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Sodium hydrosulfide mitigates dexamethasone-induced osteoblast dysfunction by interfering with mitochondrial

Jun Ma1, Qiang Fu1, Zhu Wang2

  • 1Department of Orthopedic Trauma Surgery, Changzheng Hospital, The Second Military Medical University, Huangpu District, Shanghai, People's Republic of China.

Biotechnology and Applied Biochemistry
|June 8, 2019
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Sodium hydrosulfide (NaHS) protects osteoblasts from glucocorticoid-induced injury. NaHS improves mitochondrial function and Sirt1/PGC1α expression, mitigating bone mass damage in osteoporosis.

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glucocorticoidshydrogen sulfideosteoporosis

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Endocrinology

Background:

  • Glucocorticoids (GCs) induce osteoporosis, characterized by bone mass damage and osteoblast dysfunction.
  • Hydrogen sulfide (H2S) plays a role in GC-induced osteoblast dysfunction.
  • Osteoporosis is a significant clinical complication of long-term GC therapy.

Purpose of the Study:

  • To investigate the effects of Sodium hydrosulfide (NaHS) on osteoblast function and mitochondrial activity in dexamethasone (DEX)-induced osteoporosis models.
  • To examine the impact of NaHS on Sirt1 and PGC1α expression in DEX-treated osteoblasts.
  • To elucidate the protective mechanisms of NaHS against GC-induced osteoblast injury.

Main Methods:

  • Osteoblastic MC3T3-E1 cells were treated with dexamethasone (DEX) and NaHS.
  • Cell viability, M-CSF levels, and alkaline phosphatase (ALP) activity were assessed.
  • Mitochondrial function was evaluated by measuring superoxide production, membrane potential, and ATP levels.
  • Sirt1 and PGC1α protein expression was determined using Western blot analysis.
  • Sirt1 gene silencing was performed to confirm its role.

Main Results:

  • DEX treatment decreased cell viability and ALP activity while increasing M-CSF levels, effects attenuated by NaHS.
  • NaHS partially reversed DEX-induced mitochondrial dysfunction, including reduced membrane potential and ATP generation, and increased superoxide production.
  • DEX reduced Sirt1 and PGC1α protein expression, which was partially restored by NaHS.
  • Silencing Sirt1 abolished the protective effects of NaHS against DEX-induced cellular and mitochondrial damage.

Conclusions:

  • NaHS alleviates DEX-induced osteoblastic MC3T3-E1 cell injury.
  • NaHS protects osteoblasts by improving mitochondrial function and modulating Sirt1/PGC1α expression.
  • Sirt1 is crucial for the protective effects of NaHS against GC-induced osteoblast damage, highlighting its therapeutic potential in osteoporosis.