Effects of Nimodipine on Neural Tube Development in Early Chick Embryos.
Source: PubMed, NCBI / U.S. National Library of Medicine
Although nimodipine is the only calcium channel blocker routinely used for the treatment of aneurysmal subarachnoid hemorrhage, its precise mechanism of action remains unknown. Therefore, this study investigated the effects of nimodipine on many cells in the body due to its effect on calcium channels and neural tube development, especially in pregnancy. A total of 100 fertile and 0-day-old specific pathogen-free (SPF) eggs of White Leghorn weighing 65 ± 5 g were used. SPF eggs were randomly divided into four groups: a control group and three different dose groups. SPF eggs were incubated for 28 h under appropriate temperature and humidity conditions. At the end of 28 h, nimodipine was subblastodermicly administered using a Hamilton microinjector at three different doses. At 48 h, all eggs were hatched, and the embryos were removed from the embryonic membranes. Then, morphological, histopathological, cell proliferation (PCNA), and genetic analyses were performed. The results of the morphological analysis revealed that when the frequency of neural tube patency was evaluated among the experimental groups, a statistically significant difference was determined between the control group and all groups (p < 0.001). Furthermore, the mean crown-rump length and somite number of the embryos were dose-dependently lower than the control group (p < 0.001). Nimodipine exposure dose-dependently decreased the PCNA and
Abstract
Although nimodipine is the only calcium channel blocker routinely used for the treatment of aneurysmal subarachnoid hemorrhage, its precise mechanism of action remains unknown. Therefore, this study investigated the effects of nimodipine on many cells in the body due to its effect on calcium channels and neural tube development, especially in pregnancy. A total of 100 fertile and 0-day-old specific pathogen-free (SPF) eggs of White Leghorn weighing 65 ± 5 g were used. SPF eggs were randomly divided into four groups: a control group and three different dose groups. SPF eggs were incubated for 28 h under appropriate temperature and humidity conditions. At the end of 28 h, nimodipine was subblastodermicly administered using a Hamilton microinjector at three different doses. At 48 h, all eggs were hatched, and the embryos were removed from the embryonic membranes. Then, morphological, histopathological, cell proliferation (PCNA), and genetic analyses were performed. The results of the morphological analysis revealed that when the frequency of neural tube patency was evaluated among the experimental groups, a statistically significant difference was determined between the control group and all groups (p < 0.001). Furthermore, the mean crown-rump length and somite number of the embryos were dose-dependently lower than the control group (p < 0.001). Nimodipine exposure dose-dependently decreased the PCNA and increased the caspase-3, with this change being significant between the experimental groups. In conclusion, nimodipine exposure delayed neural tube closure in chicken embryos by suppressing proliferation and apoptosis induction. Nimodipine exposure delayed neurogenesis and development in early chick embryos.