Abstract. Epimedium, a traditional Chinese herb, has been used for the remedy of coronary heart disease, impotence and osteoporosis in traditional oriental medicine. However, despite extensive pharmacological studies, the molecular mechanism of the anti-heart failure effect of epimedium is little known. In the present study, we investigated the pharmacological action mechanism of ethanol extract of epimedium (EPI-ext) on isoproterenol-induced congestive heart failure (CHF) in rats. Isoproterenol administration resulted in severe heart failure, as shown by the increased levels of left ventricular (LV) weight index and heart rate, as well as LV end diastolic pressure, and by the decreased levels of LV systolic pressure, maximal rate of LV pressure rise, and maximal rate of LV pressure decline. EPI-ext dose-dependently reversed the changes of these cardiac morphometric and hemodynamic parameters. In addition, EPI-ext significantly inhibited the serum levels of tumor necrosis factor α, norepinephrine, angiotensin II and brain natriuretic peptide in rats with CHF and improved the histological changes including cadiocyte hypertrophy, cadiocyte degeneration, inflammatory infiltration, and cardiac desmoplasia. Furthermore, the expression and activities of matrix metalloproteinase-2 and -9, which regulate collagen production, were also blocked by EPI-ext. Moreover, myocardial apoptosis was remarkably attenuated by EPI-ext through the regulating Bcl-2/Bax axle. In conclusion, EPI-ext ameliorates LV dysfunction and cardiac remodeling through down-regulating matrix metalloproteinase-2 and -9 activity and myocardial apoptosis in rats with CHF.

Coastal waters are polluted by heavy metals to varying degrees, posing potential risks to marine ecology and human health. In May 2006, the pollution levels, sources, and ecological risks of heavy metals (Cu, Pb, Zn, Cd, Hg, and As) in seawater, surface sediments, and living organisms were studied in Jiuzhen Bay in Fujian, China. This study identified Hg (0.26–0.72 µg/L) and As (20.3–31.5 µg/L) pollution in the seawater of Jiuzhen Bay. In sediments, heavy Pb pollution (946 µg/g dw) was only detected at one station at a level posing very serious potential risk, while Hg pollution (0.052–0.087 µg/g dw) was observed at three stations at a level posing serious potential risk. No heavy metal pollution was detected in sediments at other stations. The concentrations of five heavy metals (Cu, Zn, As, Cd, and Pb) exceeded the corresponding National Quality Standards for oysters, indicating heavy pollution, based on an ecological risk assessment. In clams, two heavy metals (Pb and As) exceeded the standards, indicating light pollution, based on an ecological risk assessment. No heavy metal pollution was found in fish or shrimps. The heavy metals in the seawater and sediments of Jiuzhen Bay are mainly derived from the river discharges of Luxi and Wujiang Rivers although sewage discharge along the coast of Jiuzhen Bay is another source of heavy metal pollution at some stations. Given the pollution of Pb, Hg, and As in seawater and sediments at some stations within the bay, the potential risks of Pb, Hg, and As in living organisms to both the marine ecology and human health deserve increased attention.

The effects of iron deficiency on the cochlea were studied in growing rats fed with a basic iron-deficient diet for 80 days. The electrophysiological changes (auditory thresholds raised more than 15 dB) were observed in 47% of the cochleas of iron-deficient rats. When these organs of Corti were examined by scanning electron microscopy, abnormalities of outer or inner hair cells were found, as follows: (1) fusion and torsion of the stereocilia, (2) coalescence of adjacent stereocilia in the same row, (3) loss of sensory hair stiffness, and (4) loss of stereocilia. Within each lesion, the neighbouring supporting cells and their microvilli showed no damage. The findings indicate that cochlear impairment can be induced by iron deficiency. The peroxidative mechanisms responsible for the lesions of stereocilia in iron deficiency are discussed.

Cochlear changes were studied in 141 growing rats raised on a basic iron-deficient diet for 7–100 days; 130 rats served as normal or chronic anemia controls. Electrophysiological findings showed that the incidence of an auditory threshold elevation of more than 15 dB was 31.85 % in the iron-deficient rats, but it was unchanged in all the control animals. The main cochlear histopathological changes induced by iron deficiency were strial atrophy and reduction of spiral ganglion cells. It is concluded that the observed anomalies may be attributed solely to iron deficiency of the cochlear tissue.