Lung cancer is a leading cause of cancer-related deaths globally, with current treatments having significant limitations, including drug resistance, metastasis, and tumor heterogeneity. This study investigated the anticancer potential of isalpinin, a flavonoid isolated from Paphiopedilum dianthum, against non-small cell lung cancer (NSCLC) cell lines A549, H23, and H460. Isalpinin significantly inhibited NSCLC cell viability in a dose- and time-dependent manner; H23 and H460 cells showed greater sensitivity (IC₅₀ a ~ 44 μM at 48 h) compared to A549 cells (IC₅₀ 82 μM). Isalpinin suppressed proliferation, migration, and anchorage-independent growth, particularly in H23/H460 cells. Mechanistically, it induced apoptosis via increased ROS production and Bcl-2 downregulation, particularly in H23 and H460 cells. In a molecular docking analysis, isalpinin was found to directly bind to the ATP-binding pocket of AKT1, as confirmed by reduced Akt/GSK3β phosphorylation. These results suggest that isalpinin showed a potent multi-target natural compound against NSCLC that disrupts the key hallmarks of malignancy and pro-survival signaling. However, its subtype-specific efficacy warrants further in vivo studies and an investigation of combinatorial therapeutic approaches to elucidate its clinical potential.

Background: Increased consumption of sugar-sweetened beverages (SSBs) is associated with obesity and metabolic health risks.Objective: This study determined the relationship between SSB intake and body composition, with a focus on visceral fat accumulation among Thai university students.Material and Methods: A cross-sectional study was conducted with 387 university students aged 19-22 years. Dietary intake was assessed using a 3-day, 24-hour dietary recall conducted on three consecutive day to quantify SSB consumption. Body composition metrics, including body mass index (BMI), fat mass, and visceral fat levels (VFL), were measured using bioelectrical impedance analysis. Statistical analyses, including t-tests and linear regression, were used to identify the associations between SSB intake and body composition.Results: Sweetened tea, particularly freshly prepared iced milk tea, was most frequently consumed. High sugar consumption from SSB (≥ 24 g/day) was significantly associated with increased fat mass (16.9 ± 9.9 vs. 14.8 ± 7.8 kg, p = 0.021), BMI (22.6 ± 5.0 vs. 21.3 ± 4.2 kg/m², p = 0.007), and VFL > 9 (83.3% vs. 16.7%, p = 0.013). Sugar intake increased progressively across BMI categories: underweight (25.21 g/day), normal-weight (28.78 g/day), overweight (32.18 g/day), and obese (34.00 g/day). Participants with a VFL above 9 consumed over 40 g/day of SSB-derived sugar. At VFL exceeding 10, males had an average BMI of 30.06 ± 2.40 kg/m², whereas females exhibited a dramatically higher BMI of 41.20 ± 3.27 kg/m².Conclusions: Excessive SSB consumption, particularly sweetened tea, is strongly associated with higher visceral fat and unfavorable body composition in young adults. Public health interventions targeting reduced SSB intake are urgently required to address obesity and metabolic health risks. Further longitudinal studies are recommended to confirm causality and inform dietary guidelines.

Lung cancer remains a major clinical challenge, with therapy resistance in non-small-cell lung cancer (NSCLC) driving the search for novel selective agents. This study demonstrates that 2,3′-dihydroxy-5′-methoxystilbene exhibits significant anticancer activity in NSCLC cell lines (A549, H23, and H460) while displaying substantially lower toxicity toward normal NIH/3T3 fibroblasts. The compound reduced the viability of H23 and H460 cells after 48 h. (IC50: 23.39 ± 3.27 μM and 24.20 ± 2.61 μM, respectively), with NIH/3T3 cells remaining comparatively resistant (IC50 > 100 μM). At 25 μM, it suppressed proliferation by approximately 40% in H23, 30% in H460, and 20% in A549 cells, and dose-dependently impaired colony formation and migration, leading to near-complete migration arrest in H460 cells. Apoptosis induction peaked at 19% in H23, 17% in H460, and 8% in A549 cells at 25 μM. Mechanistic studies and molecular modeling revealed AKT-dependent activity, with decreased p-AKT and p-GSK3β levels (0.70 and 0.75 in H23; 0.65 and 0.70 in H460 at 25 μM), without changes in total protein expression. Combination treatment with cisplatin yielded synergistic effects in A549 (CI = 0.83) and H460 (CI = 0.94) cells, but antagonistic effects in H23 cells (CI = 1.32). These findings identify 2,3′-dihydroxy-5′-methoxystilbene as a selective AKT-targeting stilbene with promising anticancer potential and context-dependent chemosensitizing activity in NSCLC cells.

