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摘要 Male mice in the AOM/DSS model were randomly divided into 4 groups: Model group, Model+AAV-NC group, Model+AAV/NC+BBD group, and Model/OE-SNTB1+BBD group. After one week of adaptive feeding, mice were injected with 12.5mg/kg AOM. After one week, they were given 2.5% DSS to induce the construction of colitis-associated colon cancer (CAC) model. SNTB1 gene overexpression plasmid was packaged and recombinant virus particles were obtained. The colon tissue of the mice was infected with the virus particles. At the beginning of each round of DSS, mice in the Model+AAV-NC and Model+AAV/NC+BBD groups were injected with 100ul of empty adenovirus, while mice in the Model/OE-SNTB1+BBD group were injected with 100ul of SNTB1 overexpression adenovirus. After the first round of DSS feeding ended, mice were given BaBaoDan (250mg/kg) for long-term intervention. Tissue analysis was conducted on day 67 of the experiment. The general living conditions of the mice and their weight were observed. An in viv
咨询记录 · 回答于2023-03-29
翻译 中译英
我这边已经机翻好了,需要您帮我看看语法什么的,检查和更改一下
亲 发来看看呢
发文字哦
中文摘要目的:通过体内外实验,在体外水平研究八宝丹(BaBaoDan,BBD)治疗大肠癌细胞的作用机制,检验SNTB1是否是八宝丹发挥治疗大肠癌功能的潜在靶点;以及在体内水平研究检验八宝丹是否通过调控SNTB1的表达,影响p38MAPK信号通路活化,参与调控结肠炎相关性肠癌(CAC)的发生发展,从而为临床应用八宝丹治疗CAC奠定基础,也为结肠炎相关性结肠癌的治疗提供了基因治疗新的思路。方法:1.体外培养SNTB1、LOVO肠癌细胞,采用慢病毒感染和嘌呤霉素筛选构分别构建大肠癌稳转细胞株,将2株细胞分为HCT-116/NC组、HCT-116/OE组及LOVO/NC组、LOVO/OE组;采用MTT法、细胞克隆球形成实验、Transwell、Invasion实验分别检测转染后各组细胞的活力、增殖、迁移侵袭能力; qPCR法检测转染后各组SNTB1的表达情况;WB检测过表达组细胞中SNTB1的表达是否被上调以及MAPK12、PMAPK12表达能力。
AbstractObjective: To investigate the mechanism of BaBaoDan (BBD) in the treatment of colorectal cancer cells in vitro and in vivo, and to test whether SNTB1 is a potential target for BaBaoDan to exert its therapeutic effect on colorectal cancer cells; "And in vivo level studies to test whether Babao Dan can regulate the expression of SNTB1, affect the activation of p38MAPK signaling pathway, and participate in the regulation of the occurrence and development of colitis associated colon cancer
Abstract:The objective of this study is to investigate the mechanism of BaBaoDan (BBD) in treating colorectal cancer (CRC) cells in vitro and in vivo, and to verify whether SNTB1 is a potential target for the therapeutic effect of BBD on CRC. The study also aims to examine whether BBD can affect the activation of p38MAPK signaling pathway by regulating the expression of SNTB1 in vivo and participate in the regulation of the occurrence and development of colitis-associated colon cancer (CAC), thus laying a foundation for the clinical application of BBD in the treatment of CAC and providing a new approach to gene therapy for colitis-associated colon cancer.Methods:SNTB1 and LOVO CRC cells were cultured in vitro, and stable cell lines of CRC were constructed by lentivirus infection and puromycin screening. The two cell lines were divided into HCT-116/NC group, HCT-116/OE group, LOVO/NC group, and LOVO/OE group. MTT assay, cell clone sphere formation experiment, Transwell, and Invasion
(CAC), thereby laying the foundation for the clinical application of BBD in the treatment of CAC and providing a new gene therapy approach for colitis-associated colon cancer.Methods: SNTB1 and LOVO colorectal cancer cells were cultured in vitro, and stable cell lines were constructed using lentivirus infection and puromycin screening. The cells were divided into HCT-116/NC, HCT-116/OE, LOVO/NC, and LOVO/OE groups. The cell viability, proliferation, migration, and invasion ability of each group after transfection were assessed using MTT assay, cell clone sphere formation experiment, Transwell, and Invasion assay. qPCR was used to detect the expression of SNTB1 in each group after transfection, and WB was used to detect whether the expression of SNTB1 was upregulated and the expression ability of MAPK12 and PMAPK12 in the overexpressed cells.
