Stimulating the Expression of Sphingosine Kinase 1 (SphK1) is Beneficial to Reduce Acrylamide-Induced Nerve Cell Damage

Abstract

Background: Sphingosine kinase 1 (SphK1) is the main rate-limiting enzyme that catalyzes the production of sphingosine 1-phosophate (S1P) from sphingosine (Sph). It has a certain role in the protection of nerve damage. However, the role of acrylamide (ACR) in nerve damage is currently unclear. Methods: In our current research, liquid chromatography triple quadrupole tandem mass spectrometer (LC-MS/MS) and reverse transcription-PCR (RT-qPCR) were used to detect S1P content in serum and SphK1 content in whole blood in the ACR contact and non-contact groups. In vitro experiments, SphK1 in human neuroblastoma cell (SH-SY5Y) was activated by adding SphK1 specific activator phorbol 12-myristate 13-acetate (PMA). Our research adopted cell viability assay, flow cytometry, western blot, RT-qPCR and related protein detection at mitogen activated protein kinases (MAPK) signaling pathway. The results of the population study showed that the contents of SphK1 and S1P in the ACR contact group were lower than those in the non-contact group. Results: The results of in vitro experiments showed that the expression of SphK1 decreased with the increase of ACR concentration. Activating SphK1 can improve the survival rate of SH-SY5Y cells and decrease the apoptosis rate. Activating SphK1 in SH-SY5Y cells can regulate MAPK signaling, including enhancing the phosphorylation of extracellular signal-regulated protein kinases (ERK) and inhibiting the phosphorylation of c-Jun N-terminal kinases (JNK) and p38. Conclusion: These results suggest that activating SphK1 can protect the nerve cell damage caused by ACR. This study will provide new ideas for the prevention of neurological damage caused by ACR.