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The time changes of endogenous salusin-β in septic rats

Salusin-α and salusin-β are newly found bioactive peptides of 28 and 20 amino acids, respectively, which are widely distributed in the hematopoietic system, endocrine system, and central nervous system. Salusins exert cardiovascular effects, including hypotension and bradycardia; promote vascular inflammation; and so on. However, little information is available yet on the relationships of salusin-β with sepsis. In this study, we investigated the distribution and content of endogenous salusin-β in septic rats. A total of 72 specified pathogen-free (SPF) male Sprague-Dawley (SD) rats were randomly divided into control group (sham operation, n = 36) and experimental group (n = 36) with sepsis rat model by cecal ligation and puncture (CLP). The model group rats were sacrificed after 6, 12, and 24 h of treatment. The concentration of salusin-β in spleen, stomach, small intestine, hypothalamus, and serum specimens was detected by enzyme-linked immunosorbent assay (ELISA). It showed that salusin-β was endogenously generated in rat tissues, including spleen, stomach, small intestine, hypothalamus, and serum. The content of salusin-β in the spleen was higher than that in other tissues. The content of salusin-β in the spleen, stomach, and small intestine, together with the serum level of salusin-β, increased significantly at 6 h after CLP compared with the control group (P < 0.05). The content of salusin-β in spleen and serum peaked at 12 h, and in small intestine, it reached the summit at 24 h. Meanwhile, no significant fluctuations in salusin-β content were observed in the stomach. The content of salusin-β in hypothalamus began to increase at 6 h, and a significant increase appeared 12 h after CLP (P < 0.05). In conclusion, this study shows that the time-dependent alterations of salusin-β in septic rats suggest that salusin-β might be involved in the pathogenesis of sepsis.