亲 这个太长了吧,8毛钱很难做到啊
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Objective: To investigate the mechanism of BaBaoDan (BBD) in the treatment of colorectal cancer cells in vitro and in vivo, and to verify whether SNTB1 is a potential target for BBD to exert its therapeutic effect on colorectal cancer cells. Additionally, the study aims to examine whether BBD can affect the activation of p38MAPK signaling pathway by regulating the expression of SNTB1 in vivo and participate in the regulation of the occurrence and development of colitis-associated colon cancer (CAC), thus laying a foundation for the clinical application of BBD in the treatment of CAC and providing a new gene therapy approach for colitis-associated colon cancer.Methods: SNTB1 and LOVO colorectal cancer cells were cultured in vitro, and stable cell lines were constructed using lentivirus infection and puromycin screening. The cells were divided into HCT-116/NC, HCT-116/OE, LOVO/NC, and LOVO/OE groups. The cell viability, proliferation, migration, and invasion ability of each group after
中文摘要目的:通过体内外实验,在体外水平研究八宝丹(BaBaoDan,BBD)治疗大肠癌细胞的作用机制检验SNTB1是否是八宝丹发挥治疗大肠癌功能的潜在靶点;以及在体内水平研究检验八宝丹是否通过调控SNTB1的表达,影响p38MAPK信号通路活化,参与调控结肠炎相关性肠癌(CAC)的发生发展,从而为临床应用八宝丹治疗CAC奠定基础也为结肠炎相关性结肠癌的治疗提供了基因治疗新的思路。方法:1体外培养SNTB1、LOVO肠癌细胞,采用慢病毒感染和漂岭霉素筛选构分别构建大肠癌稳转细胞株,将2株细胞分为HCT-116/NC组、HCT-116/OE组及LOVO/NC组、LOVO/OE组;采用MTT法、细胞克隆坏成实觉Iranswellnvasion:染后各组细胞的活力、增殖、迁移侵袭能力:qPCR法检测转染后各组SNTB1的表达情况:WB检测过表达组细胞中SNTB1的表达是否被上调以及MAPK12PMAPK12表达能力。2.将构建成功后的大肠癌稳转细胞株采用MTT法、细胞克隆球形成实验、Transwell、invasionScratch实验分别检测转染后各组细胞的活力、增殖迁移侵袭、转移能力:qPCR法检测转染后各组SNTB1的表达情况WB检测过表达组细胞中SNTB的表达是否被上调以及MAPK12、PMAPK12表达能力,以检测八宝丹对SNTB1介导的大肠癌细胞模型的影响。
这段的
SNTB1 adenovirus was constructed, and male Balb/c mice were randomly divided into 5 groups: Model group, Model/OE-NC group, Model/OE group, Model/Sh-NC group, and Model/Sh group. The general living conditions of the mice, as well as their weight and fecal occult blood were observed. The virus infection of the colon tissue was observed using an in vivo imaging system. The virus infection effect was verified using frozen sections, and the expression of SNTB1, MAPK12, and PMAPK12 in colon tissue was detected using IHC. RT-PCR was used to detect the differences in SNTB1 mRNA expression in colon tissue among the groups of mice, and Western blot was used to detect the expression of SNTB1, MAPK12, and PMAPK12.
