Protective effect of total aralosides of Aralia elata (Miq) Seem (TASAES) against diabetic cardiomyopathy in rats during the early stage, and possible mechanisms
Total aralosides of Aralia elata (Miq) Seem (TASAES) from Chinese traditional herb Longya Aralia chinensis L was found to improve cardiac function. The present study was to determine the protective effects of TASAES on diabetic cardiomyopathy, and the possible mechanisms. Therefore, a single dose of...
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Veröffentlicht in: | Experimental & molecular medicine 2009, 41(8), , pp.538-547 |
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Sprache: | eng |
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Zusammenfassung: | Total aralosides of
Aralia elata
(Miq) Seem (TASAES) from Chinese traditional herb Longya Aralia chinensis L was found to improve cardiac function. The present study was to determine the protective effects of TASAES on diabetic cardiomyopathy, and the possible mechanisms. Therefore, a single dose of streptozotocin was used to induce diabetes in Wister rats. Diabetic rats were immediately treated with low, medium and high doses of TASAES at 4.9, 9.8 mg/kg and 19.6 mg/kg body weight by gavage, respectively, for eight weeks. Cardiac function was evaluated by
in situ
hemodynamic measurements, and patch clamp for the L-type Ca
2+
channel current
(
I
Ca
2+
-L)
and transient outward K
+
channel current (I
to
). Histopathological changes were observed under light and electron microscope. The expression of pro-fibrotic factor, connective tissue growth factor (CTGF) was monitored using immunohistochemistry staining. Compared with diabetic group, medium and high doses, but not low dose, of TASAES showed a significant protection against diabetes-induced cardiac dysfunction, shown by increased absolute value of left ventricular systolic pressure (LVSP) and maximum rates of pressure development (±dp/dt
max
), and enhanced amplitude of
I
Ca
2+
-L
(
P
< 0.05). Histological staining indicated a significant inhibition of diabetes-caused pathological changes and up-regulation of CTGF expression (
P
< 0.05). The results suggest that TASAES prevents diabetes-induced cardiac dysfunction and pathological damage through up-regulating
I
Ca
2+
-L
in cardiac cells and decreasing CTGF expression. |
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ISSN: | 1226-3613 2092-6413 |
DOI: | 10.3858/emm.2009.41.8.059 |