Menopause is characterized by a decline in estrogen levels, leading to symptoms such as vasomotor instability, osteoporosis, and increased cardiovascular and cognitive risk. Hormone replacement therapy (HRT) remains the gold standard for managing menopausal symptoms; however, concerns regarding its long-term safety, including elevated risks of cancer and cardiovascular events, have prompted interest in alternative therapies. Phytoestrogens, particularly the isoflavones daidzein and genistein, are plant-derived compounds structurally similar to 17β-estradiol (E2) and capable of binding estrogen receptors. Found abundantly in soybeans and red clover, these compounds exhibit selective estrogen receptor modulator (SERM)-like activity, favoring ERβ over ERα, which underlies their tissue-specific effects. In vitro, in silico, and in vivo studies demonstrate their ability to modulate estrogenic pathways, inhibit oxidative stress, and influence reproductive and neurological function. Clinical trials show that daidzein and genistein, especially in equol-producing individuals, can reduce vasomotor symptoms such as hot flashes and night sweats. While results across studies vary, consistent findings support their safety and modest efficacy, particularly for women unable or unwilling to use HRT. Pharmacokinetic studies reveal moderate bioavailability and interindividual variability due to gut microbiota metabolism. At dietary levels, these compounds are generally safe, although high-dose supplementation is discouraged in individuals with hormone-sensitive cancers. Emerging evidence suggests lifelong consumption of soy-based foods may reduce cancer risk. In conclusion, daidzein and genistein represent promising, well-tolerated natural alternatives to conventional HRT, offering symptom relief and additional health benefits. Further research is warranted to optimize dosing, improve clinical outcomes, and clarify long-term safety in diverse populations, particularly with genetic variations in isoflavone metabolism.

The skin is the largest organ that performs a variety of the body’s essential functions. Impairment of skin structure and functions during the aging process might severely impact our health and well-being. Extensive evidence suggests that reactive oxygen species play a fundamental role in skin aging through the activation of the related degradative enzymes. Here, the 16 Thai medicinal plant species were screened for their potential anti-skin aging properties. All extracts were investigated for total phenolic and flavonoid contents, antioxidant, anti-elastase, and anti-tyrosinase activities, as well as the binding ability of compounds with target enzymes by molecular docking. Among all the plants screened, the leaves of A. occidentale and G. zeylanicum exhibited strong antioxidants and inhibition against elastase and tyrosinase. Other potential plants include S. alata leaf and A. catechu fruit, with relatively high anti-elastase and anti-tyrosinase activities, respectively. These results are also consistent with docking studies of compounds derived from these plants. The inhibitory actions were found to be more highly positively correlated with phenolics than flavonoids. Taken together, our findings reveal some Thai plants, along with candidate compounds as natural sources of antioxidants and potent inhibitors of elastase and tyrosinase, could be developed as promising and effective agents for skin aging therapy.

Nam Wah banana (Musa paradisiaca L.) is the most common banana cultivar in Thailand. Large amounts of its non-consumable byproducts are considered undervalued and thrown as waste. Exploring the potential utilization and application of banana byproducts for human benefit can add to their value and minimize the risk of threats. This study aimed to investigate phytochemicals, antioxidant and anti-inflammatory activities, and toxicity of Nam Wah banana byproducts. Five banana plant parts, including the midrib, leaf, peduncle, unripe and ripe peels, were extracted using hexane, ethyl acetate, ethanol, and water. Among the extracts tested, the ethyl acetate leaf extract showed the strongest antioxidant capacity and anti-inflammatory activity, probably through the inhibition of inducible nitric oxide synthase (iNOS) and 15-lipoxygenase (15-LOX). Positive correlations existed between the activities and the total phenolic/flavonoid content of banana byproducts. An in silico docking analysis demonstrated that flavonoid glycosides in banana byproducts, such as kaempferol-3-O-rutinoside and rutin, may bind to inducible iNOS, whereas omega-3-polyunsaturated fatty acids, such as eicosapentaenoic acid, may bind to 15-LOX and cyclooxygenase-2 (COX-2). The extracts showed either low or no toxicity. These findings suggest that banana byproducts are a natural source of antioxidant and anti-inflammatory compounds. It is recommended that additional investigations be conducted to explore their potential therapeutic applications in treating disorders linked with oxidative stress or inflammation. This research has the potential to enhance the value of banana byproducts.

