Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/198649
Type: Artigo de periódico
Title: Diltiazem And Verapamil Protect Dystrophin-deficient Muscle Fibers Of Mdx Mice From Degeneration: A Potential Role In Calcium Buffering And Sarcolemmal Stability.
Author: Matsumura, Cintia Yuri
Pertille, Adriana
Albuquerque, Tereza C P
Santo Neto, Humberto
Marques, Maria Julia
Abstract: The lack of dystrophin in mdx mice and in Duchenne muscular dystrophy causes sarcolemmal breakdown and increased calcium influx followed by myonecrosis. We examined whether the calcium channel blockers diltiazem and verapamil protect dystrophic muscles from degeneration. Mdx mice received daily intraperitoneal injections of diltiazem or verapamil for 18 days, followed by removal of the sternomastoid, diaphragm, tibialis anterior, and cardiac muscles. Control mdx mice were injected with saline. Both drugs significantly decreased blood creatine kinase levels. Total calcium content was significantly higher in mdx muscles than in control C57Bl/10. Verapamil and diltiazem reduced total calcium content only in diaphragm and cardiac muscle. Histological analysis showed that diltiazem significantly attenuated myonecrosis in diaphragm. Immunoblots showed a significant increase of calsequestrin and beta-dystroglycan levels in some diltiazem- and verapamil-treated muscles. Possible interactions of these drugs with the sarcoplasmic reticulum and sarcolemma may also contribute to the improvement of the dystrophic phenotype.
Subject: Animals
Calcium
Calcium Channel Blockers
Calsequestrin
Creatine Kinase
Diltiazem
Disease Models, Animal
Dystroglycans
Female
Male
Mice
Mice, Inbred C57bl
Mice, Inbred Mdx
Muscle Fibers, Skeletal
Muscular Dystrophy, Animal
Sarcolemma
Verapamil
Rights: fechado
Identifier DOI: 10.1002/mus.21188
Address: http://www.ncbi.nlm.nih.gov/pubmed/19145649
Date Issue: 2009
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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