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Updated: Jan 23, 2026
An In Vitro Approach to Study Mitochondrial Dysfunction: A Cybrid Model
Published on: March 9, 2022
Sodium hydrosulfide mitigates dexamethasone-induced osteoblast dysfunction by interfering with mitochondrial function
1Department of Orthopedic Trauma Surgery, Changzheng Hospital, The Second Military Medical University, Huangpu District, Shanghai, People's Republic of China.
Abstract:
Osteoporosis is one of the clinical complications of long-term treatment with glucocorticoids (GCs), characterized by systemic damage of bone mass and osteoblast dysfunction. Hydrogen sulfide was found to be involved in GCs-induced osteoblast dysfunction. Osteoblastic MC3T3-E1 cell and mitochondrial function were determined by cell viability, M-CSF level, and ALP activity and superoxide production, membrane potential, and ATP level, respectively. The purpose of this research was to explore the impact of NaHS on osteoblastic MC3T3-E1 cell function as well as on Sirt1 and PGC1α expression in dexamethasone (DEX)-treated osteoblast cells. DEX-treated MC3T3-E1 cells exhibited decreased cell viability and ALP activity, as well as increased M-CSF level; all these changes were dramatically attenuated by NaHS. DEX-treated cells also displayed mitochondrial dysfunction, namely decreased mitochondrial membrane potential and ATP generation and increased superoxide generation, which were partly reversed by NaHS. We confirmed decreased Sirt1 and PGC1α protein expression in DEX-treated MC3T3-E1 cells by Western blot, which was also partly reversed by NaHS. Silencing of Sirt1 abrogated the protective effect of NaHS against DEX-induced cell damage and mitochondrial dysfunction. NaHS alleviates DEX-induced osteoblastic MC3T3-E1 cell injury by improving mitochondrial function.
Insights
Sodium hydrosulfide (NaHS) protects osteoblasts from glucocorticoid-induced injury. NaHS improves mitochondrial function and Sirt1/PGC1α expression, mitigating bone mass damage in osteoporosis.
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.
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