Water Extract of Lotus Leaf Alleviates Dexamethasone-Induced Muscle Atrophy via Regulating Protein Metabolism-Related Pathways in Mice.

Muscle atrophy is an abnormal condition characterized by loss of skeletal muscle mass and function and is primarily caused by injury, malnutrition, various diseases, and aging. Leaf of lotus (Nelumbo nucifera Gaertn), which has been used for medicinal purposes, contains various active ingredients, including polyphenols, and is reported to exert an antioxidant effect. In this study, we investigated the effect of water extract of lotus leaf (LL) on muscle atrophy and the underlying molecular mechanisms of action. Amounts of 100, 200, or 300 mg/kg/day LL were administered to dexamethasone (DEX)-induced muscle atrophy mice for 4 weeks. Micro-computed tomography (CT) analysis revealed that the intake of LL significantly increased calf muscle volume, surface area, and density in DEX-induced muscle atrophy mice. Administration of LL recovered moving distance, grip strength, ATP production, and body weight, which were decreased by DEX. In addition, muscle damage caused by DEX was also improved by LL. LL reduced the protein catabolic pathway by suppressing gene expression of muscle atrophy F-Box (MAFbx; atrogin-1), muscle RING finger 1 (MuRF1), and forkhead box O (FoxO)3a, as well as phosphorylation of AMP-activated kinase (AMPK). The AKT-mammalian target of the rapamycin (mTOR) signal pathway, which is important for muscle protein synthesis, was increased in LL-administered groups. The HPLC analysis and pharmacological test revealed that quercetin 3-O-beta-glucuronide (Q3G) is a major active component in LL. Thus, Q3G decreased the gene expression of atrogin-1 and MuRF1 and phosphorylation of AMPK. This compound also increased phosphorylation levels of mTOR and its upstream enzyme AKT in DEX-treated C2C12 cells. We identified that LL improves muscle wasting through regulation of muscle protein metabolism in DEX-induced muscle atrophy mice. Q3G is predicted to be one of the major active phenolic components in LL. Therefore, we propose LL as a supplement or therapeutic agent to prevent or treat muscle wasting, such as sarcopenia.

Exploring the Potential of Olive Flounder Processing By-Products as a Source of Functional Ingredients for Muscle Enhancement.

Olive flounder (OF) is a widely aqua-cultivated and recognized socioeconomic resource in Korea. However, more than 50% of by-products are generated when processing one OF, and there is no proper way to utilize them. With rising awareness and interest in eco-friendly bio-materialization recycling, this research investigates the potential of enzymatic hydrolysis of OF by-products (OFB) to produce functional ingredients. Various enzymatic hydrolysates of OFB (OFBEs) were generated using 11 commercial enzymes. Among them, Prozyme 2000P-assisted OFBE (OFBP) exhibited the highest protein content and yield, as well as low molecularization. The muscle regenerative potential of OFBEs was evaluated using C2C12 myoblasts, revealing that OFBP positively regulated myoblast differentiation. In an in vitro Dex-induced myotube atrophy model, OFBP protected against muscle atrophy and restored myotube differentiation and Dex-induced reactive oxygen species (ROS) production. Furthermore, zebrafish treated with OFBEs showed improved locomotor activity and body weight, with OFBP exhibiting outstanding restoration in the Dex-induced muscle atrophy zebrafish in vivo model. In conclusion, OFBEs, particularly OFBP, produce hydrolysates with enhanced physiological usability and muscle regenerative potential. Further research on its industrial application and mechanistic insights is needed to realize its potential as a high-quality protein food ingredient derived from OF processing by-products.

A Combined Angelica gigas and Artemisia dracunculus Extract Prevents Dexamethasone-Induced Muscle Atrophy in Mice through the Akt/mTOR/FoxO3a Signaling Pathway.

Since skeletal muscle atrophy resulting from various causes accelerates the progression of several diseases, its prevention should help maintain health and quality of life. A range of natural materials have been investigated for their potential preventive effects against muscle atrophy. Here, ethanol extracts of Angelica gigas and Artemisia dracunculus were concentrated and dried, and mixed at a ratio of 7:3 to create the mixture CHDT. We then evaluated the potential for CHDT to prevent muscle atrophy and explored the mechanisms involved. CHDT was orally administered to C57BL/6 mice daily for 30 days, and dexamethasone (Dex) was intraperitoneally injected daily to induce muscle atrophy from 14 days after the start of oral administration. We found that CHDT prevented the Dex-induced reductions in muscle strength, mass, and fiber size, likely by upregulating the Akt/mTOR signaling pathway. In addition, CHDT reduced the Dex-induced increase in the serum concentrations of pro-inflammatory cytokines, which directly induce the degradation of muscle proteins. These findings suggest that CHDT could serve as a natural food supplement for the prevention of muscle atrophy.