Picea mongolica, known for its remarkable tolerance to cold, drought, and salinity, is a key species for ecological restoration and urban greening in the "Three Norths" region of China. MYB transcription factors are involved in plant responses to abiotic stress and synthesis of secondary metabolites. However, studies are limited regarding the MYB transcription factors in P. mongolica and their roles in salt stress tolerance. In this study, 196 MYBs were identified based on the genome of Picea abies and the transcriptome of P. mongolica. Phylogenetic analysis classified the MYB transcription factors into seven subclasses. The R2R3-MYB subclass contained the maximum number of genes (84.77%), while the R-R and R1R2R3 subclasses each represented the smallest proportion, at about 0.51%. The MYB transcription factors within the same subclass were highly conserved, exhibiting similar motifs and gene structures. Experiments with varying salt stress gradients revealed that P. mongolica could tolerate the salt concentration up to 1 000 mmol/L. From the transcriptome data of P. mongolica exposed to salt stress (1 000 mmol/L) for 0, 3, 6, 12, and 24 h, a total of 34 differentially expressed MYBs were identified, which suggested that these MYBs played a key role in regulating the response to salt stress. The proteins encoded by these differentially expressed genes varied in length from 89 aa to 731 aa, with molecular weights ranging from 10.19 kDa to 79.73 kDa, isoelectric points between 4.80 and 9.91, and instability coefficients from 41.20 to 70.99. Subcellular localization analysis indicated that most proteins were localized in the nucleus, while three were found in the chloroplasts. Twelve MYBs were selected for quantitative real-time PCR (qRT-PCR), which showed that their expression patterns were consistent with the RNA-seq data. This study provides valuable data for further investigation into the functions and mechanisms of MYB family members in response to salt stress in P. mongolica.
Picea/physiology* ; Transcription Factors/classification* ; Salt Stress/genetics* ; Phylogeny ; Plant Proteins/genetics* ; Salt Tolerance/genetics* ; Gene Expression Regulation, Plant

Objective: To investigate the effect of sirtuin 2(SIRT2) on the proliferation and migration of cardiac fibroblasts(CFs)in C57BL/6 mice under angiotensin II(Ang Ⅱ) stimulation. Methods : The hearts were taken from 1 to 2 days C57BL/6 milk mice. After cutting and digesting, CFs were extracted by different adhesion centrifugation. After CFs attachment, the cells were cultured under control medium and Ang Ⅱ(100 nmol/L) medium and treated using OE-SIRT2 plasmid to overexpression the SIRT2 gene. RT-qPCR was used to detect mRNA expression of SIRT2 proliferating cell nuclear antigen(PCNA), periostin(POSTN)and type Ⅰ collagen procollagen A1(Col1A1), Western blot assay was used to measure the protein expression levels of SIRT2, PCNA, POSTN and Col1A1, CCK-8 assay and EdU assay were used to evaluate CFs proliferation rate, Transwell experiment was used to assess CFs migration activity. Results: Compared with control group, Ang Ⅱ stimulation led to down-regulation of SIRT2 expression in CFs, increased collagen expression, and promoted CFs proliferation and migration. The expression of SIRT2 was up regulated in CFs treated with OE-SIRT2 plasmid under Ang Ⅱ stimulation, Col1A1, POSTN and PCNA expression was down regulated, and CFs proliferation and migration ability decreased. Conclusion Overexpression of SIRT2 can inhibit the proliferation and migration of CFs under Ang Ⅱ stimulation, indicating that SIRT2 may be a key regulatory point in the onset and progression of cardiac fibrosis.

Perimenopausal depression seriously affects women's physical and mental health.It is caused primarily by gonadal function decline,which is typically characterized by low mood,anxiety,slow thinking,and loss of interest,and is accompanied by autonomic dysfunction and endocrine dysfunction.The pathogenesis of perimenopausal depression remains unclear and controversial.Many scholars have conducted scientific research that is based on animal models of perimenopausal depression.Indeed,a good animal model of perimenopausal depression is the basic premise for studying its pathophysiological mechanisms and for facilitating reliability of the scientific result.Therefore,this paper combines the modern research mechanisms of perimenopausal depression and the current status of animal models in China,and provides an overview,evaluation,and generalization of the modeling method,principles and result,to provide a scientific basis and reference for the selection of suitable animal models for scientific research experiments.

