Короткий опис (реферат):
Plasma galsectin-3 is increased in setting of STZ-diabetes in rats. Inhibition of H2S endogenous production could apparently enhance this effect, when NaHS administration led to reduction in plasma galectin-3. Thus, H2S system can be integrated in pathogenesis of diabetic complications through modulation of proinflammatory and profibrogenic mediator galectin-3.