Xiaotao Hou

Large amounts of banana leaves are discarded as agricultural waste during banana harvesting; however, they are rich in bioactive compounds with promising exploitation potential. The ethyl acetate fraction contains the highest levels of total phenolics and total flavonoids together with strong antioxidant activity, which renders it a candidate source of natural antioxidants. In our current study, HPLC fingerprints were constructed for ten batches of ethyl acetate extracts from banana leaves (BLEA), and fingerprint similarity evaluation coupled with statistical analysis of common peak areas was carried out. Meanwhile, an HPLC quantitative method was developed to simultaneously determine eight characteristic components. The similarity values between the fingerprints of ten batches and the reference fingerprint ‘R’ ranged from 0.791 to 0.988. Cluster analysis (CA) and orthogonal partial least squares discriminant analysis (OPLS-DA) yielded consistent results, revealing clear separation trends among samples from different batches. In this quantitative method, eight characteristic analytes showed favorable linearity within their respective concentration ranges (r ≥ 0.9997). The average recoveries ranged from 101.6% to 104.3%, with RSD of 0.32% to 0.84%, demonstrating that the quantitative method was accurate and reliable. HPLC fingerprint combined with multi-component content determination offers a scientific basis for the quality evaluation and biomass valorization of banana leaves.

Pulmonary edema, a life-threatening condition in acute lung injury/acute respiratory distress syndrome (ALI/ARDS), is driven by dysregulated inflammation,

Marine medicinal algae represent a valuable reservoir of bioactive metabolites for anticancer drug discovery, yet the efficient identification of target-relevant compounds from chemically complex marine matrices remains challenging. In this study, an integrated cathepsin B-oriented strategy was developed to discover, prioritize, isolate, and validate antitumor metabolites from the brown alga Sargassum polycystum. Affinity ultrafiltration LC-MS was first applied to screen CTSB-binding constituents from the crude extract, followed by molecular docking, molecular dynamics simulation, and gray relational analysis for multidimensional candidate prioritization. Seven CTSB-binding metabolites were characterized, including chlorogenic acid, caffeic acid, cynarin, loliolide, taxifolin, senkyunolide H, and dihydroactinidiolide, with binding degrees of 73.99–85.61% at 2.5 U/mL CTSB. Molecular docking showed predicted binding affinities ranging from −6.3 to −9.4 kcal/mol, compared with −10.2 kcal/mol for the positive control CA-074Me. Integrated computational and biological evaluation identified caffeic acid, cynarin, and taxifolin as the top-ranked candidates. Preparative recovery was then achieved using counter-current chromatography combined with semi-preparative HPLC, and the isolated compounds were structurally identified by LC-MS/MS and NMR. Cellular assays in NCI-H1975 cells suggested that these metabolites reduced CTSB-associated enzymatic activity and intracellular CTSB-related fluorescence signals to different extents, with phenolic acid-type compounds exhibiting comparatively stronger effects. At the extract level, S. polycystum dose-dependently suppressed NCI-H1975 xenograft tumor growth, with inhibition rates of 48.78%, 36.58%, and 22.86% in the high-, middle-, and low-dose groups, respectively, without evident hepatorenal histopathological toxicity. This effect was associated with reduced CTSB, Ki-67, and Bcl-2 staining, increased Bax staining, enhanced apoptosis, and ultrastructural alterations in tumor tissues. Overall, this study provides a practical CTSB-oriented workflow for discovering antitumor metabolites from marine medicinal algae and supports further investigation of S. polycystum as a potential source of anti-NSCLC candidates.

