Aggregation-induced emission enhancement (AIEE) of thiolated gold nanoclusters (AuNCs) has emerged as an attractive and alternative strategy to improve their brightness. This study demonstrates Ce(III)-triggered AIEE of glutathione-capped AuNCs (GSH-AuNCs) through the coordination between two carboxylic groups of GSH and Ce(III). The cluster size and valence state of GSH-AuNCs are almost identical to those of a Ce(III)-induced assembly of GSH-AuNCs (named Ce(III)-GSH-AuNCs). More importantly, the as-prepared Ce(III)-GSH-AuNCs exhibit a higher quantum yield (up to 13%), longer luminescence lifetime, and shorter maximum luminescence peak than GSH-AuNCs. Additionally, Ce(III)-GSH-AuNCs possess redox-switchable luminescence, high salt stability, and long-term storage stability. These findings provide clear evidence that the Ce(III)-triggered aggregation of GSH-AuNCs is a crucial factor to improve the luminescence property of GSH-AuNCs. Intriguingly, the presence of adenosine triphosphate (ATP) switches off the luminescence of Ce(III)-GSH AuNCs through the significant formation of Ce(III)-ATP complexes. Furthermore, the ATP-induced luminescence quenching of Ce(III)-GSH-AuNCs can be paired with the alkaline phosphatase (ALP)–ATP system to design a turn-on luminescent probe for ALP; the limit of detection for ALP is estimated to be 0.03 U L⁻¹. Also, the biocompatibility of Ce(III)-GSH-AuNCs enables the proposed system to detect ALP in human serum and HeLa cells.

Pulmonary artery hypertension (PAH) pathology involves extracellular matrix (ECM) remodeling in cardiac tissues, thus promoting cardiac fibrosis progression. miR-29a-3p reportedly inhibits lung progression and liver fibrosis by regulating ECM protein expression; however, its role in PAH-induced fibrosis remains unclear. In this study, we aimed to investigate the role of miR-29a-3p in cardiac fibrosis progression in PAH and its influence on ECM protein thrombospondin-2 (THBS2) expression. The diagnostic and prognostic values of miR-29a-3p and THBS2 in PAH were evaluated. The expressions and effects of miR-29a-3p and THBS2 were assessed in cell culture, monocrotaline-induced PAH mouse model, and patients with PAH. The levels of circulating miR-29a-3p and THBS2 in patients and mice with PAH decreased and increased, respectively. miR-29a-3p directly targets THBS2 and regulates THBS2 expression via a direct anti-fibrotic effect on PAH-induced cardiac fibrosis. The circulating levels of miR-29a-3p and THBS2 were correlated with PAH diagnostic parameters, suggesting their independent prognostic value. miR-29a-3p targeted THBS2 expression via a direct anti-fibrotic effect on PAH-induced cardiac fibrosis, indicating miR-29a-3p acts as a messenger with promising therapeutic effects.

Two new alkaloids, 9-methoxy-18,19-dehydrocamptothecin (1) and 5- hydroxymappicine-20-O-β-glucopyranoside (2a/2b as a racemic mixture), together with nine known compounds: camptothecin (3), 9-methoxy-camptothecin (4), 5-hydroxycamptothecin (5a/5b racemic mixture), 5-hydroxy-9-methoxycamptothecin (6a/6b racemic mixture), diosmetin (7), apigenin (8), apigenin-7-O-glucopyranoside (9), rosin (cinnamyl- O-β-D-glucopyranoside) (10) and amarantholidoside IV (11) were isolated from the immature seeds of Nothapodytes foetida (Wight) Sleumer. The structures were elucidated by spectroscopic analyses. In the present research, compounds 1, 3, 4, 5a/5b and 6a/6b, also showed in vitro cytotoxicity against six cancer cell lines (HepG2, Hep3B, MDA-MB- 231, MCF-7, A549, and Ca9-22). Among them, compound 1 exhibited significant cytotoxicity against these cancer cell lines, with IC₅₀ of 0.24-6.57 μM. Furthermore, HPLC profiles were developed for qualitative and quantitative analysis of these active constituents in different parts of this plant, including mature and immature seeds, leaves, stems and roots. The results revealed that compounds 3 and 4 have the highest concentrations, which are found in the roots part of the plant.