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2016 ; 5
(ä): 146-151
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Macrophage depletion by clodronate liposome attenuates muscle injury and
inflammation following exhaustive exercise
#MMPMID28955817
Kawanishi N
; Mizokami T
; Niihara H
; Yada K
; Suzuki K
Biochem Biophys Rep
2016[Mar]; 5
(ä): 146-151
PMID28955817
show ga
Exhaustive exercise promotes muscle injury, including myofiber lesions; however,
its exact mechanism has not yet been elucidated. In this study, we tested the
hypothesis that macrophage depletion by pretreatment with clodronate liposomes
alters muscle injury and inflammation following exhaustive exercise. Male
C57BL/6J mice were divided into four groups: rest plus control liposome (n=8),
rest plus clodronate liposome (n=8), exhaustive exercise plus control liposome
(n=8), and exhaustive exercise plus clodronate liposome (n=8). Mice were treated
with clodronate liposome or control liposome for 48 h before undergoing
exhaustive exercise on a treadmill. Twenty-four hours after exhaustive exercise,
the gastrocnemius muscles were removed for histological and PCR analyses.
Exhaustive exercise increased the number of macrophages in the muscle; however,
clodronate liposome treatment reduced this infiltration. Although exhaustive
exercise resulted in an increase in injured myofibers, clodronate liposome
treatment following exhaustive exercise reduced the injured myofibers. Clodronate
liposome treatment also decreased the mRNA expression levels of inflammatory
cytokines (TNF-?, IL-1?, and IL-6) in the skeletal muscle after exhaustive
exercise. These results suggest that macrophages play a critical role in
increasing muscle injury by regulating inflammation.