Justicia procumbens prevents hair loss in androgenic alopecia mice.

The plant Justicia procumbens is traditionally used in Asia to treat fever, cough, and pain. Previous studies have reported its anticancer and anti-asthmatic properties. However, its potential for preventing androgenic alopecia (AGA) has not yet been reported. AGA is a widespread hair loss condition primarily caused by male hormones. In this study, we examined the hair loss-preventing effects of an aqueous extract of J. procumbens (JPAE) using human hair follicle dermal papilla cell (HFDPC) and a mouse model of testosterone-induced AGA. JPAE treatment increased HFDPC proliferation by activating the Wnt/ß-catenin signaling pathway. Additionally, JPAE increased the expression of Wnt targets, such as cyclin D1 and VEGF, by promoting the translocation of ß-catenin to the nucleus. Administration of JPAE reduced hair loss, increased hair thickness, and enhanced hair shine in an AGA mouse model. Furthermore, it increased the expression of p-GSK-3ß and ß-catenin in the dorsal skin of the mice. These findings imply that JPAE promotes the proliferation of HFDPC and prevents hair loss in an AGA mouse model. JPAE can therefore be used as a functional food and natural treatment option for AGA to prevent hair loss.

Geniposide attenuates muscle atrophy via the inhibition of FoxO1 in senescence-accelerated mouse prone-8.

BACKGROUND: Geniposide (GP) is an iridoid glycoside that is present in nearly 40 species, including Gardenia jasminoides Ellis. GP has been reported to exhibit neuroprotective effects in various Alzheimer's disease (AD) models; however, the effects of GP on AD models of Caenorhabditis elegans (C. elegans) and aging-accelerated mouse predisposition-8 (SAMP8) mice have not yet been evaluated. PURPOSE: To determine whether GP improves the pathology of AD and sarcopenia. METHODS: AD models of C. elegans and SAMP8 mice were employed and subjected to behavioral analyses. Further, RT-PCR, histological analysis, and western blot analyses were performed to assess the expression of genes and proteins related to AD and muscle atrophy. RESULTS: GP treatment in the AD model of C. elegans significantly restored the observed deterioration in lifespan and motility. In SAMP8 mice, GP did not improve cognitive function deterioration by accelerated aging but ameliorated physical function deterioration. Furthermore, in differentiated C2C12 cells, GP ameliorated muscle atrophy induced by dexamethasone treatment and inhibited FoxO1 activity by activating AKT. CONCLUSION: Although GP did not improve the AD pathology in SAMP8 mice, we suggest that GP has the potential to improve muscle deterioration caused by aging. This effect of GP may be attributed to the suppression of FoxO1 activity.

Geniposide-Rich Gardenia jasminoides Ellis Fruit Extract Increases Healthspan in Caenorhabditis elegans.

The human life span has been markedly extended since the 1900s, but it has not brought healthy aging to everyone. This increase in life expectancy without an increase in healthspan is a major global concern that imposes considerable health care budgets and degrades the quality of life of older adults. Dietary interventions are a promising strategy to increase healthspan. In this study, we evaluated whether a Gardenia jasminoides Ellis fruit ethanol extract (GFE) increases the life span of Caenorhabditis elegans (C. elegans). Treatment with 10 mg/mL GFE increased the life span by 27.1% when compared to the vehicle group. GFE (10 mg/mL) treatment improved healthspan-related markers (pharyngeal pumping, muscle quality, age-pigment, and reactive oxygen species accumulation) and exerted a protective effect against amyloid ß 1-42 toxicity. These effects of GFE are related to the inhibition of insulin/IGF-1 signaling and activation of SKN-1/Nrf, thereby promoting the expression of stress resistance-related genes. In addition, treatment with 10 mM geniposide, the most abundant component of GFE, improved healthspan-related markers and increased life span by 18.55% when compared to the vehicle group. Collectively, these findings demonstrate that GFE and its component geniposide increase the life span along with healthspan in C. elegans.

The innate immune signaling component FBXC-58 mediates dietary restriction effects on healthy aging in Caenorhabditis elegans.

Dietary restriction (DR) is a highly effective and reproducible intervention that prolongs longevity in many organisms. The molecular mechanism of action of DR is tightly connected with the immune system; however, the detailed mechanisms and effective downstream factors of immunity that mediate the beneficial effects of DR on aging remain unknown. Here, to investigate the immune signaling that mediates DR effects, we used Caenorhabditis elegans, which has been widely used in research, to understand the underlying molecular mechanisms of aging and immunity. We found that the F-box gene, fbxc-58, a regulator of the innate immune response, is a novel mediator of DR effects on extending the health span of C. elegans. fbxc-58 is upregulated by DR and is necessary for DR-induced lifespan extension and physical health improvement in C. elegans. Furthermore, through DR, fbxc-58 prevents disintegration of the mitochondrial network in body wall muscle during aging. We found that fbxc-58 is a downstream target of the ZIP-2 and PHA-4 transcription factors, the well-known DR mediator, and fbxc-58 extends longevity in DR through an S6 kinase-dependent pathway. We propose that the novel DR effector, fbxc-58, could provide a new mechanistic understanding of the effects of DR on healthy aging and elucidate the signaling mechanisms that link immunity and DR effects with aging.