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Acta Histochem. 2016 Jun;118(5):464-70. doi: 10.1016/j.acthis.2016.04.011. Epub 2016 May 18.

Preventive effects of electrical stimulation on inflammation-induced muscle mitochondrial dysfunction.

Author information

1
Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Kobe 654-0142, Japan.
2
Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Kobe 654-0142, Japan; Department of Physical Therapy, Osaka Yukioka College of Health Science, 1-1-41 Sojiji, Ibaraki, Osaka 567-0801, Japan.
3
Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.
4
Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, 7-10-2 Tomogaoka, Kobe 654-0142, Japan. Electronic address: fujino@phoenix.kobe-u.ac.jp.

Abstract

Cachexia is a complex metabolic syndrome associated with underlying chronic diseases and is characterized by the overexpression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), which impair muscle oxidative metabolism. We hypothesized that electrical stimulation (ES) would prevent decrement in muscle oxidative metabolism by suppressing the phosphorylation of p38 MAPK, a critical regulator of inflammatory response. Therefore, the purpose of the present study was to verify the effects of ES on inflammatory-induced decrement of oxidative metabolism in mice tibialis anterior muscles. ICR mice were randomly divided into three groups: control, lipopolysaccharide (LPS) injection for 4days, and LPS injection plus ES (LPS+ES). Cachexia was induced in the animals in the LPS groups via LPS injection (10mg/kg body weight/day, i.p.) during the intervention period. The animals in the LPS+ES group were stimulated electrically (carrier frequency, 2500Hz; modulation frequency, 100Hz; duration, 240s/day; type of contraction, isometric) during the intervention period. LPS injection resulted in decreased body and muscle wet weight and increased expression of TNF-α in plasma and skeletal muscle. In addition, LPS injection decreased indicators of mitochondrial function such as succinate dehydrogenase (SDH) and citrate synthase (CS) activity as well as the expression of PGC-1ɑ, and increased the phosphorylation of p38 MAPK. On the other hand, the intervention of ES attenuated the changes in muscle wet weight, SDH activity, CS activity, p38 MAPK, and PGC-1ɑ. These results suggest that ES could prevent decrement in muscle oxidative metabolism induced by pro-inflammatory cytokines in cachexia.

KEYWORDS:

Cachexia; Electrical stimulation; Lipopolysaccharide; Mitochondria; Skeletal muscle

PMID:
27209425
DOI:
10.1016/j.acthis.2016.04.011
[Indexed for MEDLINE]

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