3构建SNTB1腺相关病毒,将雄性Balb/c小鼠随机分成5组,Model组、ModeVOE-NC组Model/OE组、Model/Sh-NC组、Model/Sh组;观察小鼠一般生活状态和测量体重、粪便隐血情况,通过活体成像系统观察结肠组织病毒感染情况,冰冻切片验证病毒感染效果,通过IHC检测结肠组织SNTB1、MAPK12PMAPK12表达;利用RT-gPCR技术检测各组小鼠的结肠组织SNTB1mRNA表达差异,通过Westermn Blot检测SNTB1、MAPK12、PMAPK12表达。这段的
Male mice in the AOM/DSS model were randomly divided into 4 groups: Model group, Model+AAV-NC group, Model+AAV/NC+BBD group, and Model/OE-SNTB1+BBD group. After one week of adaptive feeding, mice were injected with 12.5mg/kg AOM. After one week, they were given 2.5% DSS to induce the construction of colitis-associated colon cancer (CAC) model. SNTB1 gene overexpression plasmid was packaged and recombinant virus particles were obtained. The colon tissue of the mice was infected with the virus particles. At the beginning of each round of DSS, mice in the Model+AAV-NC and Model+AAV/NC+BBD groups were injected with 100ul of empty adenovirus, while mice in the Model/OE-SNTB1+BBD group were injected with 100ul of SNTB1 overexpression adenovirus. After the first round of DSS feeding ended, mice were given BaBaoDan (250mg/kg) for long-term intervention. Tissue analysis was conducted on day 67 of the experiment. The general living conditions of the mice and their weight were observed. An in viv
4.将AOM/DSS模型小凰随机分成4组,分别是Model组、Model+AAV-NC组Model+AAV/NC+BBD组、Model/OE-SNTB1+BBD组,经适应性喂养一周后,对小鼠体内注射12.5mg/kg的氧化偶氮甲烷(AOM),一周后,给予2.5%浓度的葡聚糖硫酸钠(DSS),诱导构建结肠炎相关性结肠癌(CAC)模型。将构建的SNTB1基因过表达质粒包装、重组得到病毒颗粒,感染小鼠结肠组织部位,在每一轮DSS开始时,Model+AAV-NC组及Model+AAV/NC+BBD组小鼠注射100ul/只的空载腺病毒,Model/OE-SNTB1+BBD组小鼠注射100ul/只的SNTB1过表达腺病毒。在第一轮DSS喂养结束后odeltAAWNCRRDEB1+RRD6小鼠使用八宝丹(250mg/kg)长期干预:在实验第67天的时候进行取材分析。观察小鼠一般生活状态和检测体重,运用小动物活体成像系统观察结肠组织病毒感染情况;利用冰冻切片验证病毒感染效果,免疫组化检测SNTB1、MAPK12、PMAPK12阳性率评价长期使用八宝丹对脏器组织病理学的影响,HE染色检测结肠组织瘤体情况,RT-GPCR检测结肠组织SNTB1表达差异;Western Blot检测SNTB1蛋白、p-MAPK12/MAPK12通路的表达情况,以验证八宝丹是否是通过调控SNTB1基因影响结肠炎相关性结肠癌小鼠的发生发展。这段的
Results:The MTT experiment showed that overexpression of the SNTB1 gene can enhance the viability of HCT116 and LOVO cells (P<0.01). Compared with the HCT116/NC and LOVO/NC groups, the viability of cells in the HCT-116/OE and LOVO/OE groups was significantly increased. The colony formation experiment showed that overexpression of the SNTB1 gene can significantly promote the sphere-forming ability and proliferation of colon cancer cells. Compared with the HCT-116/NC and LOVO/NC groups, the cloning ability of cells in the HCT-116/OE and LOVO/OE groups was significantly improved, with significant differences (P<0.01). The Transwell and Invasion Scratch experiments showed that the migration, invasion, and scratch healing rate of HCT-116/OE and LOVO/OE colon cancer cells were higher than those of the HCT-116/NC and LOVO/NC groups (P<0.01), indicating that overexpression of the SNTB1 gene can promote the metastasis of colon cancer cells. qPCR detected the expression of SNTB1 in each group
