Delta Sleep-Inducing Peptide Protects Rat Liver Cells from Stress Damage

The liver, a vital organ, is highly susceptible to damage from various stressors, including psychological stress, which can lead to oxidative stress and impaired hepatocyte (liver cell) function. Foot-shock stress is a well-established animal model used to induce both acute and chronic psychological stress, mimicking conditions that can negatively impact physiological systems. While the detrimental effects of stress on liver health are recognized, the specific mechanisms by which neuropeptides might mitigate this damage remain underexplored. This study specifically aimed to investigate how delta sleep-inducing peptide (DSIP) influences lipid peroxidation and the functional state of rat hepatocytes under both acute and chronic foot-shock stress.

In rats exposed to acute foot-shock stress, administration of 120 mcg/kg DSIP effectively normalized the stress-induced elevation of malondialdehyde (MDA) levels in the liver homogenate, a key indicator of oxidative damage. Interestingly, DSIP significantly decreased catalase activity across all tested doses in this acute setting. For serum markers, an injection of DSIP at 40 mcg/kg led to an increase in aminotransferase activity. In the context of chronic foot-shock stress, DSIP demonstrated a more consistent protective effect, with all tested doses providing normalization of protein synthetic hepatocyte function and increasing the activity of antioxidant enzymes, specifically catalase and superoxide dismutase. Furthermore, malondialdehyde (MDA) content in the liver homogenate was significantly decreased by 40 mcg/kg DSIP during chronic stress, although higher doses showed an increase against a background of reduced overall antioxidative activity. Crucially, the stress-induced increase in serum alanine aminotransferase activity, a marker of liver injury, was normalized by DSIP administration at doses of 120, 360, and 1080 mcg/kg.