Background: Pueraria candollei var. mirifica (Airy Shaw and Suvat.) Niyomdham ( Pueraria mirifica ), locally known as “White Kwao Krua” or “white kudzu”, is a renowned medicinal botanical drug indigenous to Southeast Asia, particularly Thailand and Myanmar. It has long been utilized in ethnomedicine for estrogen-related conditions and age-associated functional decline. This review critically evaluates the nexus between its botanical characteristics, traditional ethnopharmacological uses, and contemporary evidence regarding its therapeutic potential. Materials and Methods: A structured literature search was conducted across multiple international and Chinese databases up to 2025, with screening based on predefined inclusion and exclusion criteria focusing on botanical identity, chemical composition, pharmacological activity, toxicological evidence, and clinical findings. Taxonomic validity and geographic distribution were verified using Plants of the World Online (POWO) and the Global Biodiversity Information Facility (GBIF). The names and chemical formulas of secondary metabolites were verified using the PubChem database, and the structures were drawn using ChemDraw 22.2. Results: Phytochemical studies on the rhizomes of P. mirifica showed that it contains 106 kinds of secondary metabolites, including benzopyrans, isoflavones and their glycosides, coumarins, steroids, fatty acids and their derivatives, and other metabolites. Pharmacological evidence demonstrates that P. mirifica exhibits potent estrogenic, anti-osteoporotic, and antioxidant activities, alongside neuroprotective and immunomodulatory effects. Clinical data suggest that its high concentration of potent phytoestrogens effectively mitigates vasomotor symptoms and urogenital syndromes in menopausal women, while positively influencing lipid metabolism and bone mineral density. Conclusion: P. mirifica represents a high-potency phytoestrogenic candidate for menopause management. Nevertheless, the translation from traditional use to clinical standardization is hindered by a lack of rigorous pharmacokinetic data and inconsistent quality control of metabolites. Future research should move beyond descriptive summaries toward mechanistic studies that define long-term safety margins and standardized dose–response relationships in order to ensure therapeutic reliability.

Objectives: KU DING tea is a traditional Chinese herbal tea traditionally used topically for inflammation. This study aimed to investigate its potential anti-UV effects. Methods: The chemical components of KU DING tea were identified using UHPLC-Q-TOF-MS. Permeability prediction was performed to assess transdermal potential. A machine learning was applied to predict anti-UV activity, and network pharmacology analysis was used to explore the potential mechanism of action. Result: A total of 76 chemical components were identified, with 21 predicted to have good transdermal potential. A machine learning Random Forest (RF) model (accuracy 0.84, F1 0.84, AUC 0.93) predicted components like salicylic acid and methyl salicylate likely possess significant anti-UV activity. Network pharmacology indicated the mechanism may involve targets MAPK14 and NFKB1, influencing the AGE-RAGE signaling pathway. Conclusions: KU DING tea is a promising natural and safe anti-UV agent, deserving further experimental validation.

Due to today's unhealthy eating habits, such as high‐fat diets (HDs), people's bodies are in a sub‐healthy or unhealthy state, in which lipid disorders are a major cause of cardiovascular disease. Peach kernel oil (PKO), a by‐product of peaches, is rich in oleic acid and linoleic acid, but there are few studies on its biological characteristics. Zebrafish is an excellent animal model for the study of lipid metabolism. This study was designed to establish a lipid disorder model of zebrafish with an ApoEa genotype defect to investigate how PKO regulates lipid disorders. According to our findings, the ApoEa heterozygote ( Het ApoEa ) zebrafish lipid metabolism disorder model could be established by feeding with HD for 5 days. Het ApoEa zebrafish fed with HD for 5 days showed a significant increase in total cholesterol, lipid accumulation in the arterial vessels, and lipid droplet abundance in liver cells accompanied by mitochondrial damage. The role of PKO in the lipid metabolism disorder model of zebrafish revealed that PKO inhibits the accumulation of lipids and decreases the formation of neutrophils induced by HD. In the in vitro high‐fat, oxidative‐stress, and inflammatory models of vascular (HUVECs) and hepatic (HepG2) cells, PKO suppressed intracellular lipid accumulation, decreased reactive oxygen species (ROS) generation, and restored cell viability after inflammatory injury. RNA‐seq analysis results showed that PKO activates the Jak‐STAT signaling pathway by inhibiting stat1b and pkr expression. Our findings suggested that PKO, as a naturally active product, has excellent potential for use in the development of foods.

