Treatment of sleep disorders promotes the long-term use of commercially available sleep inducers that have several adverse effects, including addiction, systemic fatigue, weakness, loss of concentration, headache, and digestive problems. Therefore, we aimed to limit these adverse effects by investigating a natural product, the extract of the Hibiscus syriacus Linnaeus flower (HSF), as an alternative treatment. In the electric footshock model, we measured anxiety and assessed the degree of sleep improvement after administering HSF extract. In the restraint model, we studied the sleep rate using PiezoSleep, a noninvasive assessment system. In the pentobarbital model, we measured sleep improvement and changes in sleep-related factors. Our first model confirmed the desirable effects of HSF extract and its active constituent, saponarin, on anxiolysis and Wake times. HSF extract also increased REM sleep time. Furthermore, HSF extract and saponarin increased the expression of cortical GABA_A receptor α1 (GABAAR α1) and c-Fos in the ventrolateral preoptic nucleus (VLPO). In the second model, HSF extract and saponarin restored the sleep rate and the sleep bout duration. In the third model, HSF extract and saponarin increased sleep maintenance time. Moreover, HSF extract and saponarin increased cortical cholecystokinin (CCK) mRNA levels and the expression of VLPO c-Fos. HSF extract also increased GABAAR α1 mRNA level. Our results suggest that HSF extract and saponarin are effective in maintaining sleep and may be used as a novel treatment for sleep disorder. Eventually, we hope to introduce HSF and saponarin as a clinical treatment for sleep disorders in humans.

Muscle fatigue is a major constraint on physical performance and is driven by multiple factors such as excessive oxidative stress and ATP depletion. This study investigated the protective effects of licochalcone B (LicoB), a phenolic chalcone compound isolated from Glycyrrhiza glabra Linné, on oxidative stress-induced damage in C2C12 cells. Additionally, its anti-fatigue potential was evaluated in mice subjected to exhaustive swimming. In C2C12 myotubes, LicoB significantly reduced H₂O₂-induced oxidative damage and preserved myotube integrity by scavenging free radicals. Transcriptomic analysis of C2C12 cells showed that LicoB reversed stress-induced dysregulation of antioxidant and myogenic genes, indicating protective transcriptional reprogramming. An in vivo mouse model employing weight-loaded forced swimming further supported the beneficial effects of LicoB. Four weeks of oral administration of LicoB improved physical endurance, increased liver glycogen content, antioxidant enzyme activity in muscle, and blood free fatty acid level, while reducing circulating blood corticosterone and lactate levels, as well as lipid peroxidation in muscle tissues. Upregulation of TP53-induced regulator of glycolysis and apoptosis, sirtuin 1, and peroxisome proliferator-activated receptor-γ coactivator 1α in skeletal muscles suggested enhanced mitochondrial function and reduced oxidative damage. Additionally, transcriptomic analysis of skeletal muscle indicated that LicoB induced gene programs involved in myogenesis, neuromuscular junctions, and glucose metabolism. Collectively, these findings suggest that LicoB plays multi-targeted protective roles against excessive exercise-induced muscle fatigue by attenuating oxidative stress and modulating energy metabolism. Therefore, LicoB is a promising nutraceutical candidate for improving muscle endurance and recovery after strenuous physical activity.

Traditionally, Lilium lancifolium bulb is known for its ability to nourish yin, nourish the lungs, clear the heart, soothe coughs, reduce irritability, and calm the mind. In Oriental Medicine, it is categorized as a tonic remedy for alleviating symptoms of fatigue and enhancing the strength of bones and muscles. In this study, we aimed to validate the effectiveness of the aquo-ethanolic extract of Lilli Bulbus (LBE) in a dexamethasone (DEX)-induced muscle atrophy model, both in vitro and in vivo, and elucidate its mechanism of action through muscle transcriptome analysis. The effects of LBE on the viability and myotube density of C2C12 myoblasts and differentiated C2C12 myotubes with and without DEX treatment were investigated. LBE pretreatment protected C2C12 myoblast cells and increased the muscle density of C2C12 myotubes in response to DEX. LBE showed potent free radical scavenging activities in cell-free biochemical assays as well as antioxidant activity in C2C12 myoblasts. LBE also exhibited protective effects in an experimental animal model of DEX-induced muscle atrophy, showing muscular function and motor coordination recovery. Transcriptomic analysis of three different muscle tissues from mice with DEX-induced muscle atrophy showed that the regulation of the extracellular matrix was perturbed by glucocorticoid treatment, and this perturbation was reversed by LBE treatment. Collectively, LBE alleviated skeletal muscle loss and maintained muscle function from the chronic toxicity of DEX by protecting muscle cells from various stressful conditions, as well as DEX itself, inhibiting muscle protein degradation, and preserving the muscle tissue microenvironment.

Skeletal muscle atrophy is a debilitating condition characterized by the loss of muscle mass and function. It is commonly associated with aging, chronic diseases, disuse, and prolonged glucocorticoid therapy. Oxidative stress and catabolic signaling pathways play significant roles in the progression of muscle degradation. Despite its clinical relevance, few effective therapeutic options are currently available. In this study, we investigated the protective effects of an ethanolic extract of Glycine Semen Preparata (GSP), i.e., fermented black soybeans, using in vitro and in vivo models of dexamethasone (Dexa)-induced muscle atrophy. In C2C12 myoblasts and myotubes, GSP significantly attenuated both oxidative stress-induced and Dexa-induced damages by reducing reactive oxygen species levels and by suppressing the expression of the muscle-specific E3 ubiquitin ligases MuRF1 and Atrogin-1. Moreover, GSP upregulated key genes involved in muscle regeneration (Myod1 and Myog) and mitochondrial biogenesis (PGC1α), indicating its dual role in muscle protection and regeneration. Oral administration of GSP to mice with Dexa-induced muscle atrophy resulted in improved muscle fiber integrity, increased proportion of large cross-sectional area fibers, and partial recovery of motor function. Isoflavone aglycones, such as daidzein and genistein, were identified as active compounds that contribute to the beneficial effects of GSP through antioxidant activity and gene promoter enhancement. Thus, GSP is a promising nutraceutical that prevents or mitigates muscle atrophy by targeting oxidative stress and promoting myogenesis and mitochondrial function. Further studies are warranted to standardize the bioactive components and explore their clinical applications.

Bongkyun Park, Kon Young Ji, Su-Jin Baek, Yu Ri Kim, Mudan Cai, Hyejin Shin, Yu Jin Kim, and So Min Lee. J Environ Health Sci. 2025;51:410-20. https://doi.org/10.5668/JEHS.2025.51.6.410

Herbal medicines have been used for centuries to manage various disease; however, their therapeutic mechanisms remain complex and insufficiently understood