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| Pretreatment with Baicalin Attenuates Hypoxia and Glucose Deprivation-Induced Injury in SH-SY5Y Cells |
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| KeyWord:baicalin, neuroprotection, apoptosis, caspase-3, nuclear factor-κB, N-methyl-d-aspartic acid receptor-1, hypoxia and glucose deptivation-reperfusion |
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| Abstract: |
| Objective: To explore the neuroprotective effects of baicalin against hypoxia and glucose deprivationreperfusion (OGD/RO)-induced injury in SH-SY5Y cells. Methods: SH-SY5Y cells were divided into a control group, a OGD/RO group, which was subject to OGD/RO induction; and 3 baicalin groups subject to baicalin (1, 5, 25 μmol/L) for 2 h before induction of OGD/RO (low-, medium-, and high-dose baicalin groups). Cell viability was detected by thiazolyl blue tetrazolium bromide (MTT) assay and flow cytometric analysis was used to detect cell apoptosis. Real-time polymerase chain reaction was performed to determine the mRNA expression of caspase-3 gene. Western blot analysis was conducted to determine the expression of nuclear factor (NF)-κB and N-methyl-daspartic acid receptor-1 (NMDAR1). Results: Baicalin could significantly attenuate OGD/RO mediated apoptotic cell death in SH-SY5Y cells; the apoptosis rates in the low-, medium- and high-dose groups were 12.1%, 7.9%, and 5.4%, respectively. Western blot and real-time PCR analysis revealed that significant decrease in caspase-3 expression in the baicalin group compared with the OGD/RO group (P<0.01). Additionally, down-regulation of NF-κB and NMDAR1 was observed in the baicalin group compared with those obtained from the OGD/RO group. Compared with the low-dose baicalin group, remarkable decrease was noted in the medium- and high-dose groups (P<0.01). Conclusion: Baicalin pre-treatment attenuates brain ischemia reperfusion injury by suppressing cellular apoptosis. |
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