Aim To investigate the effect of N6-methy-ladenosine(m6A)demethylase ALKBH5 on the prolif-eration and migration of cardiac fibroblasts(CFs)in-duced by high glucose.Methods Primary CFs were isolated from neonatal mouse hearts and identified u-sing optical and confocal microscopy.Cell activation was induced using a high-glucose medium(33 mmol·L-1 glucose).An ALKBH5 overexpression model was established by transfecting CFs with an ALKBH5 ex-pression vector in a high-glucose medium.The expres-sion of ALKBH5 in CFs was assessed through immuno-fluorescence staining,Western blot and RT-qPCR.Changes in m6A levels were evaluated using Dot blot a-nalysis.Additionally,Alterations in the expression of proliferating cell nuclear antigen(PCNA)and collagenⅠ,a pivotal fibrosis indicator,were measured using Western blot.The proliferation and migration ability of CFs were assessed through EdU staining and Transwell migration assay,respectively.Results Following treatment with high glucose,the expression of ALKBH5 in CFs notably decreased,while m6A level increased.This was accompanied by a significant increase in the expression of the proliferation marker PCNA and the fi-brosis marker collagen Ⅰ.Additionally,there was a sig-nificant improvement in the ability of proliferation and migration.Overexpression of ALKBH5 resulted in a significant decrease in the expressions of PCNA and collagen Ⅰ,leading to the inhibition of both proliferation and migration in CFs.Conclusion Overexpression of ALKBH5 suppresses the expression of PCNA and colla-gen Ⅰ,consequently reducing the proliferation and mi-gration of CFs,potentially through m6A methylation modification.

As the most common phenotype of type 1 neurofibromatosis(NF1),plexiform neurofibromas(pNF)exhibit early asymptomatic presentation but multisite involvement,with a risk of progression.Imaging serves as vital tool for evaluation and management of NF1-associated pNF.The progresses of imaging for evaluating NF1-related pNF were reviewed in this article.

Aim To investigate the effect of N6-methy-ladenosine(m6A)demethylase ALKBH5 on the prolif-eration and migration of cardiac fibroblasts(CFs)in-duced by high glucose.Methods Primary CFs were isolated from neonatal mouse hearts and identified u-sing optical and confocal microscopy.Cell activation was induced using a high-glucose medium(33 mmol·L-1 glucose).An ALKBH5 overexpression model was established by transfecting CFs with an ALKBH5 ex-pression vector in a high-glucose medium.The expres-sion of ALKBH5 in CFs was assessed through immuno-fluorescence staining,Western blot and RT-qPCR.Changes in m6A levels were evaluated using Dot blot a-nalysis.Additionally,Alterations in the expression of proliferating cell nuclear antigen(PCNA)and collagenⅠ,a pivotal fibrosis indicator,were measured using Western blot.The proliferation and migration ability of CFs were assessed through EdU staining and Transwell migration assay,respectively.Results Following treatment with high glucose,the expression of ALKBH5 in CFs notably decreased,while m6A level increased.This was accompanied by a significant increase in the expression of the proliferation marker PCNA and the fi-brosis marker collagen Ⅰ.Additionally,there was a sig-nificant improvement in the ability of proliferation and migration.Overexpression of ALKBH5 resulted in a significant decrease in the expressions of PCNA and collagen Ⅰ,leading to the inhibition of both proliferation and migration in CFs.Conclusion Overexpression of ALKBH5 suppresses the expression of PCNA and colla-gen Ⅰ,consequently reducing the proliferation and mi-gration of CFs,potentially through m6A methylation modification.

As the most common phenotype of type 1 neurofibromatosis(NF1),plexiform neurofibromas(pNF)exhibit early asymptomatic presentation but multisite involvement,with a risk of progression.Imaging serves as vital tool for evaluation and management of NF1-associated pNF.The progresses of imaging for evaluating NF1-related pNF were reviewed in this article.

