AIM:To observe the effect of Wnt/β-catenin signaling pathway on diabetic ulcer.METHODS:Diabetic animal model was established in the female Wistar rats by intraperitoneal injection of low-dose streptozotocin fol-lowing high-fat diet feeding.A circular wound was made on the dorsum of the rats in both control group and diabetic group. The condition of wound healing was recorded and the structures of the wound tissues were observed by HE staining in the 2 groups at 3, 7 and 14 d after wounding.The expression ofβ-catenin, GSK-3βand Rspo-3 at mRNA and protein levels in the wound tissues was detected by RT-PCR and ELISA.RESULTS:In diabetic group, the wound healing rate was lower (P<0.05), and the inflammatory cells, fibroblast cells and new capillaries in the wound tissues were fewer than those in control group.The expression of β-catenin and Rspo-3 at mRNA and protein levels in the wound tissues in control group was significantly higher than those in diabetic group, and the expression of GSK-3βwas exactly the opposite (P<0.05). CONCLUSION:The down-regulation of Wnt/β-catenin probably resultes from the decreased level of Rspo-3, which may be one of the reasons for delaying the diabetic ulcer healing.

AIM:To investigate the effects of celecoxib,a selective cyclooxygenase-2 inhibitor,on antioxidative capability and apoptosis of cardiac myocytes after myocardial infarction.METHODS:24 New Zealand rabbits were divided into three groups randomly(8 in each group):sham-operated group(sham group),myocardial infarction group(MI group),celecoxib group(Cele group,10 mg kg-1?d-1,qd,with the drugs gastric gavage for six weeks).The NO concentration,total antioxidative capability(T-AOC),the activity of constitutive nitric oxide synthase(cNOS)and inducible NOS(iNOS)in cardiac tissue homogenate,adjacent to the infracted area,were detected.The pathological changes were observed by light microscope and electron microscopy.The expressions of Bcl-2 and Bax protein in myocytes were observed using immunohistochemistry,and the degree of apoptosis were examined by TUNEL.RESULTS:Cardiac tissue in MI group presented interstitial edema,fibroplastic proliferation,inflammatory cellular infiltration,and vacuolar degeneration in cardiac myocytes.The results of electron microscopy showed that myocytes presented more changes caused by ischemic injury:widened interspace of myofibril,disordered myofibrillae,focal lysis of myofilament,ectasia of sarcoplasmic reticulum.In Cele group,the pathological changes were light,the NO-_2/NO-_3 concentration,the activity of iNOS were lower(P