Drug safety · 2006
Continuation of amiodarone therapy despite type II amiodarone-induced thyrotoxicosis.
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Uzan Laurent, Guignat Laurence, Meune Christophe, Mouly Stéphane, Weber Simon, Bertagna Xavier, Bertherat Jérôme, Thomopoulos Pierre, Duboc Denis
Аннотация
OBJECTIVE: To investigate the effects of electroacupuncture (EA) at Taichong (LR 3) and Baihui (DU 20) on myocardial hypertrophy in spontaneously hypertensive rats (SHRs).
METHODS: Thirty-six SHRs were randomly assigned to model, EA, and Losartan groups, with twelve rats per group. Twelve Wistar Kyoto rats were selected as the normal control group. Systolic blood pressure (SBP) and cardiac function were measured in all rats. Expression levels of factors associated with the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway were evaluated by Western blotting and real-time PCR. Pathological changes of the heart tissue were observed by hematoxylin-eosin staining.
RESULTS: After treatment, enhanced SBP was significantly decreased in the EA and Losartan groups compared with the model group (P < 0.01). Echocardiographic and morphological analyses revealed that enhanced end-diastolic interventricular septal thickness and left ventricular posterior wall thickness, as well as ratio of left ventricular weight to body weight were markedly diminished in the EA and Losartan groups (P < 0.01 or P < 0.05), while reduced left ventricular end-diastolic dimension and left ventricular ejection fraction were significantly ameliorated (P < 0.01). Real-time PCR and western blotting analyses showed that the expression levels of PI3K, Akt, and mTOR in SHRs were significantly up-regulated by EA and Losartan (P < 0.01), while the expression levels of PTEN and ANP were down-regulated (P < 0.01).
CONCLUSION: EA at Taichong (LR 3) and Baihui (DU 20) inhibited the development of cardiac hypertrophy and improved the cardiac function in SHRs, possibly through regulation of the PI3K/Akt/mTOR signalling pathway.
METHODS: Thirty-six SHRs were randomly assigned to model, EA, and Losartan groups, with twelve rats per group. Twelve Wistar Kyoto rats were selected as the normal control group. Systolic blood pressure (SBP) and cardiac function were measured in all rats. Expression levels of factors associated with the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway were evaluated by Western blotting and real-time PCR. Pathological changes of the heart tissue were observed by hematoxylin-eosin staining.
RESULTS: After treatment, enhanced SBP was significantly decreased in the EA and Losartan groups compared with the model group (P < 0.01). Echocardiographic and morphological analyses revealed that enhanced end-diastolic interventricular septal thickness and left ventricular posterior wall thickness, as well as ratio of left ventricular weight to body weight were markedly diminished in the EA and Losartan groups (P < 0.01 or P < 0.05), while reduced left ventricular end-diastolic dimension and left ventricular ejection fraction were significantly ameliorated (P < 0.01). Real-time PCR and western blotting analyses showed that the expression levels of PI3K, Akt, and mTOR in SHRs were significantly up-regulated by EA and Losartan (P < 0.01), while the expression levels of PTEN and ANP were down-regulated (P < 0.01).
CONCLUSION: EA at Taichong (LR 3) and Baihui (DU 20) inhibited the development of cardiac hypertrophy and improved the cardiac function in SHRs, possibly through regulation of the PI3K/Akt/mTOR signalling pathway.