Abstract
Ashitaba, Angelica keiskei Koidzumi (AK), as a traditional medicine in Korea, Japan, and China, has been known as an elixir of life having therapeutic potential. However, there is no scientific evidence to support that Ashitaba can enhance or maintain muscle strength. To find a new therapeutic agent from the medicinal plant, we evaluated the anti-myopathy effect of chalcones from ethanol extract of AK (EAK) in cellular and animal models of muscle atrophy. To examine anti-myopathy activity, EAK was treated into dexamethasone injected rats and muscle thickness and histopathological images were analyzed. Oral administration of EAK (250 or 500 mg/kg) alleviated muscle atrophic damages and down-regulated the mRNA levels of muscle-specific ubiquitin-E3 ligases. Among ten compounds isolated from EAK, 4-hydroxyderricin was the most effective principle in stimulating myogenesis of C2C12 myoblasts via activation of p38 mitogen-activated protein kinase (MAPK). In three cellular muscle atrophy models with C2C12 myoblasts damaged by dexamethasone or cancer cell-conditioned medium, 4-hydroxyderricin protected the myosin heavy chain (MHC) degradation through suppressing expressions of MAFbx, MuRF-1 and myostatin. These results suggest that the ethanol extract and its active principle, 4-hydroxyderricin from AK, can overcome the muscle atrophy through double mechanisms of decreasing muscle protein degradation and activating myoblast differentiation.
Highlights
With the increasing population of older individuals, incidence rates of various chronic diseases are increasing
To investigate the protective effect of ethanol extract of Angelica keiskei Koidzumi (EAK) against muscle atrophy induced by dexamethasone in rats, we measured body weight and gastrocnemius muscle thickness
We investigated the mechanism involved in extract of AK (EAK)-mediated muscle protection in animal by measuring mRNA levels of muscle-specific E3 ligases
Summary
With the increasing population of older individuals, incidence rates of various chronic diseases are increasing. Chronic conditions and aging can lead to skeletal muscle wasting and weakness, i.e., muscle atrophy. Cachexia is a muscle wasting condition generated by chronic diseases, such as cancer, kidney failure, and diabetes. More than 30% of pancreatic cancer patients have died of muscle atrophy accompanied by resistance to chemotherapy and therapy-related side effects [1,2]. 50% of individuals over 80 years of age who suffer from fragility fractures have sarcopenia, an age-related muscle wasting condition [3]. The severity of muscle atrophy is increasing, only megestrol acetate has been approved by U.S FDA for the treatment of cancer and AIDS induced cachexia. Megestrol acetate has shown side effects such as insomnia, skin rash, impotence
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