Factory Supply High Purity DSIP CAS NO.62568-57-4 CAS NO.62568-57-4

About DSIP

Delta sleep-inducing peptide, abbreviated DSIP, is a neuropeptide that when infused into the mesodiencephalic ventricle of recipient rabbits induces spindle and delta EEGactivity and reduced motor activities.[1]

Its aminoacid sequence is Тrр-Аlа-Gly-Gly-Asp-Ala-Ser-Gly-Glu. However, it is the only neuropeptide in history whose gene is unknown, raising serious questions regarding the actual existence of this peptide in nature.

Function

Many roles for DSIP have been suggested following research carried out using peptide analogues with a greater molecular stability and through measuring DSIP-like immunological (DSIP-LI) response by injecting DSIP antiserum and antibodies.

Decreases basal corticotropin level and blocks its release.

Stimulates release of luteinizing hormone (LH).

Stimulates release of somatoliberin and somatotrophin secretion and inhibits somatostatinsecretion.

Can act as a stress limiting factor.

May have a direct or indirect effect on body temperature and alleviating hypothermia.

Can normalize blood pressure and myocardial contraction.

It has been shown to enhance the efficiency of oxidative phosphorylation in rat mitochondria in vitro, suggesting it may have antioxidant effects.

There is also conflicting evidence as to its involvement in sleep patterns. Some studies suggest a link between DSIP and slow-wave sleep (SWS) promotion and suppression of paradoxical sleep, while some studies show no correlation.[28] Stronger effects on sleep have been noted for the synthesized analogues of DSIP.

It may have an impact on human lens epithelial cell function via the MAPK pathway, which is involved in cell proliferation, differentiation, motility, survival, and apoptosis.

It has been found to have anticarcinogenic properties. In a study on mice, injecting a preparation of DSIP over the mice's lifetime decreased total spontaneous tumor incidence 2.6-fold.

The same study found it to also have geroprotective effects: it slowed down the age-related switching-off of oestrous function; it decreased by 22.6% the frequency of chromosome aberrations inbone marrow cells and it increased by 24.1% maximum life span in comparison with the control group.