Autophagy is the sequential process whereby cell components are degraded, which can occur due to nutrient deprivation. Its regulation has an essential role in many diseases, functioning in both cell survival and cell death. Autophagy starts when mTORC1 is inhibited, resulting in the activation of several complexes to form a cargo that fuses with a lysosome, where it undergoes degradation. In this review, we describe a plant extract that is well known in Korea, namely Korean ginseng extract; we studied how its derivatives and metabolites can regulate autophagy and thus mediate the pathogenesis of certain diseases.

Panax ginseng Meyer, a traditional herbal remedy with a long history, has been widely used worldwide. Phytochemical studies have shown that its physiological activity is due to a variety of active compounds, and extensive research has demonstrated the adaptogenic potential of ginseng in various physiological and pathological contexts. However, the molecular mechanisms supporting its adaptogenic effects remain inadequately elucidated, leading to undervaluation of its adaptogenic properties. This review uses a comprehensive literature analysis to examine five major health benefits attributed to ginseng extracts or derivatives: anti-inflammatory, antioxidant, anti-fatigue, cardiovascular protection, and cognitive enhancement. Moreover, it categorizes the biomarkers identified in each efficacy study and analyzes their interaction networks using KEGG pathway information. In that way, four key biomarkers pivotal to the adaptogenic attributes of P. ginseng are identified: superoxide dismutase, tumor necrosis factor, nuclear factor erythroid 2-related factor 2, and caspase-1. These biomarkers play an integral role in the manifestation of P. ginseng's five major effects, contributing significantly to its adaptogenic efficacy. This novel approach to understanding adaptogenic mechanisms is intended to offer innovative insights into the pharmacological effects of P. ginseng and its derivatives.

The Licania genus has been used in the treatment of dysentery, diabetes, inflammation, and diarrhea in South America. Of these plants, the strong anti-inflammatory activity of Licania macrocarpa Cuatrec (Chrysobalanaceae) has been reported previously. However, the beneficial activities of this plant on skin health have remained unclear. This study explores the protective activity of a methanol extract (50–100 μg/mL) in the aerial parts of L. macrocarpa Cuatrec (Lm-ME) and its mechanism, in terms of its moisturizing/hydration factors, skin wrinkles, UV radiation-induced cell damage, and radical generation (using RT/real-time PCR, carbazole assays, flowcytometry, DPPH/ABTS, and immunoblotting analysis). The anti-pigmentation role of Lm-ME was also tested by measuring levels of melanin, melanogenesis-related genes, and pigmentation-regulatory proteins. Lm-ME decreased UVB-irradiated death in HaCaT cells by suppressing apoptosis and inhibited matrix metalloproteinases 1/2 (MMP1/2) expression by enhancing the activity of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38. It was confirmed that Lm-ME displayed strong antioxidative activity. Lm-ME upregulated the expression of hyaluronan synthases-2/3 (HAS-2/3) and transglutaminase-1 (TGM-1), as well as secreted levels of hyaluronic acid (HA) via p38 and JNK activation. This extract also significantly inhibited the production of hyaluronidase (Hyal)-1, -2, and -4. Lm-ME reduced the melanin expression of microphthalmia-associated transcription factor (MITF), tyrosinase, and tyrosinase-related protein-1/2 (TYRP-1/2) in α-melanocyte-stimulating hormone (α-MSH)-treated B16F10 cells via the reduction of cAMP response element-binding protein (CREB) and p38 activation. These results suggest that Lm-ME plays a role in skin protection through antioxidative, moisturizing, cytoprotective, and skin-lightening properties, and may become a new and promising cosmetic product beneficial for the skin.

Meniran (Phyllanthus niruri L.) is a wild plant in the Euphorbiaceae family which grows in tropical climates. The plant is known to possess antioxidant activity and is rich in phenolic compounds. Since plants with high phenolic content and high antioxidant activity are known to exhibit high tyrosinase inhibitory activity, the purpose of this study is to determine the inhibitory activity of the tyrosinase enzyme by the methanol extract of meniran (P. niruri L.) and to isolate secondary metabolites from the extract and fractions which exhibit inhibitory activity against tyrosinase. The in vitro tyrosinase inhibitory activity assay was conducted using the 96-well microplate method with kojic acid as the positive control, while the separation and purification of compounds were carried out using chromatography techniques. The methanol extract and n-hexane fraction showed tyrosinase inhibitory activity with IC₅₀ of 11.05±0.16 and 2.57±0.08 mg/ml, respectively. Three bioactive compounds were succesfully isolated from the n-hexane fraction. Based on the UV and NMR spectra, compounds 1, 2, and 3 were identified as phyllanthin, phyltetralin, and hypophyllanthin, respectively. Furthermore, phyllanthin (1) was shown to demonstrate inhibitory activity against tyrosinase with IC₅₀ of 0.6322 mM. In conclusion, both meniran extract and phyllanthin (1) were found to exhibit inhibitory acitivity against the tyrosinase enzyme. In the future they can be candidates for the treatment against hyperpigmentation and also as an active ingredient in skincare formulations.

Background: Although recent studies have established the critical roles of methyltransferases in epigenetic regulation and cellular homeostasis, the biological function of METTL25, a member of this enzyme family, is not well known. Current clinical research has identified various methyltransferases as key regulators of gene expression, yet METTL25 remains functionally uncharacterized, representing a significant knowledge gap in our understanding of methyltransferase biology. Objective: This study examines the expression patterns of METTL25 across normal human tissues and cancer contexts to identify its potential physiological and pathological roles and to understand its regulatory mechanisms in health and disease. Methods: We conducted a systematic computational analysis using large-scale publicly available transcriptomic and proteomic datasets. Expression patterns were analyzed across normal human tissues and cancer cell lines. Correlation analysis between mRNA and protein levels was performed, followed by differential gene expression analysis comparing thyroid carcinoma to normal thyroid tissue. Functional enrichment analysis was applied to identify biological pathways associated with METTL25 expression. Results: METTL25 exhibited tissue-specific expression patterns with highest expression observed in endocrine organs (thyroid, adrenal glands) and immune compartments (lymphoid tissues). Moderate correlation between mRNA and protein levels was identified (r=0.404 ; p=0.001), indicating transcriptional control of protein abundance. METTL25 expression was significantly downregulated in thyroid carcinoma compared to normal thyroid tissue (p<0.01). Higher METTL25 expression in tumors was statistically significant and positively correlated with gene signatures related to wound healing, coagulation, and hemostasis pathways. Conclusion: METTL25 functions as a tissue-restricted methyltransferase with tumor suppressor characteristics in thyroid cancer. The positive correlation between METTL25 expression and wound healing pathways was statistically significant, suggesting its involvement in tissue repair mechanisms. These findings provide the foundation for future mechanistic studies investigating METTL25's role in cancer biology and its potential as a therapeutic target.