2. Academic Validation
  3. Polygalasaponin F inhibits neuronal apoptosis induced by oxygen-glucose deprivation and reoxygenation through the PI3K/Akt pathway

Polygalasaponin F inhibits neuronal apoptosis induced by oxygen-glucose deprivation and reoxygenation through the PI3K/Akt pathway

  • Basic Clin Pharmacol Toxicol. 2020 Sep;127(3):196-204. doi: 10.1111/bcpt.13408.
Wei Xie 1 2 3,  Hade Wulin 1 4,  Guo Shao 2 3,  Liqin Wei 5,  Ruifang Qi 1 2,  Baohui Ma 1 2,  Naihong Chen 6,  Ruili Shi 1 2 3
Affiliations

Affiliations

  • 1 Department of Physiology, Baotou Medical College, Baotou, China.
  • 2 Institute of Neuroscience, Baotou Medical College, Baotou, China.
  • 3 Inner Mongolia Key Laboratory of Hypoxic Translational Medicine, Baotou Medical College, Baotou, China.
  • 4 Department of Pharmacy, Inner Mongolia International Mongolian Hospital, Hohhot, China.
  • 5 Department of Traditional Chinese Medical Science, Baotou Medical College, Baotou, China.
  • 6 Institute of Materia Medica, Chinese Academy of Medical Sciences, Beijing, China.
PMID: 32237267 DOI: 10.1111/bcpt.13408
Abstract

Cerebral ischaemia is a common cerebrovascular disease and often induces neuronal Apoptosis, leading to brain damage. Polygalasaponin F (PGSF) is one of the components in Polygala japonica Houtt, and it is a triterpenoid saponin monomer. This research focused on anti-apoptotic effect of PGSF during oxygen-glucose deprivation and reoxygenation (OGD/R) injury in rat adrenal pheochromocytoma cells (PC12) and primary rat cortical neurons. OGD/R treatment reduced viability of PC12 cells and primary neurons. This reduced viability was prevented by PGSF, as shown by MTT assay. OGD/R insult decreased expression of Bcl-2/Bax both in PC12 cells and primary neurons but elevated levels of Caspase-3 in primary neurons. However, PGSF may up-regulate expression of Bcl-2/Bax and down-regulate Caspase-3 in these particular cells. Furthermore, Bcl-2/Bax and the ratio between phosphorylated Akt and total Akt were decreased in PC12 cells treated with OGD/R, and both were increased by PGSF. Moreover, increase in the ratios of Bcl-2/Bax and phosphorylated Akt/total Akt in PC12 cells was suppressed by phosphatidylinositol 3-kinase (PI3K) inhibitor. Data suggest PGSF might prevent OGD/R-induced injury via activation of PI3K/Akt signalling. The ability of PGSF to block the effects of OGD/R appears to involve regulation of Bcl-2, Bax and Caspase-3, which are related to Apoptosis.

Keywords

anti-apoptosis; neurons; oxygen-glucose deprivation and reoxygenation (OGD/R); phosphatidylinositol 3-kinase (PI3K)/Akt; polygalasaponin F (PGSF).

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