结果:1MTT实验表明SNTB1基因过表达能增强HCT116及LOVO细胞的活力(P<0.01),与HCT116/NC组和LOVO/NC组相比,HCT-116/OE组与LOVO/OE组细胞的活力显著增加;集落形成实验表明SNTB1基因过表达能显著促进肠癌细胞成球能力与增殖情况,与HC-116/NC组和LOVO/NC组与LOVO/OE组细胞的克隆球形成能力显著提高,结果具有显著性差异(P<0.01)。Transwell、InvasionScratch实验表明转染后的HCT-116/OE组LOVO/OE组肠癌细胞其迁移侵袭及划痕应合率都高于HCT-116/NC组和LOVO/NC组(P<0.01),其结果表明过表达SNTB1基因可促进大肠癌细胞的转移。qPCR法检测转染后各组SNTB1结果显示,与HCT-116/NC组和LOVO/NC组相比,HCT116/OE组及LOVO/OE组肠癌细胞的SNTB1的mRNA表达量显著增加(P<0.01)。Western blot结果显示,与HCT116/NC组和LOVO/NC组相比,HCT116/OE组及LOVO/OE组肠癌细胞的SNTB1的蛋白表达量及pMAPK12/MAPK12的比值显著升高(P<0.01)。2.经过八宝丹干预后,MTT实验结果显示,与HCT-116/NC组及LOVO/NC组的细胞相比,HCT116/SNTB1组及LOVO/SNTB1组的肠癌细胞的增殖能力显著提高(P<0.01)HCT-116/NC+BBD组与LOVO/NC+BBD组的细胞增殖水平降低(P<0.01)。八宝丹干预过后,HCT-116/SNTB1+BBD组及LOVO/SNTB1+BBD组的肠癌细胞增殖能力有所下降(P<0.05)这些结果表明八宝丹能通过影响SNTB1基因表达水平,降低肠癌细胞的增殖情况。这段的
The Transwell, Invasion, and Scratch experiments showed that after intervention with BaBaoDan, the migration, invasion, and scratch healing rate of HCT116/NC and LOVO/NC colon cancer cells were significantly decreased (P<0.01), indicating that BaBaoDan can inhibit the metastasis of colon cancer cells. Additionally, compared with HCT116/SNTB1 and LOVO/SNTB1 overexpressing cells, the migration, invasion, and scratch healing rate of HCT116/SNTB1+BBD and LOVO/SNTB1+BBD colon cancer cells were also decreased (P<0.05). These results suggest that BaBaoDan can reduce the metastasis of colon cancer cells by affecting the expression level of the SNTB1 gene.In the qPCR experiment, it was found that the mRNA expression levels of SNTB1, MAPK12, and p-MAPK12 in HCT-116/NC+BBD and LOVO/NC+BBD groups were significantly decreased compared with the HCT-116/NC and LOVO/NC groups (P<0.05). Similarly, the mRNA expression levels of SNTB1 and MAPK12, as well as the protein expression level of SNTB1 and the
TanswellInvasion、Scratch实验表明在HCT116/NCLOVO/NC组细胞中加入八宝丹的干预后,其迁移侵袭及划痕愈合率都较NC组细胞有明显的下降(P<0.01)其结果表明使用八宝丹可抑制大肠癌细胞的转移:同时,与HCT116/SNTB1及LOVO/SNTB1过表达细胞株相比,八宝丹使用后的HCT116/SNTB1+BBD与LOVO/SNTB1+BBD组肠癌细胞的迁移侵袭及划痕愈合率都有所下降(P<0.05)。这些结果表明八宝丹能通过影响SNTB1基因表达水平,降低肠癌细胞的转移在qPCR实验中,我们发现与HCT116/NCLOVO/NC组相比,HCT-116/NC+BBDLOVO/NC+BBD组的SNTB1、MAPK12、P-MAPK12Ln&rLOVO/SNTB1组相比,HCT116/SNTB1+BBD与LOVO/SNTB1+BBD组细胞中的SNTB1、MAPK12p-MAPK12mRNA表达水平下降,表明八宝丹可降低大肠癌细胞中的SNTB1、MAPK12、P-MAPK12等基因的mRNA表达水平(P<0.05)。Westemn blot结果显示,与HCT116/NC、LOVONC组相比,HCT116/NC+BBD、LOVO/NC+BBD的SNTB1蛋白表达量、P-MAPK12/MAPK12的比值下降(P<0.01);与HCT-116/SNTB1及LOVO/SNTB1组相比,HCT116/SNTB1+BBD与LOVO/SNTB1+BBD组细胞中的SNTB1蛋白表达量、P-MAPK12mRNA表达水平下降,表明八宝丹可能是通过介导SNTB1,进而发挥调控p38MAPK信号通路,抑制大肠癌发生发展的作用。这段的
Compared with the Control group, the Model group of mice showed a decline in their living conditions (including fur luster, activity, and diet), and the Model/OE group with SNTB1 overexpression exhibited significant weight loss, bloody stool, and diarrhea (P<0.001). However, the severity of the disease in the Model/Sh group with SNTB1 knockdown was not significant, indicating that SNTB1 may be a potential target gene that promotes the development of colitis-associated colorectal cancer. The small animal live imaging results showed that after