Introduction: Sugarcane leaf (Poaceae) is a widely cultivated herbaceous plant in the tropical regions of southern China. Traditional Yao medicine has utilized its significant diuretic effects for the treatment of edema-related diseases. However, the underlying mechanisms of its diuretic activity remain unclear.Methods: This study aims to elucidate the potential mechanisms of the diuretic activity of sugarcane leaf extract using untargeted metabolomics, network pharmacology, and molecular dynamics simulations.Results and discussion: A water-loaded rat model was established to assess diuresis, and sugarcane leaf extract markedly increased urinary excretion of Na⁺, Cl^-, and other ions. Ultra-performance liquid chromatography–mass spectrometry (UPLC–MS) identified ten absorbed constituents in rat serum after sugarcane leaf extract administration. Untargeted metabolomics revealed ten endogenous differential metabolites and two key metabolic pathways modulated by sugarcane leaf extract. Network pharmacology uncovered 63 overlapping targets, among which AKT1, IL-6, TNF, STAT3, and EGFR were pinpointed as core targets implicated in the diuretic response. Molecular docking and dynamics simulations confirmed strong binding affinities between these core targets and five absorbed sugarcane leaf extract constituents. The alanine, aspartate, and glutamate metabolism pathway was highlighted as pivotal for sugarcane leaf extract-induced diuresis. Collectively, this study has elucidated the diuretic mechanism of sugarcane leaf extract, providing a scientific basis for its clinical application and the development of novel diuretic agents.

Atherosclerosis (AS) is a complex pathological process characterized by the pivotal involvement of foam cells in its pathogenesis. As the primary cellular components of arterial plaques, foam cells critically determine plaque stability. Foam cells derive mainly from macrophages, and their formation is driven by dysregulated lipid metabolism within these immune cells. Macrophage cholesterol metabolism is a highly regulated process comprising four key phases: uptake, esterification, hydrolysis, and efflux. Under physiological conditions, these four phases maintain a delicate balance. However, disruption of cholesterol homeostasis results in the excessive accumulation of intracellular lipid, promoting the formation of foam cell and inflammasome activation, thereby accelerating the atherosclerotic progression. Therefore, targeting macrophage cholesterol metabolism has emerged as a promising therapeutic approach for AS. This review summarizes the mechanisms underlying macrophage cholesterol metabolism and highlights recent progress in identifying bioactive components of traditional Chinese medicines (TCMs) that mitigate AS through the modulation of macrophage cholesterol homeostasis. These findings may offer novel insights into the development of clinically effective therapies for the prevention of AS.

Background/Objectives: Camellia nitidissima Chi (C. nitidissima), a traditional Chinese “food and medicine homology” plant, has demonstrated potential anti-tumor properties. However, its mechanisms of anti-lung cancer activity via ferroptosis remain unclear. This study aimed to construct an integrated research system of “natural product extraction-purification, bioactivity evaluation, and computational drug screening” to explore the bioactive compounds in C. nitidissima leaves targeting HMOX-1-mediated ferroptosis and their anti-lung cancer mechanisms. Methods: Active fractions were prepared using ethanol extraction combined with polyamide column chromatography. The anti-lung cancer activity was evaluated using the NCI-H1975 cell model. Ferroptosis was verified via transmission electron microscopy (TEM), biochemical indicators, a PCR Array, and immunofluorescence. The bioactive compounds were identified using UPLC-Q Exactive MS, and their binding affinity to HMOX-1 was evaluated via molecular docking and dynamics simulations, followed by cellular validation. Results: The 95% F1 fraction from the extracts of C. nitidissima leaves exhibited the strongest anti-lung cancer activity, which could be significantly reversed by Ferrostatin-1. Furthermore, it induced typical ferroptosis-related structural damage in mitochondria, including shrinkage and a reduction in size, increased membrane density, and a reduction or even the disappearance of cristae structures. At the molecular level, this fraction significantly increased the levels of oxidative stress markers (ROS↑, MDA↑, Fe²⁺↑, and GSH↓) and upregulated the expression of key ferroptosis-related genes, including HMOX-1, CHAC1, and NOX1. Using UPLC-Q Exactive MS combined with computational simulation methods, four bioactive compounds with high affinity for HMOX1 were successfully identified, including isochlorogenic acid A (−8.4 kcal/mol), isochlorogenic acid C (−8.4 kcal/mol), apigenin (−7.8 kcal/mol), and chrysin (−7.3 kcal/mol). Cellular experiments validated that these compounds exhibited dose-dependent anti-proliferative effects. Conclusions: The leaves of C. nitidissima induce anti-lung cancer effects via HMOX-1-mediated ferroptosis. Isochlorogenic acid A/C, apigenin, and chrysin were identified as key bioactive components. These findings lay the foundation for the development of natural ferroptosis-targeted drugs.