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Nitric oxide prevents atorvastatin-induced skeletal muscle dysfunction and alterations in mice.
Muscle Nerve. 2013 Jan; 47(1):72-80.MN

Abstract

INTRODUCTION

Myopathy is the most common side effect of statins. Because nitric oxide (NO) has a key role in regulating skeletal muscle function, we studied whether the NO-donating atorvastatin NCX 6560 could show a better profile on skeletal muscle function and structure compared with atorvastatin.

METHODS

C57BL/6 mice received atorvastatin 40 mg/kg/day or an equivalent dose of NCX 6560 for 2 months. Muscle function assessed by treadmill test, serum creatine kinase (CK) activity, citrate synthase (CS) activity, and muscle histology were evaluated.

RESULTS

Atorvastatin significantly (P < 0.001) reduced muscle endurance, increased serum CK by 6-fold, and induced muscle fiber atrophy. Conversely, NCX 6560 preserved muscle function, prevented CK increase and did not modify muscle structure. Interestingly, atorvastatin reduced CS activity, a marker for mitochondrial function, in gastrocnemius, diaphragm, and heart, whereas NCX 6560 prevented such decrease.

CONCLUSIONS

These findings suggest that NO may prevent statin-induced myopathy.

Authors+Show Affiliations

Department of Molecular Medicine, University of Pavia, Via Forlanini 6, 27100 Pavia, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

23042511

Citation

D'Antona, Giuseppe, et al. "Nitric Oxide Prevents Atorvastatin-induced Skeletal Muscle Dysfunction and Alterations in Mice." Muscle & Nerve, vol. 47, no. 1, 2013, pp. 72-80.
D'Antona G, Mascaro A, Monopoli A, et al. Nitric oxide prevents atorvastatin-induced skeletal muscle dysfunction and alterations in mice. Muscle Nerve. 2013;47(1):72-80.
D'Antona, G., Mascaro, A., Monopoli, A., Miglietta, D., Ongini, E., & Bottinelli, R. (2013). Nitric oxide prevents atorvastatin-induced skeletal muscle dysfunction and alterations in mice. Muscle & Nerve, 47(1), 72-80. https://doi.org/10.1002/mus.23465
D'Antona G, et al. Nitric Oxide Prevents Atorvastatin-induced Skeletal Muscle Dysfunction and Alterations in Mice. Muscle Nerve. 2013;47(1):72-80. PubMed PMID: 23042511.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitric oxide prevents atorvastatin-induced skeletal muscle dysfunction and alterations in mice. AU - D'Antona,Giuseppe, AU - Mascaro,Anna, AU - Monopoli,Angela, AU - Miglietta,Daniela, AU - Ongini,Ennio, AU - Bottinelli,Roberto, Y1 - 2012/10/05/ PY - 2012/05/15/accepted PY - 2012/10/9/entrez PY - 2012/10/9/pubmed PY - 2013/2/23/medline SP - 72 EP - 80 JF - Muscle & nerve JO - Muscle Nerve VL - 47 IS - 1 N2 - INTRODUCTION: Myopathy is the most common side effect of statins. Because nitric oxide (NO) has a key role in regulating skeletal muscle function, we studied whether the NO-donating atorvastatin NCX 6560 could show a better profile on skeletal muscle function and structure compared with atorvastatin. METHODS: C57BL/6 mice received atorvastatin 40 mg/kg/day or an equivalent dose of NCX 6560 for 2 months. Muscle function assessed by treadmill test, serum creatine kinase (CK) activity, citrate synthase (CS) activity, and muscle histology were evaluated. RESULTS: Atorvastatin significantly (P < 0.001) reduced muscle endurance, increased serum CK by 6-fold, and induced muscle fiber atrophy. Conversely, NCX 6560 preserved muscle function, prevented CK increase and did not modify muscle structure. Interestingly, atorvastatin reduced CS activity, a marker for mitochondrial function, in gastrocnemius, diaphragm, and heart, whereas NCX 6560 prevented such decrease. CONCLUSIONS: These findings suggest that NO may prevent statin-induced myopathy. SN - 1097-4598 UR - https://www.unboundmedicine.com/medline/citation/23042511/Nitric_oxide_prevents_atorvastatin_induced_skeletal_muscle_dysfunction_and_alterations_in_mice_ L2 - https://doi.org/10.1002/mus.23465 DB - PRIME DP - Unbound Medicine ER -