Elastin-derived
peptides (EDPs) contain replications of the Val-
Gly-Val-
Ala-Pro-Gly (
VGVAPG) hexapeptide. It has been described that the
VGVAPG peptide induces
reactive oxygen species (ROS) production in murine monocytes and astrocytes, human fibroblasts, and the human
neuroblastoma (SH-SY5Y) cell line. To date, there is growing evidence that
calcium channel blockers (CCBs) reduce oxidative stress and development of
inflammation in the nervous system. Therefore, the aim of the present study was to evaluate the impact of such CCBs as
Nifedipine,
Verapamil, and
MK-801 on the expression of
peroxisome proliferator-activated receptor (Pparγ), i.e. ROS-related and
inflammation-related
proteins, in mouse astrocytes exposed in vitro to the
VGVAPG peptide. The experiments showed that
Nifedipine or
MK-801 used in co-treatment with the
VGVAPG peptide potentiated the effect of this
peptide on the Pparγ level after the 24-h and 48-h treatment. Moreover, all studied compounds decreased the
VGVAPG-induced caspase-1 activity in both time intervals. The data also showed that the
VGVAPG peptide decreased the
interleukin 1 beta (IL-1β) level in both studied time intervals. Upon a short-time exposure, the use of CCBs intensified the decrease in IL-1β stimulated by the
VGVAPG peptide, opposite to the longer treatment. Moreover, the
VGVAPG peptide decreased the IL-1βR1 level in both studied time intervals. After 24 h,
Nifedipine and
Verapamil potentiated the effect of the
VGVAPG peptide. The
VGVAPG peptide decreased the
catalase (Cat)
protein expression only after 24 h, whereas CCBs did not affect the expression of Cat induced by the
VGVAPG peptide. The
VGVAPG peptide increased the expression of the
superoxide dismutase 1 (
Sod1) protein. After 24 h of exposure,
Nifedipine and
Verapamil potentiated the increase in the
Sod1 protein expression. Finally, our data showed that
VGVAPG did not change the level of
estradiol (E2) in the astrocytes. Interestingly,
Nifedipine and
Verapamil in co-treatment with
VGVAPG increased the E2 level. Summarizing, it can be assumed that increased amounts of the
VGVAPG during lifetime can play a certain role in
calcium channel functioning in
neurodegenerative diseases.