Using the whole-genome data of Atractylodes lancea, members of the auxin(Aux)/indole-3-acetic acid(IAA) gene family were identified and characterized, and the effects of 1-naphthaleneacetic acid(NAA) treatment on the expression levels of this gene family were investigated, providing a foundation for further studies on the functions of the A. lancea Aux(AlAux)/IAA gene family. Members of the AlAux/IAA gene family were identified from the A. lancea whole-genome data using TBtools-Ⅱ. Bioinformatics software was employed to analyze the physicochemical properties of the encoded proteins, construct a phylogenetic tree, and predict conserved motifs and gene structures. Tissue-cultured seedlings of A. lancea were used as experimental materials, and key genes of the AlAux/IAA gene family were screened by transcriptome sequencing. The expression of key AlAux/IAA genes was analyzed after one month of NAA treatment. A total of 53 AlAux/IAA genes were identified from the A. lancea genome. Most AlAux/IAA proteins were localized in the nucleus, lacked transmembrane domains, and exhibited negative hydrophobicity. Among them, 44 AlAux/IAA genes were predicted to encode functional Aux/IAA transport proteins. Transcriptome sequencing and RT-qPCR analyses showed that the AlAux/IAA family genes exhibited spatiotemporal expression specificity, and different members displayed varying response times and intensities to NAA treatment. Tissue-specific expression analysis revealed that the AlAux/IAA gene family was generally highly expressed in flowers. This study identified the Aux/IAA gene family members in A. lancea, preliminarily analyzed their sequence characteristics, and examined their expression features in response to Aux. It is speculated that AlAux/IAA13 and AlAux/IAA38 may be involved in rooting and bud growth and development during the subculture process of A. lancea tissue-cultured seedlings. These results provide a theoretical basis for elucidating the molecular mechanisms of AlAux/IAA gene function and Aux-mediated regulation of rhizome growth in A. lancea.

This study explored the therapeutic potential and underlying mechanisms of betulinic acid(BA) in the treatment of colorectal cancer(CRC) through integrated bioinformatics analysis and in vitro experimental validation. Potential targets of BA against CRC were identified by mining multiple public databases, including BATMAN-TCM, PharmMapper, DrugBank, and GeneCards. A total of 100 overlapping targets were identified. Protein-protein interaction(PPI) network was constructed to screen for core targets. Differentially expressed genes(DEGs) in CRC patients were obtained from the cancer genome atlas(TCGA), and single-cell RNA sequencing analysis was employed to identify the specific cell clusters potentially affected by BA. Gene Ontology(GO) function and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analyses were performed on the common targets to clarify the potential signaling pathways and biological processes. Core targets were further validated through molecular docking with BA. A methyltransferase-like 3(METTL3) knockdown model was established using HCT116 colorectal cancer cells. The cells were treated with varying concentrations of BA(9.375, 18.75, 37.5, 75, and 150 μmol·L~(-1)). Cell viability was assessed using CCK-8 assay. Additionally, wound healing assays were used to assess cell migration ability, while Transwell assays were conducted to evaluate both migration and invasion ability. Western blot analysis was performed to measure the expression levels of METTL3, as well as peroxisome proliferator-activated receptors(PPAR)γ and PPARα. Network pharmacology analysis revealed that the therapeutic effects of BA on CRC were primarily associated with 100 therapeutic targets and 26 signaling pathways, with PPAR signaling pathway identified as a key pathway. Molecular docking demonstrated that BA exhibited a strong binding affinity to the core targets. In vitro experiments confirmed that BA significantly inhibited the proliferation, migration, and invasion of HCT116 cells. Western blot indicated that BA treatment downregulated METTL3 expression and reduced the expression of PPARγ and PPARα compared to the control group. These findings suggest that BA may inhibit the proliferation, migration, and invasion of CRC cells by down-regulating METTL3 expression, thereby reducing the m~6A methylation level of PPARγ and PPARα mRNA, leading to decreased mRNA stability and translational efficiency, and ultimately modulating the PPAR signaling pathway.

