Objective To investigate the role of HO-1 in the protection of rat heart from anoxia/reoxygenation induced injury and its underlying mechanism.Methods LVEDP,LVDP and dp/dtmax were analyzed by the Langendorff method in isolated rat heart.Lactate dehydrogenase(LDH), infarct area,COHb and 6-keto-PGF1? were further determined in the experiment.Results After intraperitoneal injection of HO-1 inducer hemin,CO concentration in rat blood enhanced(P

AIM: To investigate the role of HO-1 in protection of rat hearts against anoxia/reoxygenation-induced injury and its underlying mechanism. METHODS: Cardiac contractility, lactate dehydrogenase (LDH) and infarct area were analyzed by the Langendorff method in isolated rat hearts. RESULTS: After intraperitoneal injection of HO-1 inducer hemin, CO concentration in rat blood enhanced (P

AIM: The objectives of the present study were to examine the effect of Jumi(JM) extraction on relaxation of isolated rat aortic rings,and to elucidate its mechanisms.METHODS: The thoracic aortic rings with and without endothelium of male Sprague-Dawley rats were mounted on a bath system.Vasodilatation of aortic rings preconstricted with 10-6 mol/L of phenylephrine(PE) was measured.RESULTS: JM extraction(0.5-8 g/L) caused a concentration-dependent relaxation in aortic rings.The extent of relaxation was larger in endothelium-intact aortic rings than that in endothelium-denuded aortic rings.Both L-NAME [a nitric oxide synthase(NOS) inhibitor] and high potassium(20 mmol/L KCl) partly abolished the relaxation action of JM extraction in endothelium-intact aortic rings.Pretreatment with L-NAME also inhibited the relaxation response to JM extraction in endothelium-denuded aortic rings.After incubation with JM extraction,NOS activities enhanced both in endothelium-intact and endothelium-denuded aortic rings.CONCLUSION: JM extraction causes relaxation of aortic rings through endothelium-dependent and independent pathways.The mechanisms might be involved in NOS and endothelium-derived hyperpolarizing factor.

Objective To observe the effect of Bushen Gutai mixture on uterine blood supply of rat model of abortion induced by hydroxyurea tablets combined with mifepristone through PKA-CREB signal pathway and its mechanism of calming fetus.Methods 60 pregnant rats of SPF grade SD rats were prepared by closing cages at 2∶1.According to the order of pregnancy,60 pregnant rats were randomly divided into 6 groups with 10 rats in each group:Bushen Gutai mixture group(low,middle and high dose),normal pregnancy group,model group and Di qu progesterone group.On the 1st to 9th day of pregnancy,except the normal group,the pregnant rats in each group were gavaged with hydroxyurea tablets at 5∶00 pm every day(450 mg·kg-1),and at 10∶00 am on the 10th day of pregnancy.Mifepristone tablets were given by intragastric administration(4.0 mg·kg-1).At 9∶00 am every day from the 1st to 9th day of pregnancy,Bushen Gutai mixture was given to the low,middle and high dose groups(0.5,1.0,2.0 g·kg-1),didrone group(3.02 mg·kg-1),model group and normal pregnancy group with 0.9%normal saline.24 hours after the last administration of pentobarbital sodium(50 mg kg-1),all pregnant rats were killed by intraperitoneal injection of pentobarbital sodium,and the uterine decidual tissue of pregnant rats was bluntly isolated in sterile environment.Hematoxylin-eosin(HE)staining was used to observe the lumen diameter and wall thickness of spiral artery in uterine decidual tissue.Immunohistochemical staining(IHC)was used to detect the expression of vascular endothelial growth factor(VEGF)in decidual tissues.Western blot was used to detect the protein expression of phosphorylated protein kinase A,protein kinase A,phosphorylated cyclic adenosine monophosphate response element binding protein,Cyclic Adenosine monophosphate response element binding protein and aquaporin 5 in the decidua of pregnant rats.The apoptosis of decidual cells was detected by in situ end labeling(TUNEL)of DNA fragmentation.Results Compared with the model group,the wall thickness of spiral artery was higher than that in other groups(P<0.05),the lumen diameter was lower than that in other groups(P<0.05)and the expression of VEGF protein was lower than that of other groups(P<0.01).Compared with the model group,the apoptosis level of decidual cells in uterine decidua of abortive rats in high,middle and low dose groups of Bushen Gutai mixture and diqu progesterone group decreased in varying degrees.Bushen Gutai mixture can up-regulate the levels of p-PKA/PKA and p-CREB/CREB in uterine decidua(P<0.01)and promote the expression of AQP5 protein in uterine decidua of abortion rats(P<0.01).Conclusion Bushen Gutai mixture can improve uterine blood supply of aborted rats by activating PKA and CREB phosphorylation,up-regulating AQP5 expression,promoting physiological recasting of spiral artery and high expression of Vascular endothelial growth factor.