Castillo Alicia, Ruzmetov Nargiz, Harvey Kevin A, Stillwell William, Zaloga Gary P, Siddiqui Rafat A
Cellular Biochemistry Laboratory, Methodist Research Institute, Clarian Health Partners, Indianapolis.
J Mol Genet Med. 2005 Jul 28;1(1):18-25. doi: 10.4172/1747-0862.1000006.
Phenylephrine (PE) induces cardiac hypertrophy through multiple signaling pathways including pathways involving protein kinase C (PKC) activation. Docosahexaenoic acid (DHA), an omega-3 fatty acid, has been shown to reduce the PE-induced hypertrophic responses. However, the effects of DHA on PKC activation and translocation are controversial. The present study investigates the effect of DHA on PE-induced activation of PKC. The results indicate that PE induces PKCalpha translocation (from cytosol to plasma membranes) and activation in cardiomyocytes during the hypertrophic responses. Although DHA itself has no significant effect on basal PKC translocation and activation, it effectively reduced PE-stimulated PKC translocation and activation. The results of the present study suggest a possible mechanism explaining how dietary fish oil may inhibit development of cardiac hypertrophy and therefore may be an attractive dietary agent for preventing cardiac hypertrophy in patients with heart failure.
去氧肾上腺素（PE）通过多种信号通路诱导心脏肥大，包括涉及蛋白激酶C（PKC）激活的通路。二十二碳六烯酸（DHA）是一种ω-3脂肪酸，已被证明可减少PE诱导的肥大反应。然而，DHA对PKC激活和转位的影响存在争议。本研究调查了DHA对PE诱导的PKC激活的影响。结果表明，在肥大反应过程中，PE诱导心肌细胞中PKCα转位（从细胞质到质膜）并激活。尽管DHA本身对基础PKC转位和激活没有显著影响，但它有效地减少了PE刺激的PKC转位和激活。本研究结果提示了一种可能的机制，解释了膳食鱼油如何抑制心脏肥大的发展，因此可能是预防心力衰竭患者心脏肥大的一种有吸引力的膳食剂。
