Adaptation to heat of cardiomyoblasts in culture protects them against heat shock: role of nitric oxide and heat shock proteins

摘要

Dosed adaptation to environmental factors is an efficient non-drug means for increasing the resistance of organs or the body as a whole. Earlier, we demonstrated that nitric oxide (NO) plays an important role in adaptive defense of the body, in particular due to activation of heat shock protein (HSPs) synthesis. A key question has remained open: to what extent the formation of adaptive defense depends on central mechanisms and to what extent on the intracellular mechanisms immediately responding tothe adapting factor, and whether the NO-dependent activation of HSP synthesis plays a role in adaptation of isolated cells. In the present study we looked into a possibility of producing the protective effect of adaptation to heat in cell culture. A 6-day adaptation to heat reduced by 17 percent the fall of metabolic activity induced by heat shock in cardiomyoblasts H9c2. The development of adaptation was associated with increased NO production. Treatment of cells with the inhibitor of NO synthase L-NNA (100 mu M) prevented the development of adaptive protection. Adaptation of cell culture enhanced synthesis of HSP70 but not HSP27. Blockade of HSP70 synthesis with quercetin (50 mu M) left unchanged the protective effect of adaptation. Inhibition of NOsynthesis restricted the adaptation-induced HSP70 synthesis. Therefore, the formation of adaptation at the cell level may result from a direct action of an environmental factor without participation of neuro-humoral factors. The process of such adaptation involves the NO-dependent mechanisms divorced from the activation of HSP70 synthesis.