Benzo[a]pyrene (B[a]P) is known to inhibit neurodifferentiation and induce neurodegeneration. Agarwood or Aquilaria crassna (AC), a plant with health-promoting properties, may counteract the neurotoxic effects of B[a]P by promoting neuronal growth and survival. This study investigated the protective effect of AC leaf ethanolic extract (ACEE) on the B[a]P-induced impairment of neuronal differentiation. A transcriptomic analysis identified the canonical pathway, the biological network, and the differentially expressed genes (DEGs) that are changed in response to neuronal differentiation and neurogenesis. Several genes, including CXCR4, ENPP2, GAP43, GFRA2, NELL2, NFASC, NSG2, NGB, BASP1, and NEUROD1, in B[a]P-treated SH-SY5Y cells were up-regulated after treatment with ACEE. Notably, a Western blot analysis further confirmed that ACEE increased the protein levels of GAP43 and neuroglobin. B[a]P treatment led to decreased phosphorylation of Akt and increased phosphorylation of ERK in SH-SY5Y cells; however, ACEE was able to reverse these effects. Clionasterol and lupenone were identified in ACEE. Molecular docking showed that these two phytochemicals had significant interactions with CXCR4, GDNF family receptor alpha (GFRA), and retinoid X receptors (RXRs). In conclusion, ACEE may be a potential alternative medicine for the prevention of impaired neuronal differentiation and neurodegenerative diseases.

A critical causative factor of oxidative stress and inflammation leading to several skin complications is ultraviolet-B (UVB) irradiation. Lignosus rhinocerus (LR), or tiger milk mushroom, is native to Southeast Asia. Cold water extract of an LR cultivar, TM02® (xLr®) is a promising anti-oxidant and anti-inflammatory source. However, the effects of xLr® on UVB-induced photoaging have never been elucidated. This study investigated the protective effects of xLr® and its high, medium, and low molecular weight (HLR, MLR, and LLR, respectively) fractions against UVB irradiation using in vivo Caenorhabditis elegans (C. elegans) model. The investigation revealed a significant lifespan extension of xLr® and its fractions in UVB-irradiated C. elegans, which could be mediated by the regulation of genes associated with anti-oxidant (daf-16 and sod-3) and apoptosis (cep-1, hus-1, ced-13, and egl-1) pathways. xLr® significantly reduced the ROS production in C. elegans and increased the DAF-16 nuclear translocation compared to untreated worms. Additionally, the SOD-3 expression was increased in the xLr®-treated worms. Hence, it suggests that the different components in xLr® work synergistically to protect against UVB irradiation. Our findings may be beneficial for the application of xLr® as a treatment against UVB-induced cellular damage and photoaging.

Cognitive impairment encompasses a clinical spectrum ranging from mild cognitive impairment to dementia, particularly Alzheimer’s disease (AD), and involves interconnected pathological processes including cholinergic dysfunction, oxidative stress, neuroinflammation, mitochondrial impairment, amyloid-β accumulation, tau hyperphosphorylation, and synaptic loss. Herbal medicines have attracted increasing attention because their complex phytochemical composition may provide multi-target neuroprotective effects. This narrative review aimed to summarize current preclinical and clinical evidence on herbal medicines and traditional herbal formulations for cognitive impairment, with emphasis on their mechanisms, therapeutic potential, safety, and translational limitations. Relevant evidence from in vitro studies, animal models, randomized clinical trials, systematic reviews, and meta-analyses was narratively synthesized. The review considered single herbal medicines, standardized extracts, isolated phytochemicals, and traditional multi-herbal formulations, together with their reported cognitive outcomes and molecular targets. Preclinical studies suggest that selected herbal preparations may modulate pathways implicated in cognitive impairment through acetylcholinesterase and butyrylcholinesterase inhibition, antioxidant and mitochondrial protection, suppression of neuroinflammatory signaling, modulation of amyloidogenic and tau-related pathways, and enhancement of BDNF/TrkB- and CREB-associated neuroplasticit; however, clinical evidence remains limited and heterogeneous. Clinical studies of Bacopa monnieri, Panax ginseng, Crocus sativus, and several traditional Chinese, Korean, and Persian formulations have reported improvements in memory and global cognitive measures, including MMSE, MoCA, and ADAS-cog scores. However, evidence remains constrained by heterogeneity of products, small sample sizes, short treatment periods, inconsistent outcome measures, limited biomarker integration, and incomplete long-term safety assessment. Herbal medicines show potential as preventive, complementary, or adjunctive approaches for cognitive impairment, but they cannot yet be considered established replacements for conventional therapy. Standardized products, rigorous pharmacokinetic and toxicological evaluation, disease-relevant models, and adequately powered multicenter trials are required to support evidence-based clinical application.