanisms of medical ozone on sepsis- associated kidney injury (S-AKI) induced by lipopolysaccharide in mice. Using enzyme-linked immunosorbent assay, renal histopathological evaluation, detection of renal function biochemical indicators, immunofluorescence staining, and Western blot analysis, the effects of intraperitoneal injection of ozone on inflammation, coagulation, and renal tissue in mice were systematically detected.The results demonstrated that ozone treatment significantly reduced circulating levels of the specific markers (citrullinated histone H3 and myeloperoxidase-DNA complexes) from neutrophil extracellular traps (NETs) in S-AKI mice, with a suppression on inflammatory and tissue factor expression in renal tissue. Furthermore, ozone effectively improved microcirculation dysfunction, reduced tubular damage and interstitial inflammatory infiltration, thereby alleviating pathological changes of kidneys of S-AKI mice. Mechanistic studies revealed that ozone enhances phagocytic clearance of tissue factor-rich microparticles (TF-MPs) by activating the 5'-monophosphate-activated protein kinase (AMPK) / scavenger receptor (SR)-A1 signaling pathway in macrophages. In Sr-a1-/- mice, renoprotective effect of ozone was completely abolished, confirming the critical role of SR-A1 in this mechanism. In summary, this study demonstrates that medical ozone promotes macrophage clearance of TF-NETs complexes through the AMPK/SR-A1 signaling axis, exerting dual protective effects on mice through anti-inflammatory action and microcirculation improvement, which provides novel intervention targets and therapeutic strategies for S-AKI treatment.

Objective To investigate if basic fibroblast Growth factor (bFGF) can penetrate placental barrier, alleviate rat brain damage and stimulate fetal rat neurons proliferation. Methods BFGF labeled with 125 I was injected peritoneally to pregnant rats, and tissue distribution of radioactivity of 125 I in different organs was detected. Thirty two of pregnant Waister rats were randomly divided at 15 d of gestational age into four groups: normal control, uteri distressed control, bFGF treatment, and bFGF prevention. Fetal rats in the latter three groups suffered from distress in uteri in an animal model of perinatal asphyxia. Proliferated neurons in fetal rat brains were counted in each group. Results 125 I bFGF has been found in fetal brain, heart, lung and spleen, etc. Under high power microscope, proliferated neurons in fetal rat brains were counted in each group, they are: (4.5 ?2.4), (5.8?3.1), (17.2?5.4); (18.1?5.8), ( F=128,P