β-丙氨酸对氧糖剥夺/复氧损伤神经元作用及机制OA

Objective To investigate the role of the β-alanine(β-Ala)/silent information regulator 6(SIRT6)/hypoxia-indu-cible factor-1α(HIF-1α)signaling pathway in neurons with oxygen-glucose deprivation/reoxygenation(OGD/R)injury.Methods Rat cortical neurons were used to establish an in vitro model of OGD/R injury.CCK-8 assay was used to observe the viability of neurons treated with β-Ala,and Western blot was used to measure the expression levels of SIRT6 and HIF-1α in neurons after β-Ala treatment.After neurons with OGD/R injury were treated with both β-Ala and an SIRT6 inhibitor,Western blot was used to measure the protein expression level of HIF-1α in each group,and CCK-8 colorimetry was used to measure the viability of neurons in each group.The neurons without treatment were established as control group.Results Compared with the control group,the OGD/R group had a reduction in the viability of neurons,and compared with the OGD/R group,the OGD/R+1 000 μmol/L β-Ala group had a significant increase in the viability of neurons(F=343.30,P＜0.01).Western blot showed that compared with the control group,the OGD/R group had an increase in HIF-1α expression and a reduction in SIRT6 expression,and compared with the OGD/R group,the OGD/R+β-Ala group had a reduction in HIF-1α expression and an increase in SIRT6 expression(F=16.13,10.08;P＜0.05).Western blot and CCK-8 assay showed that compared with the OGD/R+β-Ala group,the group treated with OGD/R+β-Ala+SIRT6 inhibitor had a significant increase in HIF-1α expression(F=22.24,P＜0.01)and a significant re-duction in the viability of neurons(F=33.64,P＜0.01).Conclusion β-Ala exerts a neuroprotective effect against OGD/R-in-duced neuronal injury by regulating the SIRT6/HIF-1α signaling pathway.