Dongli Li

Phytochemical investigation of the 95% ethanol extract from the twigs and leaves of Nanhaia speciosa (Champ. ex Benth.) J. Compton & Schrire led to the isolation of twelve terpenoids. They consist of three new norsesquiterpenoids (1–3), six known norsesquiterpenoids (4–9), two known sesquiterpenoids (10–11), and one known monoterpenoid (12). The structures of the previously undescribed compounds were elucidated by analysis of spectroscopic data and quantum chemical calculations. Notably, compound 2 features an oxidative cleavage between C-5 and C-6 of the six-membered ring, yielding a highly rare seco-norsesquiterpenoid skeleton. Furthermore, compound 10 exhibited moderate antiproliferative activity against A549 cells (IC₅₀ = 13.7 ± 1.8 μM). This study significantly enriches the chemical profile of the aerial parts of N. speciosa.

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) deposition, oxidative stress, ferroptosis, and mitochondrial dysfunction, while effective therapeutic interventions remain limited. Epidemiological evidence indicates that tea and flavonoids with antiaging properties lower AD risk. In this study, untargeted metabolomic profiling identified isovitexin as a differentially abundant flavonoid in postfermented dark tea (DT), and Caenorhabditis elegans (C. elegans) AD models were employed to evaluate its anti-AD potential and elucidate the underlying molecular mechanisms. The results showed that isovitexin significantly extended lifespan, reduced Aβ accumulation, and improved neuromuscular function, demonstrating marked neuroprotective effects. Mechanistically, isovitexin mitigated Aβ-triggered toxicity through SKN-1 signaling, accompanied by the attenuation of Aβ-evoked ferroptosis and mitochondrial dysfunction. Collectively, these results broaden the therapeutic potential of dark tea flavonoids and support further investigation of isovitexin as a candidate for mitigating Aβ-induced neurodegeneration.

1. Drug-induced liver injury is the leading cause of acute liver injury (ALI), with acetaminophen (APAP) recognised as the most common causative agent (Yuan and Kaplowitz 2013). Although current th...

Purpose This study aims to evaluate the in vitro effect of 8α-tigloyloxyhirsutinolide-13-O-acetate (THA) on human prostate cancer cells and to examine its in vivo inhibitory effect on tumor growth in a mouse xenograft model. Methods In this study, the androgen-independent prostate cancer (AIPC) cell line PC-3 was employed. To investigate the effects of THA, we assessed cell proliferation, migration, invasion, apoptosis, and cell cycle distribution using MTT, wound healing, Transwell invasion, colony formation assays, Hoechst-33342 staining and flow cytometry. A mouse xenograft tumor model was established, and treatment groups received THA. The expression levels of p-STAT3, p-AKT, p-Erk1/2, CDK2, cyclin E1, MMP9, Bcl-2, Bax, and survivin were analyzed by Western blotting. Tumor formation and progression were evaluated by monitoring tumor volume. Results Our study showed that THA strongly inhibited cell growth and induced apoptosis, as well as caused cell cycle arrest at the S phase in PC-3 cells. THA also strongly suppressed cell migration and invasion, and decreased spheroid and colony formation. Animal experiment showed that THA inhibited the growth of PC-3 xenograft tumor in nude mice. Studies on mechanisms of actions showed that the potent anti-prostate cancer effects of THA were associated with inhibition of STAT3, AKT, and Erk1/2 pathways. Conclusion Our findings demonstrate that the potent anti-prostate cancer activity of THA is associated with inhibition of the STAT3, AKT, and Erk1/2 pathways. These data lend support to the further investigation of THA as a potential therapeutic agent against prostate cancer.

Felodipine (FEL), a first-line antihypertensive drug, suffers from low oral bioavailability due to its poor aqueous solubility and first-pass metabolism. T

The roots of Millettia speciosa Champ., a medicinal-edible plant, contain bioactive polysaccharides (MSCPs) that demonstrate potential prebiotic effects. Studies in diet-induced obese (DIO) mice have shown that MSCPs can modulate gut microbiota dysbiosis, suppress appetite, and ultimately alleviate obesity. However, the mechanism by which MSCPs regulate appetite and ameliorate obesity-associated metabolic dysfunction through modulating the gut microbiota still requires further investigation. In this study, we observed that MSCPs improved diet-induced obesity to the same extent as the pair-fed group, suggesting that MSCPs can ameliorate obesity in DIO mice by reducing appetite and energy intake. Through RT-qPCR, Western blot, and immunohistochemical experiments, it was found that MSCPs regulate the expression of appetite-related peptides and activate the JAK2/STAT3 signaling pathway to improve obesity in DIO mice; however, MSCPs did not ameliorate obesity in leptin receptor-deficient (db/db) mice, indicating that the leptin pathway is a critical target for treating DIO mice. Furthermore, MSCPs beneficially modulate gut microbiota; fecal microbiota transplantation experiment (FMT) restored the gut microbiota structure in mice, and the FMT group still alleviated obesity through the same signaling pathway. Additionally, 16S rRNA gene sequencing revealed that both MSCPs and FMT upregulated beneficial microbiota such as Lachnospiraceae_UCG_006 and Faecalibaculum, and promoted the production of short-chain fatty acids (SCFAs). Notably, in db/db mice, although MSCPs significantly elevated SCFAs levels, they failed to ameliorate obesity or metabolic disorders, further confirming that the leptin pathway serves as a critical requirement for MSCPs-mediated obesity improvement. In summary, MSCPs may alleviate obesity in DIO mice by enriching Lachnospiraceae_UCG_006 and Faecalibaculum to promote SCFAs production, thereby modulating the leptin pathway.

C ₂₀ H ₂₀ FNO ₂ , monoclinic, P 2 ₁ / c , a = 18.0094(6) Å, b = 8.5146(2) Å, c = 12.3716(4) Å, β = 106.891(4)°, V = 1815.26(11) Å ³ , Z = 4, R _gt ( F ) = 0.0499, wR _ref ( F ² ) = 0.1470, T = 170 K.