[Salidroside inhibits clinorotation-induced apoptosis in pulmonary microvascular endothelial cells]

Nan Fang Yi Ke Da Xue Xue Bao. 2011 Apr;31(4):649-52.
[Article in Chinese]

Abstract

Objective: To investigate the inhibitory effect of salidroside (Sal) on pulmonary microvascular endothelial cell (HPMEC) apoptosis induced by simulated microgravity and its mechanism.

Methods: Human pulmonary microvascular endothelial cells cultured in vitro were divided into control group, clinorotation group and clinorotation+Sal pretreatment groups. Microgravity was simulated by clinorotation. The apoptotic rate of HPMECs was detected by flow cytometry using Annexin V-FITC staining, and the expressions of bcl-2, bax, and caspase-3 at the mRNA and protein levels were determined by real-time PCR and Western blotting, respectively.

Results: A 72-h clinorotation significantly induced apoptosis in HPMECs. Real-time PCR results demonstrated a significantly lowered bcl-2 but increased bax and caspase-3 mRNA expressions in clinorotation group as compared with those in the control group. Western blotting showed that clinorotation inhibited the protein expressions of PI3K and p-AKT and increased caspase-3 protein expression. Salidroside significantly inhibited the cell apoptosis, reversed the expressions of Bcl-2 and Bax, and attenuated the decrease in the protein expression of PI3K and phosphorylation level of AKT. Salidroside also antagonized the activation of caspase-3.

Conclusion: PI3K/AKT pathway and caspase 3 are involved in the apoptosis of HPMVECs induced by clinorotation, and the effect of clinorotation can be reversed by salidroside, suggesting the potential value of salidroside for application in spaceflight.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Apoptosis / drug effects*
  • Caspase 3 / metabolism
  • Cell Line
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects
  • Glucosides / pharmacology*
  • Humans
  • Lung / blood supply
  • Phenols / pharmacology*
  • Signal Transduction
  • Weightlessness*

Substances

  • Glucosides
  • Phenols
  • CASP3 protein, human
  • Caspase 3
  • rhodioloside