Adiponectin is a peptide hormone secreted exclusively by adipocytes, and obesity is an established risk factor for breast cancer. We have, thus, evaluated the associations of anthropometric measures of adiposity and adiponectin with the development of breast cancer in a case-control study. Questionnaire information, anthropometric measures, and blood samples were taken before treatment from 244 incident cases with breast cancer, including 141 premenopausal and 103 postmenopausal cases, and 244 controls admitted for health examination at the Tri-Service General Hospital, Taipei between 2004 and 2005. Plasma levels of adiponectin were measured by RIA. The relationship between anthropometric measures of adiposity and breast cancer risk was modified by menopausal status, with a significant increase in risk observed in postmenopausal but not premenopausal women. Moreover, a fairly robust inverse association of adiponectin with the risk was observed only in postmenopausal women (adjusted odds ratio (OR), 0.55; 95% confidence interval (CI), 0.23-0.97), but not in premenopausal women. Additionally, the plasma adiponectin levels tended to be inversely associated with estrogen receptor (ER)-positive (adjusted OR, 0.53; 95% CI, 0.27-0.98) but not ER-negative breast tumors. Furthermore, the associations of adiponectin with breast cancer risk overall and by menopausal and ER status remained after adjustment for obesity indices. These results suggest that adiponectin may have an independent role in breast carcinogenesis, particularly in the postmenopausal and ER-positive breast cancer risk.

The objective of this study was to determine chemiluminescence (CL) antioxidant activities and neuroprotective effects of astaxanthin, beta-carotene (β-carotene), and canthaxanthin on undifferentiated rat pheochromocytoma (PC12) cells. We performed three CL antioxidant assays, and the three carotenoids showed varying degrees of antioxidant activity, with astaxanthin exhibiting the highest antioxidant activity than the other two samples. Results of a pyrogallol-luminol assay revealed β-carotene to have higher antioxidant activity than canthaxanthin, whereas cupric sulfate-Phen-Vc-hydrogen peroxide (H₂O₂) assay showed canthaxanthin to have higher antioxidant activity than β-carotene. Luminol-H₂O₂ assay showed the antioxidant activity series as canthaxanthin > β-carotene at 62.5-1000 μg/mL and β-carotene > canthaxanthin at 1000-4000 μg/mL. Astaxanthin exhibited partial neuroprotective activity against H₂O₂ and the strongest neuroprotective activity against amyloid beta-peptide(25-35) [(Aβ)(25-35)]-induced undifferentiated PC12 cell deaths at 0.5-5.0 μM. Canthaxanthin showed partial neuroprotective activity in Aβ(25-35)-induced undifferentiated PC12 cell deaths at 1.0-5.0 μM. Astaxanthin protected undifferentiated PC12 cells from the damaging effects of H₂O₂ and Aβ(25-35) by the following ways: (1) scavenging superoxide anion radicals, hydroxyl radicals, and H₂O₂; (2) securing cell viability; (3) suppressing the production of reactive oxygen species; and (4) eliminating calcium ion influx. Our results conclusively show that astaxanthin has the merit as a potential neuron protectant.

Background: Alzheimer's disease (AD) is one of the common neurodegenerative disorders among elderly. The

In this study we have found that the crude extract of Psoraleae Fructus inhibited acetylcholinesterase activity in vitro and ameliorated impairment of the inhibitory avoidance response and of the water maze spatial performance caused by scopolamine in rats. Among all fractions, the chloroform fraction showed the best inhibitory effect on acetylcholinesterase activity and could reduce the scopolamine-induced inhibitory avoidance response impairment. Psoralen and isopsoralen, two major constituents of the chloroform fraction of Psoraleae Fructus identified by high performance liquid chromatography, also reduced the extent of the inhibitory avoidance response impairment. The results suggest that psoralen and isopsoralen are the major active ingredients of Psoraleae Fructus responsible for the progressive reversal of scopolamine-induced amnesia, whose effects are partially associated with inhibition of AchE activity and hence activation of the central cholinergic neuronal system.

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