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Neuromuscular function during aging is protected in baicalein‐treated C57BL/6 mice
Author(s) -
Bhattacharya Arunabh,
Walsh Michael,
Hamilton Ryan,
Singh Rashmi,
Rahman Mizanur,
Rodriguez Karl,
Chaudhuri Asish,
Sharma Ramaswamy
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.651.2
Subject(s) - baicalein , sarcopenia , sciatic nerve , medicine , muscle atrophy , endocrinology , stimulation , atrophy , chemistry , pharmacology
The loss of muscle mass and strength during aging is a debilitating condition leading to altered metabolism and the loss of independence in older adults. The causes of this condition, known as sarcopenia, are not known. We previously reported an increase in arachidonic acid and its metabolite 12‐hydroxyeicosatetraenoic acid (12‐HETE), which is generated by 12/15‐lipoxygenase (12/15‐LO), in sciatic nerves of old (28–30 months) C57Bl/6 mice. To determine if 12/15‐LO activity contributes to the age‐related decline in muscle and nerve function, we treated middle‐aged (24 mo old) mice with the 12/15‐LO inhibitor baicalein for 14–16 weeks. Compared to baseline measurements, baicalein treatment improved hindlimb muscle force generated by electrical stimulation. Baicalein treatment partially prevented the decline in fatigue observed in vehicle‐treated old mice compared to baseline. These improvements occurred without any change in muscle mass or sciatic nerve conduction velocity. Baicalein treatment was associated with a reduction in oxidative and ubiquitin modifications to proteins in sciatic nerves from old mice, which may be due to elevated proteasome activity and altered stress response in sciatic nerves from baicalein‐treated mice. Our data suggest that lipid metabolites generated by 12/15‐LO may contribute to the age‐related loss of muscle strength observed during aging. Support or Funding Information National Institutes of Health (K01AG038555) and American Federation for Aging Research (AB), K99/R00 Pathway to Independence Award (AG049940‐01A1) (KR), T32 AG021890‐08 (NIA) National Service Research Award to Postdoctoral Fellow Training Grant on the Biology of Aging to Steven N. Austad for trainee (RTH) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .