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[Effect of insulin on apoptosis of cultured human trophoblast cells and its mechanism]. | LitMetric

[Effect of insulin on apoptosis of cultured human trophoblast cells and its mechanism].

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

Department of Obstetrics and Gynecology, Xijing Hospital, China.

Published: September 2003

AI Article Synopsis

  • The study aimed to investigate how insulin affects the process of apoptosis (cell death) in cultured human trophoblast cells, which are important for pregnancy.
  • Human trophoblast cells were exposed to H2O2 to induce apoptosis, with three groups: a control group, a group treated with H2O2 only, and a group treated with both insulin and H2O2.
  • The results showed that insulin significantly reduced the apoptosis rate caused by H2O2, potentially by lowering caspase-3 activity and increasing Bcl-2 protein levels, suggesting it has a protective effect on these cells.

Article Abstract

Aim: To explore the effect of insulin on apoptosis of cultured human trophoblast cells and its possible mechanism.

Methods: Human trophoblast cells from early pregnancy women were cultured and divided into 3 groups; normal control group; H2O2, treatment group and insulin plus H2O2 treatment group. H2O2 was used to induce apoptosis of trophoblasts cells. Apoptotic rate was detected by flow cytometry. The effects of insulin on Bcl-2 expression and caspase-3 activity were also detected.

Results: H2O2 might induce apoptosis of trophoblast cells and typical morphological features of apoptotic cells was observed under electron microscope. Flow cytometry detection exhibited that insulin could reduce markedly H2O2-induced apoptotic rate of trophoblasts cells (P < 0. 01). Bcl-2 expression rate inH,O, treatment group was significantly lower than that in control group (P < 0. 01), while caspase-3 activity was distinctly higher than that in control group (P < 0. 01).

Conclusion: Insulin could inhibit apoptosis of human trophoblasts cells induced by H2O2, which be may through decreased caspase-3 activity and increased Bcl-2 protein expression.

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