Objective: In an effort to inform evidence-based guidelines for clinical practice, we performed a meta-analysis to systematically evaluate the safety and efficacy of Kangai injection (KAI) plus platinum-based chemotherapy for stage III/IV non-small cell lung cancer (NSCLC). Methods: Randomized controlled trials (RCTs) comparing KAI plus platinum-based chemotherapy (experimental group) to chemotherapy alone (control group) were electronically retrieved from the Cochrane Library, PubMed, EMbase, Web of Science, Chinese National Knowledge Infrastructure (CNKI), Chinese Biological Medicine (CBM) Database, Wanfang Database, and the VIP Database for Chinese Technical Periodicals. RCTs published from the date of inception to July 5, 2018, were included. All trials were assessed for methodological quality in accordance with the Cochrane Reviewer's Handbook for Systematic Reviews of Intervention. Meta-analysis was performed using RevMan5.3 Software and Comprehensive Meta-Analysis (CMA) 2.0. Results: The final analysis included 35 RCTs involving 2,618 patients. Our meta-analysis revealed that KAI combined with platinum-based chemotherapy was associated with significantly greater objective response rate (ORR) (RR=1.36, 95% CI: 1.25-1.49, P<0.00001) and disease control rate (DCR) (RR=1.14, 95% CI: 1.09-1.18, P<0.00001), improvements in quality of life (QOL) (RR=1.75, 95% CI: 1.59-1.93, P<0.00001), and decreases in the incidence of gastrointestinal reactions (RR=0.64, 95% CI: 0.54-0.77, P<0.00001), leukocytopenia (RR=0.54, 95% CI: 0.46-0.63, P<0.00001) and thrombocytopenia (RR=0.52, 95% CI: 0.36-0.76, P=0.0007) when compared with chemotherapy alone. In addition, combined treatment was associated with greater regulation of tumor immune function, as indicated by increases in the proportion of NK, CD3 + , and CD4 + cells (MD=2.27, 95% CI: 1.18-3.36, P<0.0001; MD=12.86, 95% CI: 11.64-14.08, P<0.00001; and MD=5.48, 95% CI: 2.68-8.28, P=0.0001) and decreases in the percentage of CD8 + cells (MD=-2.37, 95% CI from-4.51 to-0.23, P=0.03). Conclusions: From the available evidence, our results indicate that KAI plus platinum-based chemotherapy could be more effective in improving clinical efficacy, decreasing the incidence of adverse reactions and regulating the tumor immune function than chemotherapy alone in the treatment of stage
Background. Astragali Radix-Curcumae Rhizoma (ARCR), a classic drug pair, has been widely used for the treatment of gastric intraepithelial neoplasia (GIN) in China. However, the underlying mechanisms of this drug pair are still unknown. Thus, elucidating the molecular mechanism of ARCR for treating GIN is imperative. Methods. The active components and targets of ARCR were determined from the TCMSP database, and the differentially expressed genes related to GIN were identified from the GSE130823 dataset. The protein-protein interaction (PPI) network and ARCR-active component-target-pathway network were constructed by STRING 11.0 and Cytoscape 3.7.2, respectively. In addition, a receiver operating characteristic curve (ROC) was conducted to verify the key targets, and enrichment analyses were performed using R software. Molecular docking was carried out to test the binding capacity between core active components and key targets. Results. 31 active components were obtained from ARCR, among which 22 were hit by the 51 targets associated with GIN. Gene Ontology (GO) functional enrichment analysis showed that biological process (BP), molecular function (MF), and cellular component (CC) were most significantly enriched in response to a drug, catecholamine binding, and apical part of the cell, respectively. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated ARCR against GIN through regulation of neuroactive ligand-receptor interaction, nitrogen metabolism, calcium signaling pathway, chemical carcinogenesis-receptor activation, drug metabolism, gap junction, and cancers. In the PPI network, 15 potential targets were identified, of which nine key targets were proven to have higher diagnostic values in ROC. Molecular docking revealed a good binding affinity of active components (quercetin, bisdemethoxycurcumin, and kaempferol) with the corresponding targets (CYP3A4, CYP1A1, HMOX1, DRD2, DPP4, ADRA2A, ADRA2C, NR1I2, and LGALS4). Conclusion. This study revealed the active components and molecular mechanism by which ARCR treatment is effective against GIN through regulating multipathway, such as neuroactive ligand-receptor interaction, nitrogen metabolism, and calcium signaling pathway.
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