Developmental endothelial locus-1 enhances ER calmodulin expression, mitigates ER stress, suppresses inflammation, and attenuates neuronal apoptosis.

Hao Wang; Kangxue Chen; Yuyan Zhang; Kuijun Jiang; Zhonglei Sun

This study aimed to investigate the impact of developmental endothelial locus-1 (Del-1) on sarcoplasmic reticulum Ca2 ATPase 2 (SERCA2) and its potential effects on spinal cord injury (SCI). A total of 48 mice were randomly assigned to the sham group, SCI group, and SCI CE group. Each group was further divided into two subgroups. The Del treatment subgroup received tail-vein injections of Del-1 (1 μg/d) for a consecutive week, while the other group was injected with an equivalent volume of normal saline. After 1 week of experimentation, the mice were euthanized, and the spinal cord was extracted for further analysis. Initially, the impact of Del-1 on SERCA2 in the spinal cord was assessed using western blotting analysis. Subsequently, the effects of Del-1 on stress, inflammation, and apoptosis in the endoplasmic reticulum (ER) of SCI mice were analyzed through Western blotting analysis and fluorescent TUNEL. Finally, the study utilized Western blotting analysis and fluorescent TUNEL analysis to examine the consequences of Del-1 blocking SERCA2 on ER stress, inflammation, and apoptosis in mice. The results revealed that Del-1 treatment significantly increased the expression of SERCA2 in the spinal cord (P 0.05). In conclusion, this study proposed that Del-1 could reduce ER stress, inflammatory response, and nerve cell apoptosis in spinal cord injury by enhancing the expression of SERCA2.

NEURONS; WESTERN immunoblotting; SPINAL cord; SARCOPLASMIC reticulum; SPINAL cord injuries

Journal of Chinese Pharmaceutical Sciences, 2024, Vol 33, Issue 9, p795

1003-1057

Academic Journal

10.5246/jcps.2024.09.059