Objective To evaluate the potential of the BIBP-H fluorescent probe in the detection of the oxidative stress levels after cerebral ischemia-reperfusion(CIRI).Methods In vitro,the potential of BIBP-H probe was in detection of oxidative stress was first assessed with fluorescence imaging in rat neuroblastoma(B104)cells after L-glutamic acid stimulation.And then,the effects of edaravone and dexborneol(EDA)and glutathione(GSH)pretreatment on the fluorescence intensity were evaluated.Later,a totally of 28 male C57BL/6 mice were randomly assigned into four groups:transient middle cerebral artery occlusion(tMCAO)group,EDA+tMCAO group,GSH+tMCAO group,and sham group.After 1.5 h ischemia and 12 h reperfusion,the mice were treated with BIBP-H via tail vein injection.In vivo,ex vivo,and tissue fluorescence imaging were utilized to evaluate the probe's cerebral ischemia-reperfusion injury(CIRI).Results ① BIBP-H probe did not exhibit fluorescence signals in cultured B104 cells,but showed red fluorescence in B104 cells treated with L-glutamic acid.The signals significantly decreased when pretreated with EDA or GSH.② Both the sham-operated mice intravenously injected with the BIBP-H probe and the tMCAO mice without injection of the probe showed negative results in in vivo fluorescence imaging.③ tMCAO mice treated with BIBP-H exhibited red fluorescence signals in the ischemic hemisphere in vivo,with significantly reduced fluorescence intensity after EDA or GSH infusion during reperfusion ④ The fluorescence area examined with BIBP-H was consistent the cerebral infarction area detected with triphenyltertrazolium.Conclusions The BIBP-H probe effectively monitored oxidative stress levels both in vivo and in vitro,demonstrating its potential in CIRI detection.

Objective To evaluate the potential of the BIBP-H fluorescent probe in the detection of the oxidative stress levels after cerebral ischemia-reperfusion(CIRI).Methods In vitro,the potential of BIBP-H probe was in detection of oxidative stress was first assessed with fluorescence imaging in rat neuroblastoma(B104)cells after L-glutamic acid stimulation.And then,the effects of edaravone and dexborneol(EDA)and glutathione(GSH)pretreatment on the fluorescence intensity were evaluated.Later,a totally of 28 male C57BL/6 mice were randomly assigned into four groups:transient middle cerebral artery occlusion(tMCAO)group,EDA+tMCAO group,GSH+tMCAO group,and sham group.After 1.5 h ischemia and 12 h reperfusion,the mice were treated with BIBP-H via tail vein injection.In vivo,ex vivo,and tissue fluorescence imaging were utilized to evaluate the probe's cerebral ischemia-reperfusion injury(CIRI).Results ① BIBP-H probe did not exhibit fluorescence signals in cultured B104 cells,but showed red fluorescence in B104 cells treated with L-glutamic acid.The signals significantly decreased when pretreated with EDA or GSH.② Both the sham-operated mice intravenously injected with the BIBP-H probe and the tMCAO mice without injection of the probe showed negative results in in vivo fluorescence imaging.③ tMCAO mice treated with BIBP-H exhibited red fluorescence signals in the ischemic hemisphere in vivo,with significantly reduced fluorescence intensity after EDA or GSH infusion during reperfusion ④ The fluorescence area examined with BIBP-H was consistent the cerebral infarction area detected with triphenyltertrazolium.Conclusions The BIBP-H probe effectively monitored oxidative stress levels both in vivo and in vitro,demonstrating its potential in CIRI detection.

The purpose of this research is to investigate the therapeutic effects of losartan potassium on 5/6 nephrectomy rats with chronic heart failure(CHF)and to explore the mechanism. 24 Rats were randomly divided into three groups namely sham group(Sham), pathology group(Nx)and losartan potassium group(Lst), respectively. CHF model in rats were induced by 5/6 nephrectomy. At the 7th week, rats of Lst group were given losartan potassium(50 mg/L)for consecutive 2 weeks. Then all rats were measured for hemodynamic parameters, cardiac index, creatinine, urea nitrogen in serum, and expressions of CD133, VEGFR2, Sox2, cleaved Caspase-3 and Bcl-2 in heart. Compared with Nx group, rats of Lst group improved cardiac and renal functions: decreased LVDP, LVEDP, cardiac index, creatinine, urea nitrogen and increased LVSP. Furthermore, losartan potassium up-regulated gene expression of CD133, VEGFR2, Sox2 and protein level of Bcl-2, and down-regulated cleaved Caspase-3 protein expression. Results suggest that losartan potassium can improve cardiac function of rats with CHF which may be correlated with mobilizing bone marrow stem cells, increasing endothelial progenitor cells(EPCs)level in heart, repairing endothelial function, and inhibiting myocardial apoptosis.