This study aims to investigate the molecular mechanism by which ginsenoside Rb_1(G-Rb1) ameliorates hypoxia/reoxygenation(H/R) injury in H9c2 cardiomyocytes by the copper transporter 1(CTR1) ubiquitination-mediated regulation of cuproptosis. H9c2 cardiomyocytes were used to study the effects of different concentrations of G-Rb1 on the cell injury. The cells were grouped as follows: control, H/R model, H/R+G-Rb1, H/R+verapamil(H/R+Ver, positive control), and H/R+tetrathiomolybdate(H/R+TTM, a cuproptosis inhibitor). Cell viability was assessed by the CCK-8 assay, while apoptosis was detected by flow cytometry. The levels of lactate dehydrogenase(LDH) and creatine kinase isoenzyme(CK-MB) were measured by ELISA. Intracellular Cu~+ levels were measured via a fluorescent probe, and the expression and distribution of ferredoxin 1(FDX1) were analyzed by immunofluorescence. Furthermore, the protein and mRNA levels of CTR1, FDX1, and lipoic acid synthetase(LIAS) were determined by Western blot and quantitative real-time PCR, respectively. Molecular docking was performed to analyze the binding affinity between G-Rb1 and its potential targets, revealing the underlying mechanisms. To explore the degradation pathway of CTR1, this study treated the cells with cycloheximide and the proteasome inhibitor MG132. Subsequently, co-immunoprecipitation was employed to measure the ubiquitination level of CTR1 and the interaction between neural precursor cell expressed, developmentally down-regulated 4-like(NEDD4L) and CTR1. The results demonstrated that G-Rb1 significantly enhanced the viability of H/R-induced H9c2 cardiomyocytes, inhibited apoptosis, and reduced the release of LDH and CK-MB. G-Rb1 promoted the ubiquitination of CTR1, regulated the CTR1/FDX1/LIAS cuproptosis pathway, and reduced intracellular Cu~+ accumulation, thereby alleviating the H/R injury of cardiomyocytes. This protective effect may be associated with the inhibition of apoptosis and the regulation of protein ubiquitination-mediated degradation pathways. This study elucidates a novel mechanism by which G-Rb1 ameliorates cardiomyocyte injury through the CTR1 ubiquitination-mediated regulation of the cuproptosis pathway, providing a theoretical foundation for the development of cardioprotective drugs.

The current study aims to elucidate the underlying pharmacological mechanisms of the Tibetan medicine Renqing Mangjue against hepatic fibrosis using a research strategy integrating network pharmacology and experimental verification. Through the combination of a rat hepatic fibrosis model induced by diethylnitrosamine(DEN) and the analysis of clinical transcriptome data from the GEO database, the characteristics of its pharmacological effects were objectively evaluated, and its mechanism of action was systematically analyzed. The experimental results showed that the intervention of Renqing Mangjue significantly reduced the levels of serum hepatic fibrosis markers, including procollagen type Ⅲ(PCⅢ), collagen type Ⅳ(Ⅳ-C), and laminin(LN). Specifically, the medium-dose group showed a decrease of 37.8%, 47.1%, and 36.6% respectively compared with the model group(all P < 0.05) and a reduced collagen deposition in the liver tissue. The mechanism study found that it down-regulated the expressions of protein arginine methyltransferase 1(PRMT1), histone H4 arginine 3 dimethylation(H4R3me2a), plasminogen activator inhibitor-1(PAI-1), and monocyte chemoattractant protein 1(MCP-1) and inhibited the PRMT1/H4R3me2a/PAI-1/MCP-1 signaling axis, thereby inhibiting the activation of hepatic stellate cells and the excessive deposition of the extracellular matrix. This study is the first to clarify that Renqing Mangjue may exert an anti-hepatic fibrosis effect through the epigenetic regulation pathway, providing an experimental basis for its clinical application and offering a new paradigm for modern research on Tibetan medicine compounds.

To investigate the molecular mechanism by which salidroside inhibits the proliferation of gastric cancer (GC) cells through upregulation of miR-1343-3p.

