Research progress of ginger in the treatment of gastrointestinal tumors

Cancer seriously endangers human health.Gastrointestinal cancer is the most common and major malignant tumor,and its morbidity and mortality are gradually increasing.Although there are effective treatments such as radio-therapy and chemotherapy for gastrointestinal tumors,they are often accom-panied by serious side effects.According to the traditional Chinese medicine and food homology theory,many materials are both food and medicine.Moreover,food is just as capable of preventing and treating diseases as medicine.Medicine and food homologous herbs not only have excellent pharmacological effects and activities but also have few side effects.As a typical medicinal herb with both medicinal and edible uses,some components of ginger have been shown to have good efficacy and safety against cancer.A mass of evidence has also shown that ginger has anti-tumor effects on digestive tract cancers(such as gastric cancer,colorectal cancer,liver cancer,laryngeal cancer,and pancreatic cancer)through a variety of pathways.The aim of this study is to investigate the mechanisms of action of the main components of ginger and their potential clinical applications in treating gastrointestinal tumors.

To explore the mechanism of Yigong San anti-gastric cancer and immune regulation

BACKGROUND Yigong San(YGS)is a representative prescription for the treatment of digestive disorders,which has been used in clinic for more than 1000 years.However,the mechanism of its anti-gastric cancer and regulate immunity are still remains unclear.AIM To explore the mechanism of YGS anti-gastric cancer and immune regulation.METHODS Firstly,collect the active ingredients and targets of YGS,and the differentially expressed genes of gastric cancer.Secondly,constructed a protein-protein interaction network between the targets of drugs and diseases,and screened hub genes.Then the clinical relevance,mutation and repair,tumor microenvironment and drug sensitivity of the hub gene were analyzed.Finally,molecular docking was used to verify the binding ability of YGS active ingredient and hub genes.RESULTS Firstly,obtained 55 common targets of gastric cancer and YGS.The Kyoto Encyclopedia of Genes and Genomes screened the microtubule-associated protein kinase signaling axis as the key pathway and IL6,EGFR,MMP2,MMP9 and TGFB1 as the hub genes.The 5 hub genes were involved in gastric carcinogenesis,staging,typing and prognosis,and their mutations promote gastric cancer progression.Finally,molecular docking results confirmed that the components of YGS can effectively bind to therapeutic targets.CONCLUSION YGS has the effect of anti-gastric cancer and immune regulation.

Mechanism of pachymic acid in the treatment of gastric cancer based on network pharmacology and experimental verification

BACKGROUND Pachymic acid(PA)is derived from Poria cocos.PA has a variety of pharmacological and inhibitory effects on various tumors.However,the mechanism of action of PA in gastric cancer(GC)remains unclear.AIM To investigate the mechanism of PA in treating GC via the combination of network pharmacology and experimental verification.METHODS The GeneCards and OMIM databases were used to derive the GC targets,while the Pharm Mapper database provided the PA targets.Utilizing the STRING database,a protein-protein interaction network was constructed and core targets were screened.The analyses of Gene Ontology,Kyoto Encyclopedia of Genes and Genomes(KEGG),and gene set enrichment analysis were conducted,and molecular docking and clinical correlation analyses were performed on the core targets.Ultimately,the network pharmacology findings were validated through in vitro cell assays,encompassing assessments of cell viability,apoptosis,cell cycle,cloning,and western blot analysis.RESULTS According to network pharmacology analysis,the core targets were screened,and the PI3K/AKT signaling pathway is likely to be the mechanism by which PA effectively treats GC,according to KEGG enrichment analysis.The experimental findings showed that PA could control PI3K/AKT signaling to prevent GC cell proliferation,induce apoptosis,and pause the cell cycle.CONCLUSION Network pharmacology demonstrated that PA could treat GC by controlling a variety of signaling pathways and acting on a variety of targets.This has also been supported by in vitro cell studies,which serve as benchmarks for further research.

Network pharmacology study and in vitro experimental validation of Xiaojianzhong decoction against gastric cancer