injection of adenovirus for 2-3 weeks, the colon tissues of the Model/OE-NC group, Model/OE group, Model/Sh-NC group, and Model/Sh group of mice showed strong fluorescence under the small animal live imaging system, indicating that the adenovirus had infected the colon tissues. The IHC staining results showed that compared with the Model group, the positive expression levels of SNTB1, MAPK12, and p-MAPK12 in the colon tissues of the Model/OE group
3与Control组相比,Model组小鼠生活状态(皮毛光泽、活动状态、饮食等)下降,SNTB1过表达的Model/OE组小鼠出现明显的体重下降便血及腹泻(P<001),而SNTB1敲减的Model/Sh组小鼠疾病严重程度则不明显,表明SNTB1可能是促进肠炎相关性肠癌发展过程中的潜在靶基因。小动物活体成像结果显示,在注射腺病毒2~3周后,Model/OE-NC组、Model/OE组、Model/Sh-NC组、Model/Sh组小鼠的结肠组织在小动物活体成像系统下观察可呈强荧光,说明腺病毒已感染了结肠组织。IHC染色结果发现,与Model组相比,Model/OE组结肠组织中SNTB1、MAPK12PMAPK12的阳性表达量明显升高(P<0.01),而Model/Sh组SNTB1、MAPK12PMAPK12的阳性表达量降低。qPCR实验结果显示与Model组相比,Model/OE组SNTB1的mRNA表达量显著增高(P<0.05),而Model/Sh中的SNTB1mRNA表达量显著降低(P<0.05)。Western blot结果显示,与Model组相比,SNTB1过表达组的SNTB1蛋白表达量、P-MAPK12/MAPK12的比值升高(P<0.01)而SNTB1敲减组的SNTB1蛋白表达量、PMAPK12/MAPK12的比值显著降低(P<001)。这段的
The results of the study showed that Ba Bao Dan could inhibit the proliferation and metastasis of colorectal cancer cells by regulating the expression of SNTB1 and the p38MAPK signaling pathway in the cells, as well as relieve the disease activity index, improve the survival status and pathological condition of mice. SNTB1 may be an important target for Ba Bao Dan to inhibit the development of colitis-associated colorectal cancer. Keywords include Ba Bao Dan, SNTB1, p38MAPK12 signaling pathway, colitis-associated colorectal cancer, metastasis.After intervention with Ba Bao Dan, the results of the sample showed that compared with the Model+AAV-NC group, the disease activity of mice in the Model/NC+BBD group and the Model/OE-SNTB1+BBD group improved, with a decrease in severity, weight loss, and relief of rectal bleeding and diarrhea index (P<0.05). IHC staining results showed that compared with the Model+AAV-NC group, the number of SNTB1 MAPK12 and P-MAPK12 positive cells in the Model+
4.加入八宝丹干预后,取材结果显示,与Model+AAV-NC组相比,Model/NC+BBD组及Model/OE-SNTB1+BBD组小鼠疾病活动情况有所改善,严重程度降低,体重下降、便血及腹泻指数有所缓解(P<0.05)。IHC染色结果发现,与Model+AAV-NC组相比,Model+AAV/NC+BBD组SNTB1MAPK12、P-MAPK12阳性细胞数量显著降低(P<001),而Model/OE-SNTB1+BBD(P<005)组的SNTB1、MAPK12、p-MAPK12阳性率也有所下降(P<0.05)。HE染色结果显示,与Model+AAV-NC组相比,Model+AAV/NC+BBD组的小鼠结肠组织炎症细胞浸润的情况有所缓解,肠道组织结构更为完整(P<0.05)。qPCR实验结果显示,与Model+AAV-NC组相比,Model+AAV/NC+BBD组SNTB1的mRNA表达量显著下降(P<0.01);Model/OE-SNTB1+BBD组SNTB1的mRNA表达量有所下调(P<005)。Westernblot结果显示,与Model+AAV-NC组相比MAPK12/MAPK12的比值显著降低(P<0.01)而Model/OE-SNTB1+BBD组SNTB1蛋白表达量、pMAPK12/MAPK12的比值有所下降(P<005)。结论:SNTB1可能是八宝丹抑制结肠炎相关性结肠癌生成的重要靶标,过表达SNTB1能增强肠癌细胞的活力、增殖及转移能力,加重结肠炎相关性结肠癌小鼠的疾病严重程度。而使用八宝丹干预后,八宝丹可通过介导大肠癌细胞中SNTB1的表达,调控p38MAPK信号通路,进而发挥抑制大肠癌细胞增殖及转移的作用。同时八宝丹也可以靶向调节SNTB1的表达,缓解疾病活动指数,改善小鼠生存状态及病理情况;八宝丹也可以调控p38MAPK信号通路,从而发挥其抑制大肠癌转移和治疗大肠癌的目的。关键词:八宝丹,SNTB1,p38MAPK12信号通路,结肠炎相关性结肠癌,转移这段的
亲 完结了哦
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