Prostate cancer(PCa) is a common malignant tumor among elderly men, with high incidence and mortality rates worldwide, posing a serious threat to human health. Traditional treatments face limitations, highlighting the urgent need for novel therapeutic strategies. Recent studies on the regulatory mechanisms of micro ribonucleic acid(microRNA, miRNA) in tumor development has identified miRNA as new targets for PCa diagnosis and treatment. Traditional Chinese medicine(TCM), with its multi-mechanism, multi-target, and multi-pathway regulatory properties, shows promising potential in miRNA-based PCa therapy. This review summarized recent findings on miRNA' roles in PCa and research progress of TCM intervention and found that a variety of miRNA played important regulatory roles in cell differentiation, proliferation, apoptosis, invasion, metastasis, immune microenvironment, and drug resistance, and their potential as biomarkers for PCa diagnosis, prognosis, and therapy, indicating the potential to be a biomarker for the diagnosis, prognosis evaluation, and treatment of PCa. The review concluded that the active components of TCM(terpenoids, flavonoids, alkaloids, and others) and compounds(Yishen Tonglong Decoction, Shenhu Decoction, Zhoushi Qiling Decoction, Fuzheng Yiliu Decoction, and Qilan Formula) could regulate the expression of their downstream target genes by acting on specific miRNA and affect the above biological behaviors of PCa cells, thus playing a role in the treatment of PCa. This review aims to provide a theoretical basis for miRNA as potential biomarkers and therapeutic targets for PCa and suggest new avenues for further development of targeted therapy strategies against miRNA.

Objective To investigate the gene expression and regulatory mechanisms of mouse embryonic fibroblasts (MEFs) under inflammatory conditions, aiming to elucidate the role of MEFs in inflammatory responses and provide a foundation for discovering anti-inflammatory drugs that act by modulating MEF function. Methods MEFs cultured in vitro were divided into the following groups: lipopolysaccharides (LPS)-treated group, inflammatory conditioned medium (CM)-treated group, and control group, which were treated with LPS, CM, and equal volume solvent, respectively. Transcriptome sequencing was used to analyze the effects of two stimuli on gene expression profile of MEFs. Real time fluorescence quantitative PCR (RT-qPCR) was employed to verify the transcription levels of highly expressed genes of MEFs induced by CM. ELISA was performed to determine the concentrations of cytokines in cell supernatants. Finally, the regulatory effects of CM on the activation of signaling pathways in MEFs were analyzed by immunoblotting. Results Transcriptome analysis showed that both LPS and CM induced the transcription of a large number of genes in MEFs. Compared with LPS, CM potentiated the mRNA transcription of some acute phase proteins, inflammatory cytokines, chemokines, matrix metalloproteinases (MMP), prostaglandin synthetases, and colony-stimulating factors. The transcriptome analysis was verified by RT-qPCR. The results of ELISA showed that CM treatment significantly increased the secretion of interleukin 6 (IL-6), C-C motif chemokine ligand (CCL2), and C-X-C motif chemokine ligand (CXCL1) by MEFs compared with LPS. Mechanism study showed that both LPS and CM induced the phosphorylation of nuclear factor-κB p65 (NF-κB p65), p38 mitogen-activated protein kinase (p38 MAPK), extracellular regulated protein kinases 1/2 (ERK1/2), and TANK-binding kinase (TBK) in MEFs, and CM strongly stimulated the phosphorylation of signal transducer and activator of transcription 3 (STAT3) in MEFs. Conclusion Both LPS and CM can induce transcription and protein secretion of various inflammation-related genes in MEFs. CM can partly enhance LPS-induced activation of MEFs, and the mechanism may be related to the enhancement effect of CM on the activation STAT3 signaling pathway.

This study investigated the secondary metabolites in the product of rice fermentation with Alternaria alternata and their activity of down-regulating thymosin beta 10(TMSB10) protein expression. The secondary metabolites of A. alternata were separated and purified by various chromatographic separation techniques, including silica gel column chromatography, Sephadex LH-20 column chromatography, and semi-preparative high-performance liquid chromatography. Their structures were identified by spectral techniques such as nuclear magnetic resonance spectroscopy(NMR), infrared spectroscopy(IR), and high-resolution electrospray ionization mass spectrometry(HR-ESI-MS) and comparison with literature data. A total of 10 compounds were isolated and identified, including two new compounds(1S,3S)-2,3-dihydro-3,6-dihydroxy-8-methoxy-1-methylcyclopenta[c][2]benzopyran-5(1H)-one(1), 3,3a, 6-trihydroxy-8-methoxy-1-methyl-2,3,3a, 9b-tetrahydrocyclopenta[c]isochromen-5(1H)-one(2), and the eight known compounds are alternariol 9-methyl ether(3), 1-deoxyrubralactone(4),(3aR)-3,3a-dihydro-1,6-dihydroxy-8-methoxy-3a-methylcyclopenta[c][2]benzopyran-2,5-dione(5), altechromone A(6), alternariol(7), altenuene(8), altenusin(9), and 3'-hydroxyalternariol 5-O-methyl ether(10). The effects of these compounds on TMSB10 expression were tested. Compound 7 showed a significant down-regulation effect on TMSB10 expression with an inhibition rate of 40.5%. The results showed that benzopyrone compounds of A. alternata have the activity of down-regulating the expression of TMSB10 protein, providing theoretical basis and research value for the study of non-small cell lung cancer.

