Green tea extract decreases muscle pathology and NF-kappaB immunostaining in regenerating muscle fibers of mdx mice.
OBJECTIVE
Duchenne muscular dystrophy is a debilitating genetic disorder characterized by severe muscle wasting and early death in afflicted boys. The primary cause of this disease is mutations in the dystrophin gene resulting in massive muscle degeneration and inflammation. The purpose of this study was to determine if dystrophic muscle pathology and inflammation were decreased by pre-natal and early dietary intervention with green tea extract.


METHODS
Mdx breeder mice and pups were fed diets containing 0.25% or 0.5% green tea extract and compared to untreated mdx and C57BL/6J mice. Serum creatine kinase was assessed as a systemic indicator of muscle damage. Quantitative histopathological and immunohistochemical techniques were used to determine muscle pathology, macrophage infiltration, and NF-kappaB localization.


RESULTS
Early treatment of mdx mice with green tea extract significantly decreased serum creatine kinase by approximately 85% at age 42 days (P< or =0.05). In these mice, the area of normal fiber morphology was increased by as much as approximately 32% (P< or =0.05). The primary histopathological change was a approximately 21% decrease in the area of regenerating fibers (P< or =0.05). NF-kappaB staining in regenerating muscle fibers was also significantly decreased in green tea extract-treated mdx mice when compared to untreated mdx mice (P< or =0.05).


CONCLUSIONS
Early treatment with green tea extract decreases dystrophic muscle pathology potentially by regulating NF-kappaB activity in regenerating muscle fibers.
Evans
Nicholas P
NP
Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, 338 Wallace Hall, Blacksburg, VA 24061, USA. nievans@vt.edu
Call
Jarrod A
JA
Bassaganya-Riera
Josep
J
Robertson
John L
JL
Grange
Robert W
RW
D000375:Aging; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D004305:Dose-Response Relationship, Drug; D005260:Female; D008264:Macrophages / Q000187:drug effects; D008297:Male; D051379:Mice; D018101:Mice, Inbred mdx; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D020388:Muscular Dystrophy, Duchenne / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D016328:NF-kappa B / Q000378:metabolism*; D009336:Necrosis / Q000473:pathology / Q000517:prevention & control; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011897:Random Allocation; D012038:Regeneration / Q000187:drug effects*; D013662:Tea / Q000737:chemistry*
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015415:Biomarkers; D016328:NF-kappa B; D010936:Plant Extracts; D013662:Tea