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Monotropein attenuates oxidative stress via Akt/mTOR-mediated autophagy in osteoblast cells

Yao Shi1, Xiao-Yan Liu2, Yi-Ping Jiang2

  • 1School of Pharmacy, Second Military Medical University, Shanghai, 200433, China; School of Pharmacy, Inner Mongolia Medical University, Huhhot, 010000 China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|November 8, 2019
PubMed

Insights

Monotropein protects osteoblasts from oxidative stress by enhancing autophagy via the Akt/mTOR pathway. This natural compound shows promise for treating osteoporosis by reducing cellular damage and promoting bone health.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Pharmacology

Background:

  • Oxidative stress is a key factor in osteoporosis development.
  • Autophagy, a cellular process, can mitigate oxidative stress and is a potential therapeutic target for osteoporosis.
  • Monotropein, an iridoid glycoside used in traditional Chinese medicine, promotes osteoblastic bone formation.

Purpose of the Study:

  • To investigate if autophagy mediates the protective effects of monotropein against oxidative stress in osteoblasts.
  • To elucidate the underlying mechanism of monotropein's action, particularly its involvement with the Akt/mTOR pathway.

Main Methods:

  • Osteoblasts were exposed to hydrogen peroxide (H2O2) to induce oxidative stress.
  • Monotropein's effects on reactive oxygen species (ROS) generation, cell viability, and apoptosis were assessed.
  • Autophagy markers (Beclin1, LC3-II/LC3-I ratio), oxidative stress markers (malondialdehyde, catalase, superoxide dismutase), and signaling pathway proteins (Akt, mTOR, p70S6K, 4EBP1) were analyzed using western blotting and biochemical assays.
  • The role of the Akt/mTOR pathway was confirmed using pathway activators (SC79, MHY1485).

Main Results:

  • Monotropein inhibited H2O2-induced ROS generation and protected osteoblasts from oxidative damage and apoptosis.
  • Monotropein treatment increased autophagy, evidenced by elevated Beclin1 expression and LC3-II/LC3-I ratio.
  • Monotropein attenuated oxidative stress markers and reduced the phosphorylation of Akt, mTOR, p70S6K, and 4EBP1.
  • Activation of Akt or mTOR pathways suppressed the autophagy induced by monotropein, indicating the pathway's involvement.

Conclusions:

  • Monotropein enhances autophagy in osteoblasts under oxidative stress, at least partly through the Akt/mTOR signaling pathway.
  • The protective effects of monotropein against oxidative stress in osteoblasts are mediated by autophagy.
  • Monotropein represents a potential therapeutic agent for osteoporosis treatment due to its antioxidant and autophagy-modulating properties.
Keywords:
Akt/mTOR signaling pathwayApoptosisAutophagyMonotropeinOsteoblast

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