目的：开发肽-树状聚合物-紫杉醇偶联物，用于治疗293t和l132细胞系中的异种1期非小细胞肺癌（nsclc）。方法：采用nhs方法制备树状大分子-紫杉醇共轭物（pamam-ptx），并用于合成肽类-树状大分子-紫杉醇共轭物（ge-pamam-ptx）。测量了pamam-ptx和ge-pamam-ptx的粒度。

... evaluate the therapeutic efficacy of Tf-Glu-PTX and its potential cytotoxicity, cell viability assays were carried out in cancer cells (MCF7) and normal cells (293T). The results in Fig. 4A...

细胞冷冻与复苏是细胞培养的常规工作，可以解决细胞因为连续继代造成的退变或转化。 细胞冻存及复苏的基本原则是 慢冻快融，实验证明这样可以最大限度的保存细胞活力。 复苏细胞应采用快速融化的方法，这样可以保证细胞外结晶在很短的时间内即融化，避免由于缓慢融化使水分渗入细胞内形成胞内再结晶对细胞造成损伤。 三、步骤： （一）材料准备： 1. 仪器：净化工作台、 离心机、恒温水浴箱、冰箱（4℃、-20℃、-80℃）、倒置显微镜、培养箱、微量加样器。 2. 耗 …

2022年5月20日 · HEK-293人胚肾细胞：是用5型腺病毒75株系转化，含有Ad5 E1区的人胚肾亚三倍体细胞系，是一种E1区缺陷互补细胞系。 它是加拿大McMaster University 的F.L.Graham与J.S.Miley于1976年用DNA转染技术构建而成。 该细胞为人类腺病毒载体扩增的宿主。 可表达异常的玻连蛋白的细胞表面受体，由整合素β1亚单位和玻连蛋白受体α-v亚单位组成。 HEK-293T人胚肾细胞：人胚肾细胞293细胞插入SV40 T-抗原基因后产生的高转染效率的衍生株称为293T。 …

2025年2月21日 · 在 hepg2 细胞中，ptx + rnp-oct/cs/nps 对 pd-l1 基因的编辑效率达到了 55.8%，在稳定表达绿色荧光蛋白的 293t 细胞（gfp-293t）中，rnp-oct/cs/nps 也成功编辑了 gfp 基因。

PAMAM-PTX, GE-PAMAM-PTX, PAMAM and PTX was evaluated by 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide (MTT) assay using 293T cell lines. In vitro cellular uptake assay of PAMAM-PTX and GE-PAMAM-PTX and PTX at concentrations ranging from 0.01 to 0.5µM for 8 h was carried out in NSCLC cell lines 293T and L132.

2017年5月4日 · Purpose: To develop peptide-dendrimer-paclitaxel conjugates for the treatment of heterogeneous stage 1 non small cell lung cancer (NSCLC) in 293T and L132cell line. Method: Dendrimer-paclitaxel conjugates (PAMAM-PTX) were prepared by NHS method and the conjugates were used for the synthesis of peptide-dendrimer …

Phase-contrast microscopy images of untreated 293T cells (A), 293T cells treated with DMSO only (B), and 293T cells treated with 5 nM PTX (C), 10 nM PTX (D), 50 nM PTX (E) and 100 nM...

The identified proteins in 293T cell-derived exosomes were analyzed by GO (B) biological process, (C) cellular component, and (D) molecular function annotation, as well as (E) KEGG pathway and (F...

Then the chemotherapeutic drugs, such as PTX, the ncRNAs, such as miR-551-3p, immune molecules, such siPDL1, were released into the tumor microenvironment (TME). Thereafter, the internalization of engineered exosomes led to tumor cell death, such as ferroptosis