BACKGROUND Cancer is one of the most serious threats to human health worldwide.Conventional treatments such as surgery and chemotherapy are associated with some drawbacks.In recent years,traditional Chinese medicine treatment has been increasingly advocated by patients and attracted attention from clinicians,and has become an indispensable part of the comprehensive treatment for gastric cancer.AIM To investigate the mechanism of Xiaojianzhong decoction(XJZ)in the treatment of gastric cancer(GC)by utilizing network pharmacology and experimental validation,so as to provide a theoretical basis for later experimental research.METHODS We analyzed the mechanism and targets of XJZ in the treatment of GC through network pharmacology and bioinformatics.Subsequently,we verified the impact of XJZ treatment on the proliferative ability of GC cells through CCK-8,apoptosis,cell cycle,and clone formation assays.Additionally,we performed Western blot analysis and real-time quantitative PCR to assess the protein and mRNA expression of the core proteins.RESULTS XJZ mainly regulates IL6,PTGS2,CCL2,MMP9,MMP2,HMOX1,and other target genes and pathways in cancer to treat GC.The inhibition of cell viability,the increase of apoptosis,the blockage of the cell cycle at the G0/G1 phase,and the inhibition of the ability of cell clone formation were observed in AGS and HGC-27 cells after XJZ treatment.In addition,XJZ induced a decrease in the mRNA expression of IL6,PTGS2,MMP9,MMP2,and CCL2,and an increase in the mRNA expression of HOMX1.XJZ significantly inhibited the expression of IL6,PTGS2,MMP9,MMP2,and CCL2 proteins and promoted the expression of the heme oxygenase-1 protein.CONCLUSION XJZ exerts therapeutic effects against GC through multiple components,multiple targets,and multiple pathways.Our findings provide a new idea and scientific basis for further research on the molecular mechanisms underlying the therapeutic effects of XJZ in the treatment of GC.

MiR-204-3p overexpression inhibits gastric carcinoma cell proliferation by inhibiting the MAPK pathway and RIP1/MLK1 necroptosis pathway to promote apoptosis

BACKGROUND Gastric carcinoma(GC)is the third most frequent cause of cancer-related death,highlighting the pressing need for novel clinical treatment options.In this regard,microRNAs(miRNAs)have emerged as a promising therapeutic strategy.Studies have shown that miRNAs can regulate related signaling pathways,acting as tumor suppressors or tumor promoters.AIM To explore the effect of miR-204-3p on GC cells.METHODS We measured the expression levels of miR-204-3p in GC cells using quantitative real-time polymerase chain reaction,followed by the delivery of miR-204-3p overexpression and miR-204-3p knockdown vectors into GC cells.CCK-8 was used to detect the effect of miR-204-3p on the proliferation of GC cells,and the colony formation ability of GC cells was detected by the clonal formation assay.The effects of miR-204-3p on GC cell cycle and apoptosis were detected by flow cytometry.The BABL/c nude mouse subcutaneous tumor model using MKN-45 cells was constructed to verify the effect of miR-204-3p on the tumorigenicity of GC cells.Furthermore,the study investigated the effects of miR-204-3p on various proteins related to the MAPK signaling pathway,necroptosis signaling pathway and apoptosis signaling pathway on GC cells using Western blot techniques.RESULTS Firstly,we found that the expression of miR-204-3p in GC was low.When treated with the lentivirus overexpression vector,miR-204-3p expression significantly increased,but the lentivirus knockout vector had no significant effect on miR-204-3p.In vitro experiments confirmed that miR-204-3p overexpression inhibited GC cell viability,promoted cell apoptosis,blocked the cell cycle,and inhibited colony formation ability.In vivo animal experiments confirmed that miR-204-3p overexpression inhibited subcutaneous tumorigenesis ability in BABL/c nude mice.Simultaneously,our results verified that miR-204-3p overexpression can inhibit GC cell proliferation by inhibiting protein expression levels of KRAS and p-ERK1/2 in the MAPK pathway,as well as inhibiting protein expression levels of p-RIP1 and p-MLK1 in the necroptosis pathway to promote the BCL-2/BAX/Caspase-3 apoptosis pathway.CONCLUSION MiR-204-3p overexpression inhibited GC cell proliferation by inhibiting the MAPK pathway and necroptosis pathway to promote apoptosis of GC cells.Thus,miR-204-3p may represent a new potential therapeutic target for GC.

面向ECDSA的低复杂度多标量乘算法设计

随着电子商务的飞速发展,信息安全的重要性日益剧增。密码技术在信息安全中可以确保数据在通信过程中的安全、保密、完整且不被篡改。诸如ECDSA等数字签名算法为安全电子商务提供了关键技术。ECDSA设计架构通常采用不同的多标量乘算法和单标量乘算法分别进行运算处理,从而导致计算复杂度提升。针对该问题,提出了一种面向ECDSA的低复杂度多标量乘算法,该算法采用取模法构建联合多基链算法,对不能同时被基底{2,3}整除的部分进行3^(x)2^(y)取模运算,对得到的余数进行预处理。与现有联合多基链算法采用的贪心法相比,所生产的基链长度减小,有效地降低了多标量乘法的计算复杂度。实验结果表明,在curve-P256曲线下多标量乘和单标量乘的复杂度分别降低了约9.84%~30.75%和3.88%~26.81%;在联合处理的情况下,复杂度至少降低了约16.65%;预计算点相较于wNAF和联合多基链算法减少了约25.00%。通过Python搭建模型,相较于现有算法至少提高了14.80%的运行速度。

