Latest ArticlesThe MYC transcription factor is a core regulator in the jasmonic acid signaling pathway, widely involved in plant growth and development, secondary metabolism, stress response, and hormone signal transduction. Based on the genomic data of Lonicera japonica, this study identified members of the LjMYC gene family through bioinformatics methods, and analyzed their physicochemical properties, evolutionary relationships, conserved domains and gene structures, as well as promoter cis-acting elements. The expression patterns of this gene family in different tissues, different flowering stages, and under methyl jasmonate (MeJA) treatment were also investigated. The results showed that a total of 25 LjMYC genes were identified in Lonicera japonica, distributed across eight chromosomes. Subcellular localization prediction indicated that 22 LjMYCs proteins were localized in the nucleus, LjMYC13 and LjMYC14 in chloroplasts, and LjMYC4 in the cytoplasm. Cis-acting element analysis revealed that the promoter regions of the LjMYCs gene contain elements responsive to light, growth and development, hormones, and stress. RT-qPCR analysis demonstrated that eight genes, including LjMYC8, exhibited tissue-specific expression in floral organs. The expression trends of ten genes, including LjMYC1, were generally consistent during the flowering process (S1-S6): Expression was slightly lower at S2 than at S1, increased at S3, slightly decreased at S4, and remained high at S5 and S6. Exogenous MeJA treatment promoted flowering, whereas delayed flowering treated with sodium diethyldithiocarbamate trihydrate (DIECA). Except for LjMYC20, MeJA treatment induced the expression of nine members, including LjMYC1, while DIECA treatment suppressed their expression. This study systematically reveals the fundamental characteristics of the LjMYC gene family and its expression patterns in different tissues, flowering stages, and in response to jasmonic acid signaling, providing key insights for exploring the functions of this gene family in jasmonic acid signal transduction in Lonicera japonica.
A total of four alkaloid compounds, serratinine A (1), fawcettimine (2), 7-hydroxylycopodine (3), and huperzine I (4) were isolated from Huperzia serrata by AB-8 macroporous adsorption resin, Octadecylsilyl, Sephadex LH-20 and silica gel column chromatography combined with the semi-pre HPLC. The isolated compounds were structurally characterized by mass spectrometry (MS), nuclear magnetic resonance spectroscopy (NMR), X-ray single crystal diffraction and circular dichroism (CD). Among them, compound 1 was a square crystalline form with the stereo configuration of (4R, 7S, 8S, 12S, 13S, 15S)-serratinine, named serratinine A. Compound 1 is a new serratinine alkaloid, the first crystal culture and stereo configuration of compound 1 were confirmed in this study.
Peptide therapeutics are characterized by high potency, exquisite specificity, and low toxicity, and have therefore been widely adopted for the clinical management of diverse diseases. However, their inherently low gastrointestinal permeability, rapid enzymatic degradation, and multiple physiological barriers collectively result in extremely low oral bioavailability, necessitating parenteral administration. Compared with the more convenient and patient-compliant oral route, chronic injection is associated with poor adherence and an increased incidence of adverse reactions. In recent years, extensive research has focused on permeation enhancers (PEs) based strategies to improve the oral bioavailability of peptide drugs. This review systematically summarizes the mechanisms of action and clinical applications of representative PEs-including surfactants (sodium caprylate, sodium caprate, alkyl glycosides, bile salts), chelating agents, chitosan and cell-penetrating peptides. It also summarizes related patented technologies (EligenTM, TPETM, GIPETTM, PODTM, PeptelligenceTM) to facilitate the development and clinical translation of oral peptide formulations.
Accurate authentication of components in traditional Chinese patent medicines (TCPMs) is fundamental to ensuring the safety and accuracy. Analysis of whole-GEnome (AGE) has been applied to species identification across plants, animals, and fungi. However, its applicability to the authentication of components in TCPMs remains to be evaluated. In this study, AGE was performed to identify Panax notoginseng in TCPMs. Bioinformatic analysis of nine genome assemblies from six Panax species yielded 4 289 410 specific target sequences of P. notoginseng, from which a species-specific target sequence database was constructed. Target sequences were selected and validated by Sanger sequencing. Four molecular techniques including PCR combined with agarose gel electrophoresis, PCR coupled with Sanger sequencing, TaqMan probe-based quantitative PCR, and high-resolution melting analysis were employed to detect the target sequence, thereby establishing identification methods for P. notoginseng. These assays were further applied to commercial TCPMs, all of which were successfully detected to contain P. notoginseng. Therefore, AGE enables accurate identification of components in TCPMs, offering new insights and technologies for quality control of TCPMs.
Antibody drug conjugates (ADCs) are a novel class of cancer therapeutics, structurally composed of monoclonal antibodies conjugated to cytotoxic agents via linkers. They offer advantages such as good tolerability, precise target recognition, and minimal impact on non-cancerous cells. To date, 19 ADCs have been approved for marketing, and over 300 ADCs are in various clinical trial phases. This review systematically outlines the developmental history of the three core components of ADCs—antibodies, payloads, and linkers. It aims to establish a foundational knowledge framework in ADCs development, thereby promoting technological dissemination and advancing awareness in the field. We anticipate that this review will serve as a foundational stepping stone for researchers exploring innovative ADCs therapies, igniting in-depth contemplation for this revolutionary therapeutic strategy.
