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Updated: May 31, 2026
Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
Published on: July 17, 2018
Millimeter wave treatment inhibits the mitochondrion-dependent apoptosis pathway in chondrocytes
Guangwen Wu1, Thomas Sferra, Xuzheng Chen
1Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Shangjie Minhou, Fuzhou 350108, P.R. China.
Abstract:
Millimeter wave (MW) is an electromagnetic wave with a wavelength between 1 and 10 mm and a frequency of 30-300 GHz that causes multiple biological effects, both locally and globally. MW has been widely used in clinical medicine. Although our previous work demonstrated that MW is capable of inhibiting sodium nitroprussiate (SNP)-induced apoptosis in chondrocytes, the precise mechanism of the anti-apoptotic activity remains to be elucidated. The purpose of this study was to investigate the effects of MW in SNP-induced apoptotic chondrocytes. Sprague Dawley rat chondrocytes were isolated and cultured, and the cells were counted. Cell viability was evaluated using MTT assay. Cells were then treated with SNP and MW, and flow cytometry was used to detect apoptosis. Our results showed that MW treatment inhibited a SNP-induced mitochondrion-dependent pathway of apoptosis. MW treatment inhibited the loss of plasma membrane asymmetry (externalization of phosphatidylserine), collapse of mitochondrial membrane potential, and activation of caspase-9 and caspase-3. Taken together, the results indicate that MW inhibits the mitochondrion-dependent pathway of apoptosis in chondrocytes and this may, in part, explain its clinical effect in the treatment of osteoarthritis.
Insights
Millimeter wave (MW) therapy effectively inhibits apoptosis in chondrocytes by preserving mitochondrial function and blocking key caspase activation. This finding helps explain MW
Area of Science:
- Biomedical Engineering
- Cell Biology
- Electrophysiology
Background:
- Millimeter wave (MW) therapy, utilizing electromagnetic waves (30-300 GHz), has demonstrated clinical applications.
- Previous research indicated MW's potential to inhibit chondrocyte apoptosis, but the underlying mechanisms required further investigation.
- Understanding MW's anti-apoptotic effects is crucial for optimizing its use in conditions like osteoarthritis.
Purpose of the Study:
- To elucidate the precise mechanism by which millimeter wave (MW) therapy inhibits sodium nitroprusside (SNP)-induced apoptosis in chondrocytes.
- To investigate the impact of MW on key cellular events within the mitochondrion-dependent apoptotic pathway.
Main Methods:
- Primary Sprague Dawley rat chondrocytes were isolated, cultured, and subjected to SNP-induced apoptosis.
- Cell viability was assessed using MTT assay.
- Apoptosis and mitochondrial pathway activation were analyzed via flow cytometry, examining plasma membrane asymmetry, mitochondrial membrane potential, and caspase-9/caspase-3 activity.
Main Results:
- MW treatment significantly inhibited SNP-induced apoptosis in chondrocytes.
- MW mitigated the loss of plasma membrane asymmetry and the collapse of mitochondrial membrane potential.
- MW effectively suppressed the activation of caspase-9 and caspase-3, key executioners of apoptosis.
Conclusions:
- Millimeter wave (MW) therapy exerts its anti-apoptotic effects in chondrocytes by inhibiting the mitochondrion-dependent pathway.
- MW preserves cellular integrity by maintaining plasma membrane potential and preventing mitochondrial dysfunction.
- These findings provide a mechanistic basis for the clinical efficacy of MW in treating osteoarthritis.