This study identified 8 members including NjBIN2 of the GSK3 family in Nardostachys jatamansi by bioinformatics analysis. Moreover, the phylogenetic tree revealed that the GKS3 family members of N. jatamansi had a close relationship with those of Arabidopsis. RT-qPCR results showed that NjBIN2 presented a tissue-specific expression pattern with the highest expression in roots, suggesting that NjBIN2 played a role in root growth and development. In addition, the application of epibrassinolide or the brassinosteroid(BR) synthesis inhibitor(brassinazole) altered the expression pattern of NjBIN2 and influenced the photomorphogenesis(cotyledon opening) and root development of N. jatamansi, which provided direct evidence about the functions of NjBIN2. In conclusion, this study highlights the roles of BIN2 in regulating the growth and development of N. jatamansi by analyzing the expression pattern and biological function of NjBIN2. It not only enriches the understanding about the regulatory mechanism of the growth and development of N. jatamansi but also provides a theoretical basis and potential gene targets for molecular breeding of N. jatamansi with improved quality in the future.

To investigate the expression of Acyl-CoA synthetase long-chain family member 4 (ACSL4) in liver cancer and its role in regulating ferroptosis and proliferation of liver cancer cells.

Objective To investigate the effect of baicalein (BAI) on autophagy of gastric cancer cell line BGC-823 cells by upregulating microRNA-7-5p (miR-7) and its possible mechanism. Methods The MTT method was used to screen the optimal drug concentration of BGC-823 cells treated with BAI. Real-time quantitative PCR was used to detect the transfection efficiency of BGC-823 cell line stably transfected with miR-7. The experiment was divided into control group (mimic-NC), miR-7 group (miR-7 mimic) and BAI group ( miR-7 overexpression combined with BAI treatment group). MTT assay, plate cloning assay and EdU assay were used to detect cell proliferation. The expression levels of autophagy related 16 like 1 (ATG16L1), sequestosome 1 (p62), Beclin 1, autophagy-related protein 5 (ATG5) and microtubule-assaiated protein 1 light chain3 (LC3) were detected by immunofluorescence staining and Western blot. Network pharmacology analysis to predict possible signaling pathways; Western blot was used to detect the expression levels of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway. Results 50 μmol/L BAI significantly inhibited the proliferation ability of BGC-823 cells; Compared with the control group, the expression level of miR-7 was significantly increased after BAI treatment. The cell proliferation of the miR-7 group was significantly inhibited, and the protein expression level of autophagy-related proteins and the LC3II/LC3I ratio were significantly up-regulated, which promoted the formation of autophagosomes and inhibited the formation of autophagic flow in BGC-823 cells. Compared with the miR-7 group, the BAI group could further inhibit the proliferation of BGC-823 cells, induce the formation of autophagosomes, but inhibit the production of autophagy flow. Network pharmacology analysis showed that the common target genes of BAI, gastric cancer and autophagy may be related to PI3K/AKT signaling pathway. Compared with the control group, the phosphorylation levels of p-PI3K, p-AKT and p-mTOR in the miR-7 group were significantly inhibited, and the phosphorylation levels of these proteins were further inhibited in the BAI group. Conclusion BAI-mediated miR-7 inhibits the formation of autophagosomes in BGC-823 cells by inhibiting PI3K/AKT/mTOR signaling pathway, and inhibits the generation of autophagic flow.

