Pulsed electromagnetic fields exert protective effects against osteoarthritis by inhibiting lactic acid-induced chondrocyte damage

Chuncha Bao, Yue Hou, Chengqi He
Purpose:

Therefore, this study aims to explore whether lactate affects the function of OA chondrocytes and its potential molecular mechanisms, providing new ideas for the prevention and treatment of OA with PEMF.

Methods:

This study constructed in vitro and in vivo OA models. After the PEMF intervention, kits were used to detect extracellular lactic acid levels, NADPH, and acetyl-CoA levels. The mitochondrial oxygen consumption assay kits were used to measure the oxygen consumption rate of chondrocytes to reflect cellular energy metabolism. Techniques such as small RNA interference (siRNA), plasmid transfection, lentiviral vector transfection, and molecular biology methods were employed to investigate the specific molecular mechanisms.

Results:

This study found that compared with the healthy control group, the lactate level in the serum of OA patients was significantly increased; Compared to normal chondrocytes, OA chondrocytes showed significantly increased levels of lactate, NADPH, and acetyl CoA; After treating chondrocytes with lactic acid, the expression levels of IL-6, IL-18, MMP3, and MMP13 significantly increased. At the same time, the expression of cell aging and apoptosis related molecules P21, P53, and BAX significantly increased, while the expression level of BCL2 decreased; On the contrary, after treating OA chondrocytes with LDHA siRNA, the expression levels of IL-6, IL-18, MMP3, MMP13, P21, P53, and BAX were significantly reduced, while the expression level of BCL2 was significantly increased; After using PEMFs to intervene in chondrocytes, lactate induced cell aging can be reversed, and the promoting effect of lactate on chondrocyte catabolism can be reduced; Compared with the OA+LDHA siRNA group, PEMF intervention combined with LDHA siRNA treatment of cells can significantly promote chondrocyte synthesis and metabolism levels, and improve chondrocyte aging.

Conclusion(s):

This study reports that lactic acid, as a metabolite, contributes to the induction of chondrocyte damage, while LDHAsiRNA inhibits the catabolic metabolism, inflammatory response, and senescence in OA chondrocytes. PEMFs can prevent and delay the progression of OA by reducing lactic acid levels in chondrocytes.

 

 


Implications:

This study provides a new perspective on lactate as a metabolic factor involved in the OA process, and provides effective biological evidence for the treatment mechanism of PEMFs as a recommended treatment for OA. At the same time, it provides a theoretical basis and clinical practice guidance for the rehabilitation treatment of OA cartilage injury

Funding acknowledgements:
This study was supported by the National Natural Science Foundation of China (81972146 to Chengqi He)
Keywords:
Osteoarthritis
Pulsed electromagnetic fields
Lactate
Primary topic:
Musculoskeletal
Second topic:
Basic science including molecular and cellular health
Did this work require ethics approval?:
Yes
Name the institution and ethics committee that approved your work:
The Biomedical Ethics Review Committee of West China Hospital, Sichuan University
Provide the ethics approval number:
20220224015
Has any of this material been/due to be published or presented at another national or international conference prior to the World Physiotherapy Congress 2025?:
No

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