Objective: To explore the active components, key targets, and mechanism of action of turnip in alleviating pulmonary fibrosis(PF) based on network pharmacology and animal experiments. Methods: The active components and targets of Brassica rapa L. were screened using the traditional Chinese medicine systems pharmacology database and analysis platform database, and PF-related targets were obtained from disease databases such as online mendelian inheritance of man(OMIM) and DrugBank. The intersection targets were used to construct a protein-protein interaction(PPI) network to identify core targets, followed by gene oncology(GO)/Kyoto encyclopedia of genes and genomes(KEGG) pathway enrichment analysis. In the animal experiments, a bleomycin-induced PF mouse model was established. Pathological changes in lung tissue were evaluated using HE and Masson staining. qRT-PCR was used to detect the mRNA expression of tumor necrosis factor-α(TNF-α), phosphatidylinositol 3-kinase(PI3K), and akstrain transforming 1(AKT1), and immunofluorescence staining was used to measure the protein expression of TNF-α, PI3K, and AKT1. Results: The 68 active components identified in Brassica rapa L. may regulate PI3K-Akt signaling pathway by acting on 89 potential targets such as TNF-α and AKT1. The results of animal experiments showed that polysaccharide of Brassica rapa L.(BRPs) could significantly reduce the degree of bleomycin induced pulmonary fibrosis in mice; HE and Masson staining of lung tissue showed that compared with the model group, the damage of alveolar structure, the infiltration of inflammatory cells and the deposition of collagen fibers in the BRPs treatment group were significantly reduced. Further mechanism studies showed that BRPs could significantly down-regulate the mRNA and protein expression levels of TNF-α, PI3K and AKT1 in lung tissue of pulmonary fibrosis mice. Conclusion Brassica rapa L. can synergistically alleviate pulmonary fibrosis through “multi-component, multi-target and multi-channel” approach; BRPs is one of the main active components, and plays an anti-fibrosis role by inhibiting TNF-α/PI3K Akt signaling pathway.

Objective:To develop the anti-CD30 monoclonal antibody 64Cu-1, 4, 7-trizacyclononane-1, 4, 7-triacetic acid (NOTA)-CD30 and visualize CD30 expression in lymphoma non-invasively. Methods:The CD30 expression levels of 5 cell lines (Karpas299, Raji, Daudi, Ramos, and U266) were assessed by Western blot. Cell lines with high and low CD30 expression were selected for flow cytometry to evaluate the specific binding affinity of anti-CD30 monoclonal antibody. Thirteen NSG mice were used to established CD30 positive and negative subcutaneous xenograft models. 64Cu-NOTA-CD30 was obtained and 64Cu-NOTA-immunoglobulin (Ig)G was used as the control. ImmunoPET imaging was performed 2, 24, and 48 h after the injection of 64Cu-NOTA-CD30 or 64Cu-NOTA-IgG. Finally, the biodistribution studies were conducted. Repeated-measures analysis of variance and Bonferroni test were conducted for comparison. Results:Karpas299 showed the highest CD30 expression, while Raji showed the lowest. Flow cytometry showed specific binding affinity of the anti-CD30 monoclonal antibody to the Karpas299 cell line. The radiochemical purities of the probes were both higher than 95%. In microPET, the 64Cu-NOTA-CD30 uptake of Karpas299 xenograft tumors increased over time, with (11.46±0.58), (17.60±1.16) and (19.46±0.99) percentage activity of injection dose per gram of tissue (%ID/g) at 2, 24 and 48 h respectively. The contrast to normal tissue was good at 48 h, with the tumor/heart (blood) ratio of 2.20±0.22. The uptake of 64Cu-NOTA-CD30 in Karpas299 tumor at 48 h after injection was significantly higher than that in Raji tumor ((6.10±1.03) %ID/g) and 64Cu-NOTA-IgG in Karpas299 tumor ((5.12±0.89) %ID/g; F=290.99, t values: 19.65 and 22.25, all P<0.001). The uptake of 64Cu-NOTA-CD30 and the control probe in the heart and liver decreased over time in all groups. Ex vivo biodistribution at 48 h was mainly consistent with the results of microPET in vivo. Conclusions:64Cu-NOTA-CD30 is able to visualize the expression level and distribution of CD30 non-invasively. It is promising to be applied for screening the beneficial groups and evaluating efficacy for CD30-targeted immunotherapy.

The use of monoclonal antibodies (mAbs) for cancer therapy has achieved considerable success in recent years. Approximate 17 monoclonal antibodies have been approved as cancer therapeutics since 1997. Antibody-drug conjugates (ADC) are powerful new treatment options for cancer, and naked antibodies have recently achieved remarkable success. The safety and effectiveness of therapeutic mAbs in oncology vary depending on the nature of the target antigen and the mechanisms of tumor cell killing. This review provides a summary of the current state of antibody-based cancer therapy, including the mechanisms of tumor cell killing by antibodies, tumor antigens as antibody targets, clinical effectiveness of antibodies in cancer patients and nanoparticles-based ADCs.

Objective To explore the effect of recombinant scFv (3G11)directed against type IV collagenase in combination with cisplatin on the therapy of hepatocellular carcinoma.Methods The effects of cisplatin on the type IV collagenase secreted by cancer cells were investigated by gelatin zymography analysis and Western-blot.The antitumor activity of scFv (3G11)in combination with cisplatin was evaluated by MTT assay in vitro and a mouse hepatoma 22 model in vivo.Results Cisplatin inhibited the activity of type IV collagenase.ScFv (3G11)in combination with cisplatin showed significant inhibition effects on the growth of hepatocellular carcinoma both in vitro and in vivo.The coefficient of drug interaction(CDI)was less than 1.Conclusions ScFv (3G11)in combination with cisplatin demonstrated synergetic effects on the therapy of hepatocellular carcinoma.