Study on effect of psoralidin on anti-experimental postmenopausal osteoporosis and its mechanism / 中国中药杂志

<p><b>OBJECTIVE</b>To observe the effect of psoralidine in rats with ovariectomy, and preliminarily study its mechanism.</p><p><b>METHOD</b>Sixty female Sprague-Dawley rats were divided into 5 groups: the sham operation group, the model group, the psoralidine low-dose group (4 mg x kg(-1)), the psoralidine high-dose group (16 mg x kg(-1)) and the Zhuangguzhitong capsule group, with 12 rats in each group. Thirteen weeks later, their blood and bone samples were collected to detect bone density, bone biochemistry, pathomorphology, serum E2 and CT.</p><p><b>RESULT</b>Psoralidine could up-regulate the bone density of lumbar vertebra and thighbone of rats with ovariectomy (P < 0.05), the maximum bending strength of thighbone (P < 0.05), and serum E2 and CT (P < 0.05).</p><p><b>CONCLUSION</b>Psoralidine has a good active effect on postmenopausal antiosteoporosis. Its mechanism may be related to such pathways as E2 and CT.</p>

Overactivated mitogen-activated protein kinase by anisomycin induces tau hyperphosphorylation / 生理学报

One of the pathological feathers of Alzheimer's disease (AD) is neurofibrillary tangles (NFTs), which consist of paired helical filaments (PHFs) formed by hyperphosphorylated microtubule-associated protein tau. To study the role of mitogen-activated protein kinase (MAPK) in tau hyperphosphorylation and the underlying mechanism, wild type mouse neuroblastoma cells (N2a) were dealt with different concentrations (0.1 microg/mL, 0.2 microg/mL and 0.4 microg/mL) of anisomycin (an activator of MAPK) for 6 h. The relationship between MAPK activity and tau phosphorylation at some Alzheimer-sites was analyzed, and the activities of protein kinase A (PKA) and glycogen synthase kinase-3 (GSK-3) were detected. The results showed that anisomycin activated MAPK in a dose-dependent manner, but tau hyperphosphorylation at Ser-198/199/202 and Ser-396/404 sites was only observed when the concentration of anisomycin was at the level of 0.4 microg/mL, and the alteration of tau phosphorylation at Ser-214 showed no significant difference in different groups. 0.2 microg/mL and 0.4 microg/mL of anisomycin led to an increase in the activity of GSK-3, respectively, but had no effect on the activity of PKA. Lithium chloride, a specific inhibitor of GSK-3, completely abolished the anisomycin-induced elevation of tau phosphorylation without any effect on the activity of MAPK. In conclusion, overactivation of MAPK up to a certain degree induces tau hyperphosphorylation at Ser-198/199/202 and Ser-396/404 sites, and this is probably related to the effect of activated GSK-3 by MAPK.