Pretreatment with baicalin attenuates hypoxia and glucose deprivation-induced injury in SH-SY5Y cells

Chin J Integr Med. 2016 Mar;22(3):201-6. doi: 10.1007/s11655-015-2326-8. Epub 2015 Dec 19.

Abstract

Objective: To explore the neuroprotective effects of baicalin against hypoxia and glucose deprivation-reperfusion (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.

Keywords: N-methyl-d-aspartic acid receptor-1; apoptosis; baicalin; caspase-3; hypoxia and glucose deptivation-reperfusion; neuroprotection; nuclear factor-κB.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Caspase 3 / genetics
  • Caspase 3 / metabolism
  • Cell Death / drug effects
  • Cell Hypoxia / drug effects
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Flavonoids / pharmacology*
  • Glucose / metabolism*
  • Humans
  • NF-kappa B / metabolism
  • Nerve Tissue Proteins / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Real-Time Polymerase Chain Reaction
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Reperfusion

Substances

  • Flavonoids
  • GRIN1 protein, human
  • NF-kappa B
  • Nerve Tissue Proteins
  • RNA, Messenger
  • Receptors, N-Methyl-D-Aspartate
  • baicalin
  • Caspase 3
  • Glucose