Objective To investigate the molecular mechanism of IL-6 regulating the expression of secretory phosphoprotein 1 (SPP1) in human placental-derived mesenchymal stem cells (hfPMSCs) and influencing the polarization of macrophages. Methods hfPMSCs were prepared by enzymatic digestion and cultured in a defined, serum-free medium. The morphology of hfPMSCs was observed under a microscope, and the expression of surface markers CD14, CD34, CD45, CD73, CD90, CD105, and human leukocyte antigen DR (HLA-DR) was detected by flow cytometry. hfPMSCs were treated with IL-6 at the final dosage of 100 ng/mL for 24 hours. ELISA, Western blot, and real-time quantitative PCR were used to detect the expression of SPP1 at the protein and mRNA levels; after being treated with IL-6, hfPMSCs infected with SPP1 interference lentivirus were co-cultured with activated macrophage THP-1 cells induced by 100 ng/mL lipopolysaccharide (LPS) and 80 ng/mL phorbol 12-myristate 13-acetate (PMA), and flow cytometry was used to detect the proportion of CD11c and CD206 positive cells in THP-1 cells; hfPMSCs were treated with IL-6 and/or specific inhibitors of nuclear factor kappa B p65 (NF-κB p65), SC75741, and Western blot was used to detect the expression of genes in the NF-κB signaling pathway and SPP1. Results IL-6 significantly upregulates the expression of SPP1 in protein and mRNA levels in hfPMSCs; interference of SPP1 significantly downregulates the expression of SPP1 in hfPMSCs and significantly reduces the positive cell ratio of CD206 in co-cultured macrophages; IL-6 significantly upregulates the expression of p-p65 in hfPMSCs, activating the NF-κB signaling pathway; SC75741 significantly downregulates the expression of p-p65 and SPP1 in hfPMSCs treated with IL-6. Conclusion IL-6 upregulates the expression of SPP1 through the NF-κB signaling pathway in hfPMSCs, which enhances the capability to induce macrophages to polarize towards the M2 phenotype.

To explore the potential role and mechanism of compound tetramethylpyrazine in gastric cancer therapy by using network pharmacology analysis combined with gene function annotation and clinical data analysis.

Terpene synthases (TPSs) play a crucial role in the synthesis of terpenoids that contribute to the scent profiles of flowers. However, few studies report the genome-wide analysis of TPSs gene in Jasminum sambac var. Fuzhou bifoliatum and their expression pattern in response to methyl jasmonate (MeJA). In this study, we employed bioinformatics tools for genome-wide analysis of the J. sambac TPS (DJTPS) gene family and determined the physical and chemical properties, subcellular location, protein-protein interactions, phylogenetic relationship, subfamily classification, chromosomal location and collinearity, gene structure, conserved motifs, and promoter cis-acting elements. The expression patterns of DJTPSs in different tissues and in response to MeJA treatment were analyzed based on the transcriptome data combined with quantitative real-time PCR (qRT-PCR). We identified 32 intact DJTPS genes in the genome of J. sambac, which presented uneven distribution across nine chromosomes. All the deduced proteins were hydrophilic, predominantly localized in the cytoplasm. The phylogenetic analysis classified the DJTPS genes into five subfamilies: TPS-a, TPS-b, TPS-c, TPS-e/f, and TPS-g. The results of the collinearity analysis showed a total of 10 sets of replication events in DJTPSs, most of which underwent purifying selection. A comparative analysis of TPS homologous gene pairs was performed among J. sambac var. Fuzhou bifoliatum and other six species, which revealed different number of homologous gene pairs. The number of exons and motifs was conserved within the same subfamily. DJTPS genes carried multiple elements that may be involved in the response to MeJA. In addition, the transcriptome and qRT-PCR data unveiled that several TPS genes exhibited tissue-specific expression patterns, and the genes with specific expression in flowers were the most. Upon exposure to MeJA, 14 TPS genes showcased upregulated expression 5 h or 6 h post-treatment, and DJTPS03, DJTPS04 and DJTPS21 showed significantly increased expression levels after MeJA treatment. This study provides preliminary evidence that MeJA possesses the ability to enhance the expression of DJTPS genes during the critical flowering stage, which will facilitate the synthesis of terpenoids and improve the quality of floral fragrance.