DOT快速算法及其通用架构设计

离散正交变换(discrete orthogonal transformation,DOT)被广泛应用于图像处理和视频压缩,研究其快速算法以及通用架构的设计具有重要的实际意义。由于各种视频压缩算法被广泛提出,具体类型、特定点数的DOT已经不能满足图像和视频领域的发展要求。因此,研究一种多类型、任意点数的DOT快速算法及其通用架构是一个有待解决的问题。针对以上问题,采用分治策略,提出了一种基于CORDIC的DOT快速算法、并设计出能够实现多种DOT算法的通用架构。实验结果表明,与现有算法相比,该算法在复杂度、可扩展性、流水线设计及易于VLSI实现等方面有明显优势;与现有的架构相比,该通用架构计算简单、硬件复用率高,能满足多应用需求。

有限状态熵编码的VLSI设计与实现

在处理海量数据时,以软件方式实现的Z标准(Zstd)无损压缩算法难以满足特定应用领域对压缩速度的需求.对Zstd进行硬件加速设计是解决这一问题的有效方案,尤其是针对Zstd的有限状态熵编码(finitestateentropy,FSE)的硬件加速.因此,提出一种适用于Zstd的FSE压缩、解压硬件实现架构,采用固定压缩表实现最优的硬件加速步骤;通过增加序列映射的硬件模块来降低存储空间并提高传输速度;采用软硬件协同设计方案,并对硬件实现架构进行7级流水设计.通过VisualStudio与Modelsim的联合验证平台进行验证,实验结果表明在TSMC55 nm的工艺下,系统最高频率可达到750 MHz.与软件实现相比,整体压缩速度提高了9倍以上,整体解压速度提高了约100倍.

Optimal in vitro culture conditions for murine predominant immature CD8a^＋ dendritic cells

Background The prospects of using immature CD8a^＋ dendritic cells （DC2） to establish transplant immunologic tolerance and treatments for autoimmune diseases in the future are promising. However, the methods for inducing DC2 are still being explored. The present study was aimed to investigate the optimal in vitro conditions for preparing large numbers of predominant DC2 from murine bone marrow cells. Methods Three groups of bone marrow cells cultured under different conditions were examined, namely a cytokine-induced experimental group （cytokine group）, a control group with a low concentration of granulocyte-macrophage colony stimulating factor （GM-CSF, low GM-CSF group） and a control group without endogenous cytokines. The cytokine group was cultured with 5 ng/ml GM-CSF, 25 ng/ml Fit3 ligand （FIt3L）, 20 ng/ml interleukin 4 （IL-4） and 100 ng/ml stem cell factor （SCF）. The low GM-CSF control group was cultured with 0.4 ng/ml GM-CSF, 25 ng/ml FIt3L and 100 ng/ml SCF, without IL-4. The control group without exogenous cytokines was cultured without additional cytokines. All cells were cultured at 37℃ under 5% CO2. On days 3, 7 and 16, 4-color flow cytometry was carried out to analyze the cell phenotypes, and the total cell numbers were counted to analyze the cell yields. Phase-contrast microscopy was used to observe the cell morphologies. Results The cytokine group exhibited higher proportions of typical immature CD8a^＋ DC, especially on day 3, but the total cell number and DC2 proportion decreased during prolonged culture. The low GM-CSF control group showed the same tendencies as the cytokine group on days 16 and 22, but produced higher total cell numbers （P 〈0.05） with lower DC2 proportions and cell numbers. The control group without exogenous cytokines spontaneously generated a certain proportion of DC2, but with low total cell and DC2 numbers that decreased rapidly, especially during prolonged culture （days 7 and 16, P 〈0.05）, Conclusions Culture in the presence of 5 ng/ml GM-CSF, 25 ng/ml FIt3L, 20 ng/ml IL-4 and 100 ng/ml SCF can rapidly induce large quantities of predominant immature CD8a^＋ DC from murine bone marrow cells. Therefore, these represent optimal culture conditions for preparing murine immature DC2 in vitro.

Immature CD4＋ dendritic cells conditioned with donor kidney antigen prolong renal allograft survival in rats

Background AIIogeneic transplant rejection is currently a major problem encountered during organ transplantation. The dendritic cell （DC） is the most effective powerful known professional antigen-presenting cell, and recent studies have found that DCs can also induce immune tolerance, and avoid or reduce the degree of transplant rejection. The aim of this study was to evaluate the effect of transfused immature CD4~ DCs on renal allografts in the rat model. Methods In this study, we induced CD4~ immature DCs from rat bone marrow cells by a cytokine cocktail. The immature CD4~ DCs were identified by morphological analysis and then the suppressive activity of these cells conditioned with donor kidney antigen was evaluated in vitro and in vivo. Results Immature CD4~ DCs conditioned with donor kidney antigen possessed immunosuppressive activity in vitro and they were able to prolong renal transplant survival in an allograft rat model in vivo. Conclusions Our study provides new information on efficacious renal transplantation, which might be useful for understanding the function of immature CD4~ DCs in modulating renal transplant rejection and improving clinical outcome in future studies.