Perimenopausal depression seriously affects women's physical and mental health.It is caused primarily by gonadal function decline,which is typically characterized by low mood,anxiety,slow thinking,and loss of interest,and is accompanied by autonomic dysfunction and endocrine dysfunction.The pathogenesis of perimenopausal depression remains unclear and controversial.Many scholars have conducted scientific research that is based on animal models of perimenopausal depression.Indeed,a good animal model of perimenopausal depression is the basic premise for studying its pathophysiological mechanisms and for facilitating reliability of the scientific result.Therefore,this paper combines the modern research mechanisms of perimenopausal depression and the current status of animal models in China,and provides an overview,evaluation,and generalization of the modeling method,principles and result,to provide a scientific basis and reference for the selection of suitable animal models for scientific research experiments.

Objective To analyze the active components and mechanism of action of Houttuyniae Herba-Leonuri Herba in treating systemic lupus erythematosus(SLE).Methods The main chemical components of Houttuyniae Herba-Leonuri Herba and their targets through Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP)were obtained,and the active components of the Chinese medicine according to ADME were screened;the potential therapeutic targets of SLE through Genecards database were obtained.The protein-protein interactions(PPI)network was constructed by using the STRING 12.0 database,and the potential protein functional modules in the network was mined.The molecular docking technique was used to further validate the action mechanism of components and targets which played a therapeutic role.Results A total of 198 Houttuyniae Herba-Leonuri Herba-SLE intersection targets were obtained.Core active ingredients such as isothermalone,iso-preleoheterin,kaempferol,and quercetin and core targets such as IL6,AKT1,SRC,STAT3 and EGFR were screened out.A total of 1 001 entries were screened by Gene Ontology(GO)functional enrichment analysis,which were mainly related to the reaction of proteins and their kinases,and inflammation,etc..A total of 166 pathways were enriched in Kyoto Encyclopedia of Genes and Genomes(KEGG),including cancer pathway,PI3K-Akt signaling pathway,neuroactive ligand-receptor pathway,and so on.Molecular docking results showed that the core active components of Houttuyniae Herba-Leonuri Herba had great binding activities with their core targets,which preliminarily verified the above network pharmacology results.Conclusion Houttuyniae Herba-Leonuri Herba may exerts a therapeutic effect on SLE through core ingredients such as isothermalone acting on core targets such as IL6,AKT1,SRC,STAT3 and EGFR,and regulating cancer pathway,PI3K-Akt signaling pathway and neuroactive ligand-receptor interaction.

Aim To investigate the regulatory effect of morphine postconditioning in the LSG on remodeling after myocardial infarction. Methods SD rats were randomly divided into four groups: sham operation group (Sham), myocardial infarction group (MI), myocardial infarction + saline group (Control) and myocardial infarction + morphine postconditioning group (MI + Morphine) . The rat MI model was constructed by ligating the left anterior descending coronary artery, and then morphine was given to the LSG by percutaneous posterior approach. After four weeks, the changes of cardiac function in rats were detected by ultrasound. Masson staining was used to detect fibrosis changes; the expression of Collagen I and Collagen III protein was detected by Western blot. The mRNA expression of ANP and BNP was detected by RT-qPCR. The expression of JJLOR in LSG was detected by immunofluorescence. The concentration of catecholamine in plasma and myocardial tissue was detected by ELISA. Results Compared with the sham group, the cardiac function of the MI group was significantly impaired, the myocardial tissue showed significant fibrosis changes, and the concentration of catecholamine in plasma and myocardial tissue significantly increased. Compared with the control group, the MI + Morphine group reduced myocardial fibrosis collagen deposition in rats after MI, inhibited the expression of ANP and BNP in myocardial tissue, reduced the concentration of catecholamine, and improved the cardiac function of MI rats. Immunofluorescence results showed that JJLOR was expressed in LSG after MI and increased after morphine postconditioning. Conclusions This study shows that morphine postconditioning in the LSG has a protective effect on myocardial remodeling after myocardial infarction. The mechanism may be related to the activation of JJLOR in the LSG by morphine and the reduction of catecholamine release from sympathetic nerve endings.