Ovarian cancer is a serious threat to women's health and safety. So far, people have discovered more than 130 small molecule compounds of natural origin for anti-tumor, of which approximately 50% are of microbial origin. The Acanthus ilicifolius L. species is primarily distributed in the Guangdong, Hainan, and Guangxi regions of China and grows in tidally accessible coastal areas. Recent studies have revealed that Acanthus ilicifolius L. extracts are endowed with a range of pharmacological properties, including anti-inflammatory, hepatoprotective, antioxidant, and antitumor activities. Endophytic fungi are commonly found in the healthy tissue and organs of medicinal plants. These fungi and the plants they inhabit form mutually beneficial symbiotic relationships. Endophytic fungi produce a series of secondary metabolites, with active substances having shown great economic value and applications prospects in drug research and development as well as for the biological control of plant diseases. Secondary metabolites production by endophytic fungi is regulated by specific gene clusters, and several techniques have been used to stimulate the secondary metabolic processes of fungi, including epigenetic-modification and OSMAC (one strain many compounds) strategies, co-culturing, and gene modification. Among these, epigenetic modification has been shown to be effective; this strategy involves the addition of small-molecule epigenetic modifiers to the culture medium, thereby activating silenced biosynthetic gene clusters without altering the DNA sequences of the fungi. This approach facilitates the expression of silenced genes in endophytic fungi, thereby increasing the number and diversity of secondary metabolites. Furthermore, it assists in overcoming the inhibition of microbial secondary-metabolite synthesis under laboratory conditions, and enhances silenced-gene expressions. The advent of novel analytical techniques and bioinformatics has provided a comprehensive, multifaceted, and holistic understanding of fungal metabolism through the development of metabolomics as a research platform. However, few studies have combined anti-ovarian cancer-activity screening with metabolomic approaches in the search for activity-differentiating metabolites from endophytic fungi under the intervention of epigenetic modifiers. Herein, we investigated the impact of epigenetic modifiers on the secondary metabolites of the endophytic Diaporthe goulteri fungus from Acanthus ilicifolius L. to determine their potential anti-ovarian cancer activities. Crude extracts were obtained by controlling three variables: the number of fermentation days, the type of epigenetic modifier, and its concentration, with activities screened using the CCK-8 (cell counting kit-8) method. Ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was subsequently employed for non-targeted metabolomic analysis. A multivariate statistical analysis model was constructed using principal component analysis and orthogonal partial least squares-discriminant analysis, which combines model and variable importance projection, with qualitative screening performed and significant changes (variable importance in the projection (VIP)≥1; P<0. 05) determined. Fifteen differential metabolites were identified in the fungal and epigenetic modification group, primarily comprising polyketides, amino acids, derivatives, alkaloids, and organic acids, including prenderol, glycine, valine, 2-ethylcaproic acid, rubratoxin B, finasteride, 6-silaspiro[5.5]undecane, 1-(2-nitrophenoxy)octane, heptadecene, 1-pentadecene, 11-ketoetiocholanolone, 3-(1-ethyl-1,3,3-trimethyl-2,3-dihydro-1H-inden-5-yl)butanal, N2-benzoylarginine, tabutrex, (3aR,6S,6aS)-6-(4-hydroxy-2-methoxy-2-butanyl)-4,4-dimethylhexahydro-1(2H)-pentalenone, and 8-aminoquinoline. The expressions of prenderol, 1-(2-nitrophenoxy)octane, 3-(1-ethyl-1,3,3-trimethyl-2,3-dihydro-1H-inden-5-yl)butanal, N2-benzoylarginine, and 8-aminoquinoline were downregulated, whereas the expressions of the remaining 10 substances were upregulated. Polyketides were the main components that exhibited higher expressions. This study showed that latent active differential metabolites can be searched by combining anti-ovarian cancer-activity screening with metabolomics analysis, thereby providing a reference for the further development of Acanthus ilicifolius L. resources and the subsequent targeted isolation of active compounds.

To investigate the influence of the strigolactone inhibitor Tis108 on the growth of Gastrodia elata, this study treated G. elata tuber with Tis108 solution of 10 μmol·L~(-1) and measured the content of endogenous hormone gibberellin(GA) in the tuber. By using reverse transcription-polymerase chain reaction(RT-PCR) technology, the key enzyme GeCYP714A1 gene involved in GA deactivation was cloned. Bioinformatics analysis on the GeCYP714A1 gene was carried out by using ExPASy, SWISS-MODEL, MEGA, etc., and its expression levels in different parts of G. elata were determined. The results showed that after Tis108 treatment, GA content in G. elata tuber was significantly increased, and the transcription level of the GeCYP714A1 gene was significantly decreased. The full length of the coding region of the GeCYP714A1 gene is 1 173 bp, encoding 390 amino acids. The protein has a molecular weight of 44.85 kDa, a theoretical isoelectric point of 9.83, an instability index of 49.20, an aliphatic index of 89.03, and a grand average of hydropathicity of-0.235, classifying it as an unstable, basic, hydrophilic protein, and the GeCYP714A1 protein was localized in the mitochondria, lacking a signal peptide and a transmembrane structure. Phylogenetic tree analysis revealed that GeCYP714A1 was most closely related to the DcCYP714C2(PKU78454.1) protein from Dendrobium candidum, with a sequence identity of 67.25%. The qRT-PCR analysis of the expression patterns of the GeCYP714A1 gene indicated that GeCYP714A1 had the highest transcription level in G. elata tuber, followed by stem and inflorescence. The study represented that Tis108 inhibited the transcription level of GeCYP714A1 involved in GA deactivation in G. elata tuber, thereby increasing the accumulation of GA and affecting the growth of G. elata tuber. These results provided a basis for further studies of strigolactone regulation of GA signal and tuber development in G. elata.

