Objective To investigate the pathogenesy of postmenopausal osteoporosis and the influence of leptin on osteoporosis.Methods Healthy woman volunteers with different ages were divided into four groups: 25～34 years old(n=37),35～44 years old(n=31),45～54 years old(n=30),postmenopausal women 55～65 years old(n=40),with no significant difference in BMI among each groups.The serum levels of leptin,follicle-stimulating hormone(FSH),luteinizing,hormone(LH),beta-estradiol(E_2),testosterong(T),boneglaprotein(BGP),alkaline phosphates(ALP),tatrate-resistantacid phosphatase(TRAP),interleukin-6(IL-6),plasma calcium(Ca) and phosphate(P) were detected.Results The serum levels of leptin and BGP increased with the age in the nonobese women group.The serum levels of FSH,IL-6 and TRAP increased while those of E_2 and BMD decreased in the postmenopausal women compared with other groups.Conclusion Leptin serves as an important factor in promoting bone formation during bone rebuilding of postmenopausal women.The serum levels of leptin and BGP increase and bone formation increases.The E_2 and leptin contribute to the enhancement of bone formation and bone absorption in the postmenopausal women.The level of E_2 decreases but it acts more efficiently than leptin.The bone absorption is faster than bone formation,which contributes to the pathopoiesis of osteoporosis in postmenopausal women.

Objective To explore phenotypic modulation of vascular smooth muscle cells(VSMC) and change of p38 mitogen-activated protein kinase(MAPK) expression after intimal injury of rabbit carotid arteries. Methods The model of vascular restenosis established by balloon injury of rabbit carotid common arteries was used.HE staining,immunohistochemistry staining and Western blot were used to detect the change of proliferation cell nuclear antigen(PCNA),smooth muscle ?-actin(SM?-actin),p38 expression and morphology of sham-injured arteries and injured arteries at different time points.Results ⑴The proliferating VSMC was observed on the side of the medium lumen at 1 day and on the surface of vascular lumen at 3 days after injury.The neointima was formed and gradually being thicken at 5～7 days,and the thickening was accelerated at 14～35 days after injury.⑵PCNA was negative in the medium and endothelium of sham-injured arteries.Positive cell rate of PCNA was gradually increased at 1～14 days in the medium and at 5～14 days in the neointima after injury,with the maximum rate at 14 days.However,it declined gradually after 28 days.Positive cell rate of PCNA in the neointima was slightly higher than that in the medium.⑶SM?-actin was positive in the medium,negative in the endothelium of sham-injured arteries.Positive cell area of SM?-actin initially decreased at 1 day in the medium after injury with the minimum rate at 3 days,but it increased gradually after 5 days.Expression of SM?-actin in the neointima was slightly less than that in the medium.⑷p38 expression was very low or negative in the medium of sham-injured arteries.Expression of p38 was sustained and increased at 1～35 days after injury with the most remarkable elevation at 3～14 days.Expression of p38 in the neointima was higher than that in the medium.There was positive relationship between the p38 expression and PCNA expression in the vascular wall at different time points after injury.Elevation of p38 was earlier than decrease of SM?-actin.Conclusion There was a close relationship between the phenotypic modulation and proliferating ability of VSMC.P38 participated in signal transduction of phenotypic modulation of VSMC after intimal injury.