Background: A significant amount of research has been conducted to establish the validity of acupuncture, and it has been demonstrated through animal disease model studies that acupuncture influences mitochondrial changes. However, to more accurately examine the mechanisms of acupuncture treatment effectiveness in pathological models, it is crucial to investigate changes in disease-free animals. Among various hypotheses regarding the effects of acupuncture on the body, we focused on the result that acupuncture stimulation is related to mitochondria.
Objectives: We examined the effects of acupuncture mitochondrial fission and fusionrelated mediators in disease-free Sprague Dawley (SD) rats' spleen meridian acupoints.
Methods: SD rats were divided into control, SP1, SP2, SP3, SP5, and SP9 acupuncture groups. Acupuncture was performed at each point for 10 minutes daily for four days. Peroxisome proliferator-activated receptor-gamma coactivator 1-α (PGC-1α) and fission protein 1 (Fis1) levels were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR), while dynamin-related protein 1 (DRP1), optic atrophy-1 (OPA1), mitofusin-1 (MFN1), and mitofusin-2 (MFN2) levels were assessed via western blotting. Mitochondria protein concentrations and NADH dehydrogenase activity in spleen tissues were measured using enzyme-linked immunosorbent assay (ELISA).
Results: PGC-1α expression decreased in the SP1 (p < 0.01), SP5 (p < 0.05), and SP9 (p < 0.05) groups, while Fis1 expression increased in the SP1 (p < 0.01), SP5 (p < 0.01), and SP9 (p < 0.05) groups. DRP1, OPA1, MFN1, and MFN2 levels exhibited no significant changes. Mitochondrial protein concentrations decreased in the SP2 (p < 0.01), SP3 (p < 0.01), SP5 (p < 0.01), and SP9 (p < 0.01) groups, while NADH dehydrogenase activity decreased in the SP2 (p < 0.05) and SP9 (p < 0.05) groups.
Conclusion: Acupuncture at the SP9 acupoint influenced the mitochondrial fission pathway by modulating PGC-1α and Fis1 mediators in the rat spleen under non-disease conditions.