When plants are subjected to mechanical wounding(MW)caused by insect feeding, extreme weather, and human factors, they rapidly initiate a series of response mechanisms at the transcriptional and metabolic levels, leading to changes in the content of phytohormone and secondary metabolites in plants. In this study, using the medicinal model plant Danshen(Salvia miltiorrhiza) as an example, the effect of MW on the metabolism of medicinal plants was evaluated. By virtue of qRT-PCR and LC-MS, the changes in the biosynthetic genes and contents of jasmonates(JAs) and tanshinones in response to leaf damage stimulation were detected to reveal the related patterns of transcription and metabolism in leaves and roots at different time points after MW treatment, thus exploring the response mechanism of Danshen to MW stress. The results showed that MW induction could transiently increase the expression of biosynthetic genes of Jas, with AOC and JAR beginning to increase and peaking at 2 h after induction, while AOS and OPR3 peaked at 4 h. Correspondingly, the content of OPDA, JA, and JA-Ile all peaked at 2 h. In the biosynthesis of tanshinones, the diterpene synthase genes CPS1 and KSL1 both peaked at 2 h, while the subsequent modification genes CYP450s all peaked at 4 h. The content of the four tanshinones showed a continuous increase trend within 8 h. This study provides a reference for revealing the research on secondary metabolite accumulation under MW stress and lays a foundation for further understanding the role of Jas in enhancing plant resistance, promoting the accumulation of active ingredients, and improving the quality of medicinal materials under MW stress.

To investigate the effect of sanguinarine (SAN) on proliferation and ferroptosis of colorectal cancer cells.

With the rapid development of traditional Chinese medicine and the continuous discovery of various anticancer effects of salidroside (sal), it is known that sal inhibits tumor proliferation, invasion and migration by inducing apoptosis and autophagy, regulating the cell cycle, modulating the tumor microenvironment, and controlling cancer-related signaling pathways and molecules. The microRNA (miRNA)-mRNA signaling axis can regulate the expression of target mRNAs by altering miRNA expression, thereby affecting the growth cycle, proliferation, and metabolism of cancer cells. Studies have shown that sal can influence the occurrence and progression of various malignant tumors through the miRNA-mRNA signaling axis, inhibiting the progression of lung cancer, gastric cancer, and nasopharyngeal carcinoma, with a notable time and dose dependence in its antitumor effects. Summarizing the specific mechanism of sal regulating miRNA-mRNA signaling axis to inhibit tumors in recent years can provide a new theoretical basis, diagnosis, and therapeutic methods for the research on prevention and treatment of tumors.

The function of the Trihelix transcription factor is that it plays an important role in many abiotic stresses, especially in the signaling pathway of low temperature, drought, flood, saline, abscisic acid, methyl jasmonate, and other abiotic stresses. However, there are few studies on the Trihelix gene family of ginseng. In this study, 41 Trihelix gene family members were identified and screened from the ginseng genome database, and their physicochemical properties, cis-acting elements, subcellular localization, chromosomal assignment, and abiotic stress-induced expression patterns were analyzed by bioinformatics methods. The results showed that 85% of Trihelix family members of ginseng were located in the nucleus, and the main secondary structure of Trihelix protein was random coil and α helix. In the promoter region of Trihelix, cis-acting regulatory elements related to various abiotic stresses such as low temperature, hormone response, and growth and development were identified. Through the collinearity analysis of interspecific Trihelix transcription factors of model plants Arabidopsis thaliana and ginseng, 19 collinear gene pairs were found between A. thaliana and ginseng, and no collinear gene pairs existed on chromosomes 3, 6, and 12 only. qRT-PCR analysis showed that the expression of GWHGBEIJ010320.1 was significantly up-regulated under low temperature stress, a significant response to low temperature stress. This study lays a foundation for further research on the role of the Trihelix transcription factor of ginseng in abiotic stress, as well as the growth and development of ginseng.