Steroidal saponins are major active constituents of Maidong (Ophiopogon japonicus (L. f.) Ker Gawl.), and their structures and pharmacological activities are strongly influenced by glycosylation, whereas glycosyltransferases from Maidong remain poorly studied. In this study, we performed de novo transcriptome sequencing, assembly and annotation of roots, stems and leaves of O. japonicus, and combined domain-based screening to identify and conduct phylogenetic analysis of the UDP-dependent glycosyltransferase (UGT) gene family. In total, we obtained 109 UGT candidate coding sequences (CDSs) and identified 34 full-length UGT CDSs (OjUGT1-OjUGT34). Phylogenetic analysis grouped OjUGTs together with Arabidopsis UGTs into 15 subfamilies, among which clade D (UGT73 subfamily) and clade G (UGT85 subfamily) contained relatively more members. Conserved motif analysis and multiple sequence alignment showed that 31 OjUGT proteins possess the canonical plant secondary product glycosyltransferase (PSPG) motif. Expression profiling revealed pronounced tissue-specific differences in OjUGT transcripts, with OjUGT32 (UGT73 subfamily) highly expressed in tuberous roots and OjUGT34 (UGT73 subfamily) highly expressed in leaves. Comparative analyses across species suggested lineage-specific expansion of UGT73 and UGT85 genes within Asparagaceae, which may be associated with steroidal saponin biosynthesis. By integrating phylogenetic relationships, PSPG motif conservation, three-dimensional structure prediction and tissue-specific expression patterns, we propose that OjUGT32 and OjUGT34 are likely involved in the glycosylation of steroidal saponins in O. japonicus. Overall, this study establishes the expression profile of the UGT gene family in Maidong and predicts the physicochemical properties and sequence features of OjUGTs, providing candidate genes for elucidating the glycosylation steps in steroidal saponin biosynthesis.
To identify a new treatment strategy for acute severe pneumonia and solve the bioavailability of apigenin in formulation, the research utilized dipalmitoylphosphatidylcholine (DPPC), as well as 2-hydroxypropyl-β-cyclodextrin as respiratory carriers, to develop the apigenin β-cyclodextrin inclusion complexe DPPC liposomal dry powder inhalers (ACDLDPIs). The ACDLDPIs were prepared by grinding, film-dispersion and freeze drying. The formulation was optimized by orthogonal design, and its particle size, entrapment efficiency, electric potential, in vitro release and lung deposition were studied. Lipopolysaccharide (LPS)-induced rat acute lung injury model was used to evaluate acute severe pneumonia in vivo. The optimal formulation for apigenin cyclodextrin inclusion was obtained with the mole ratio of apigenin/cyclodextrin as (2∶1), concentration of cyclodextrin as 20% and grinding time as 90 min. The optimized prescription of the ACDLDPIs was apigenin inclusion complex/DPPC (1∶2), 15 min hydration time and the mass ratio of mannitol/DPPC (1∶1). Its encapsulation efficiency was (71.46 ± 3.18)%, and the drug loading was (8.36 ± 0.42)%. The particle size was 198.6 ± 4.4 nm (before rehydration) and 221.6 ± 5.5 nm (after rehydration). The zeta potential was 15.3 ± 2.1 mV. The aerodynamic particle size was 4.28 ± 0.77 μm. The pulmonary deposition rate (FPF) was 43.02%. The experiment was approved by the Experimental Animal Ethics Committee of Tongji University Affiliated Yangpu Hospital (No: LL-2023-ZRKX-002). The pharmacodynamic evaluation of acute severe pneumonia was evaluated in vivo. ACDLDPIs group had better therapeutic effect than apigenin group. The ACDLDPIs had suitable particle size, uniform distribution, good stability, high lung deposition rate and good therapeutic effect on acute severe pneumonia in vivo. The ACDLDPIs are promising medicines for the treatment of acute severe pneumonia.
Aortic aneurysm (AA), an irreversible pathological dilation of the aorta exceeding 50% of its normal diameter, significantly increases the risk of aortic dissection and rupture-related sudden death, causing approximately 200 000 global deaths annually. AA can occur in various aortic segments and is primarily categorized into thoracic aortic aneurysm (TAA) and abdominal aortic aneurysm. TAA, though less common, has a worse prognosis. While the etiology and molecular mechanisms differ between the two types, both are closely linked to inflammatory responses and the activation of various proteases. This review will focus on the general cellular and molecular events applicable to both conditions. AA is usually asymptomatic, and even when detected via ultrasonography, it is usually monitored due to not meeting surgical criteria. As no effective medication currently exists to halt its growth or reduce rupture risk, this review will briefly cover animal and clinical drug trials to explore potential therapeutic strategies.
The therapeutic efficacy of glioma treatment has long been constrained by the inefficiency of drug delivery due to the blood-brain barrier (BBB). Angiopep-2 peptide actively targets LDL receptor-related protein 1 and efficiently crosses the BBB via LRP1-mediated endocytosis, enabling precise and efficient drug delivery to tumor cells. This offers a novel therapeutic strategy for glioma treatment. Currently, Angiopep-2 has been extensively modified onto various carrier surfaces, significantly enhancing drug accumulation at brain tumor sites. This demonstrates its immense potential in constructing BBB-crossing platforms and has greatly advanced research on brain-targeted delivery systems. This paper primarily reviews the application of Angiopep-2/LRP-1-based modified formulations in glioma treatment. It summarizes research progress across different carriers in glioma, providing a reference for future studies.
Chemotherapy-induced immune-priming cell death (ICD) is a unique form of cell death. By inducing this type of cell death through specific methods, cells can express damage-associated molecular patterns (DAMPs). These DAMPs can act as antigens to activate the host's immune system, thereby enhancing antitumor immune responses. Its clinical application has also attracted widespread attention. This review summarizes the molecular mechanisms of ICD, including pathways such as endoplasmic reticulum stress, autophagy, and necroptosis, as well as the mechanisms by which various chemotherapeutic drugs induce ICD. Additionally, this review explores the application of ICD in clinical practice, discusses its potential to provide new ideas and challenges for cancer treatment by categorizing it according to different types of cancer, and examines the possibility of applying ICD mechanisms in other diseases.
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