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Paeoniflorin Alleviates Skeletal Muscle Atrophy in Ovariectomized Mice through the ERα/NRF1 Mitochondrial Biogenesis
Ki-Sun Park1, Hyungjun Kim1, Hye Jin Kim2
1KM Science Research Division, Korea Institute of Oriental Medicine, Daejeon 34054, Korea.
Pharmaceuticals (Basel, Switzerland)
|April 23, 2022
Summary
Paeoniflorin (PNF) prevents postmenopausal muscle atrophy by restoring mitochondrial function and muscle differentiation markers. This natural compound combats inflammation and enhances muscle mass and function in mice lacking estrogen.
Area of Science:
- Biochemistry
- Cell Biology
- Muscle Physiology
Background:
- Postmenopausal muscle atrophy is linked to estrogen deficiency and inflammation, specifically tumor necrosis factor alpha (TNFα).
- Paeoniflorin (PNF), a natural compound, possesses anti-inflammatory properties and can enhance estradiol synthesis.
- Mitochondrial dysfunction plays a critical role in the pathogenesis of muscle atrophy.
Purpose of the Study:
- To investigate the potential of Paeoniflorin (PNF) in preventing and treating TNFα-induced skeletal muscle atrophy in postmenopausal conditions.
- To elucidate the underlying mechanisms of PNF action, focusing on mitochondrial biosynthesis and muscle differentiation.
- To evaluate the efficacy of PNF in an in vivo model of estrogen deficiency.
Main Methods:
- In vitro studies using differentiated myoblasts treated with TNFα and PNF.
- Analysis of muscle differentiation markers (Myogenin, Myosin Heavy Chain 3) and mitochondrial regulators (NRF1, TFAM).
- In vivo studies using ovariectomized (OVX) mice treated with PNF, assessing muscle cross-sectional area, muscle function, and mitochondrial dynamics markers (MFN1, MFN2, DRP1, FIS1).
Main Results:
- PNF treatment restored TNFα-damaged myoblasts, increasing myogenin (MyoG) and myosin heavy chain 3 (Myh3) expression and myotube diameter.
- PNF reversed TNFα-induced repression of nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM), mediated by estrogen receptor alpha (ERα).
- In OVX mice, PNF administration significantly recovered muscle cross-sectional area and improved performance in behavioral and motor function tests, restoring mitochondrial fusion and fission markers.
Conclusions:
- Paeoniflorin effectively inhibits TNFα-induced skeletal muscle atrophy in postmenopausal models by restoring mitochondrial biosynthesis and muscle differentiation.
- The mechanism involves the regulation of NRF1 and TFAM via ERα, leading to improved mitochondrial health and muscle integrity.
- PNF demonstrates therapeutic potential for preventing muscle atrophy and enhancing muscle function in postmenopausal women by combating estrogen deficiency-related mitochondrial dysfunction.