Introduction: High expression of P-glycoprotein (P-gp) has been linked to multidrug resistance (MDR) and chemotherapeutic failure. Previously, we demonstrated that rhinacanthin-C, a naphthoquinone from Rhinacanthus nasutus, was able to enhance the cytotoxicity of doxorubicin against breast cancer MCF-7 cells via direct P-gp inhibition. In this study, we looked at its effect on P-gp downregulation and the mechanism involved in the resistance of MCF-7 cells to doxorubicin. Methods: Doxorubicin-resistant MCF-7 (MCF-7/DOX) cells were exposed to rhinacanthin-C for 24-48 hours prior to the assessment of their chemosensitivity via MTT assay, P-gp activity via calcein-AM uptake assay, P-gp expression, and signaling via qRT-PCR and western blot analyses. Results: Pretreatment with 1 µM of rhinacanthin-C for 48 hours significantly enhanced cytotoxicity of doxorubicin, as well as camptothecin and etoposide, to MCF-7/DOX cells. In the rhinacanthin-C-treated cells, reduction of MDR1 mRNA and P-gp levels and increased intracellular calcein were observed. Moreover, phosphorylation of Akt, NF-ᴋB and IκB-α, along with YB-1 expression, significantly decreased after 24-hour treatment with rhinacanthin-C. In contrast, the naphthoquinone had no effect on expression levels of ERK1/2 and phosphorylated ERK1/2 under similar conditions. Conclusion: Rhinacanthin-C, at a non-cytotoxic concentration (1 µM), could downregulate P-gp expression in MCF-7/DOX cells via the inhibition of the Akt/NF-ᴋB signaling pathway and YB-1 expression. Long-term exposure to this natural naphthoquinone may increase the chemosensitivity of cancer cells with MDR phenotype.

Oxidative stress and chronic inflammation are major contributors to skin photoaging, highlighting the need for natural antioxidants with multifunctional bioactivities. This study developed an ultrasound-assisted extraction (UAE) strategy to recover an astaxanthin-rich extract from the underutilized freshwater macroalga Chara corallina and evaluated its antioxidant, anti-inflammatory, and anti-photoaging properties. Different solvent systems were evaluated for extraction efficiency, and astaxanthin-equivalent recovery was quantified by high-performance liquid chromatography with photodiode array detection (HPLC–PDA). Antioxidant activity was evaluated using the DPPH radical scavenging assay, whereas biological activities were assessed in human dermal fibroblasts and RAW264.7 macrophages using cell viability assays, quantitative real-time PCR, and extracellular matrix-related enzyme inhibition assays. The selected solvent system (48% ethanol in ethyl acetate) provided the highest astaxanthin-equivalent recovery (0.2598 ± 0.0086% w/w). The selected CCE exhibited DPPH radical-scavenging activity, modulated antioxidant- and inflammation-associated gene expression, increased COL1A2 mRNA expression, and inhibited collagenase, elastase, and hyaluronidase within the evaluated concentration range. HPLC–PDA analysis revealed a chromatographic component with retention-time and UV–visible spectral characteristics corresponding to those of an authentic astaxanthin reference standard; however, comprehensive structural and phytochemical characterization was not performed. Because CCE is a chemically complex extract, the observed biological responses cannot be attributed exclusively to astaxanthin. Overall, these findings provide an initial basis for further investigation of C. corallina as an underexplored freshwater source of carotenoid-containing bioactive extracts rather than establishing it as a commercially competitive source of natural astaxanthin.

Obesity is a major hallmark of metabolic syndrome and is strongly associated with an increased risk of cardiovascular disease progression. Sunflower sprouts are a particularly rich source of caffeoylquinic acids (CQAs), compounds recognized for their capacity to attenuate weight gain and mitigate dyslipidemia. Sunflower sprout extract (SSE) used in this study was enriched in dicaffeoylquinic acids (diCQAs) and chlorogenic acid (5‐CQA). To evaluate its effects, male Wistar rats were first induced to develop obesity by receiving a high‐fat diet for four months, after which they were given daily oral administration of SSE for an additional 12 weeks. The effects of SSE against HFD‐induced obesity were evaluated by examining liver pathology, antioxidant activity, and biochemistry, including lipid profiles and liver and renal functions. Body weight, food intake, biochemistry, and complete blood count (CBC) were monitored for 12 weeks. SSE treatment significantly decreased body weight gain (at 4 and 8 weeks), food intake (at 8 weeks), triglyceride levels (at 4 weeks), and low‐density lipoprotein (LDL) levels (at 12 weeks) in HFD rats. Total cholesterol, ALT, ALP, BUN, and uric acid levels in HFD‐control and HFD‐SSE rats were not significantly affected, while creatinine levels only increased after 8 weeks of SSE treatment in HFD rats. Importantly, SSE treatment significantly increased catalase and NQO1 expression in HFD‐fed rat liver. Collectively, these results suggested that diCQA‐rich SSE may offer beneficial effects for the management of obesity and associated metabolic disorders.