ISSN 1004-6879

CN 13-1154/R

 
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Exploring the mechanism of cordycepin in the treatment of non-small cell lung cancer based on network pharmacology and in vitro experiments
ZHANG Jiahui, JIANG Xinyu, LI Yanchao, LI Mei, CHEN Jingjing, GUO Yachun
Abstract2)      PDF (9073KB)(0)      
Objective To explore the mechanism of cordycepin (Cor) in the treatment of non-small cell lung cancer ( NSCLC ) by network pharmacology, molecular docking and in vitro experiments. Methods Multiple databases were used to search the targets of Cor and the therapeutic targets of NSCLC, and the common targets were screened out. STRING database and Cytostape were used to analyze and visualize the protein-protein interaction networks (PPI). GO and KEGG enrichment analysis was performed using the DAVID database, and the results were visualized using the online tool “Weishengxin”. AutoDock Vina was used to verify the molecular docking of Cor with the core target, and the binding energy was calculated. PyMol was used to visualize the results. MTT assay was used to detect the effect of Cor on the proliferation of NSCLC A549 cells. Western blot was used to detect the effect of Cor on the expression of core target proteins PARP1, P53 and AKT1. Results A total of 215 targets of Cor and 1238 therapeutic targets of NSCLC were screened, and 122 common targets were obtained. After PPI analysis, the core targets PARP1, P53 and AKT1 were selected according to Degree value for verification. The results of GO and KEGG enrichment analysis showed that biological process (BP) mainly involved apoptosis process, positive and negative regulation of gene expression, cellular component ( CC ) mainly involved cytoplasm and nucleus, molecular function (MF) mainly involved protein binding and enzyme binding, and signaling pathways mainly involved cancer, PI3K / AKT and other signaling pathways. Molecular docking showed that the three targets of PARP1, P53 and AKT1 were highly correlated with the treatment of NSCLC. In vitro experiments showed that Cor could inhibit the proliferation of human NSCLC A549 cells, significantly up-regulate the expression of P53 and PARP1 and down-regulate the expression of AKT1. Conclusion Cor inhibits the proliferation of human NSCLC A549 cells, and the mechanism may be related to the regulation of PARP1, P53 and AKT1 expression.
2026, 43 (1): 6-12.
The Levels and Value of HIF-1α, SP-D, and Copeptin in COPD Patients with Type II Respiratory Failure
LI Mei-xia, WU Na-na
Abstract137)      PDF (6239KB)(7)      
Objective To investigate the changes of serum hypoxia-inducing factor 1α (HIF-1α), pulmonary surfactant protein D (SP-D), and Copeptin levels in patients with chronic obstructive pulmonary disease (COPD) complicated with type II respiratory failure, and to analyze their prognostic value. Methods A total of 120 patients with COPD combined with type II respiratory failure admitted to 988 Hospital of Chinese People's Liberation Army Joint Logistic Support Force from January 2020 to January 2023 were selected as the study objects, and were divided into poor prognosis group and good prognosis group according to the survival status within 28 days of treatment. Compare clinical data and serum levels of HIF-1 , SP-D, and Copeptin between two groups. Use receiver operating characteristic curve (ROC) to analyze the predictive value of serum indicators for prognosis. Results After 7 days of treatment, the serum levels of HIF-1α, SP-D, and Copeptin in the poor prognosis group were higher than those in the good prognosis group (P<0.05); the serum levels of HIF-1α, SP-D, and Copeptin were positively correlated with APACHE II score, cTnT, NT proBNP, and CRP (P<0.05); the AUC predicted by HIF-1α+SP-D+Copeptin was higher than that predicted by single index and predicted by any two indexes (P<0.05). Conclusion The increase of serum HIF-1α, SP-D and Copeptin levels is closely related to poor prognosis and severity of COPD patients with type 2 respiratory failure, which has important clinical significance in predicting prognosis.
2024, 41 (5): 372-377.
Molecular Identification of Tick-borne Zoonotic Anaplasma and Rickettsia in Ticks
REN Qing, LI Mei-chen, ZHANG Jia-ming, DU Luan-ying, GUO Wen-ping, XIE Guang-cheng
Abstract161)      PDF (8508KB)(31)      
Objective To investigate the prevalence and species of tick-borne Rickettsiales in rural areas of Chengde City, and to provide a theoretical basis for the prevention and control of diseases caused by tick-borne Rickettsiales. Methods Total DNA was extracted from ticks collected from Sangou Town and Liugou Town of Chengde City, and the 16S rRNA gene was amplified by nested PCR to identify Rickettsiae bacteria. The heat shock protein(groEL) gene of Anaplasma and outer membrane protein A (ompA) gene of Rickettsia were amplified and sequenced for homology and phylogenetic analysis to identify the pathogens of tick-borne zoonotic Anaplasma and Rickettsia. Results A total of 336 ticks were collected from Sangou Town and Liugou Town, and all of them were identified as Haemaphysalis longicornis. The positive rate of Anaplasma was 25.3% (85/336) in ticks and 17.3% (58/336) in Rickettsia. The positive rate of Anaplasma in ticks was significantly higher than that in Rickettsia (P=0.01). The positive rates of Anaplasma capra and Anaplasma ovis were 8.3% (28/336) and 17.0% (57/336), respectively. The positive rate of Rickettsia sibirica and Rickettsia raoultii was 3.6% (12/58) and 6.3% (21/58), respectively. The positive rate of Candidatus Rickettsia jingxinensis was 7.4% (25/58). Conclusion Two zoonotic Anaplasma and three Rickettsia species were identified in H. longicornis in Chengde, indicating that Rickettsiae bacteria prevalent in rural areas around Chengde present high genetic diversity. And it is necessary to strengthen the monitoring and prevention and control of ticks and tick-borne pathogens in Chengde.
2023, 40 (3): 190-195.
Expression of LncRNA TCONS_00022381 in Gastric Cancer and Its Effect on Proliferation of SGC-7901 Cells
LI Mei-chuan, LIU Ming-wei, ZHAO Yi-na, WANG Xiao-jie, LI Xin
Abstract141)      PDF (2067KB)(156)      
Objective To detect the expression of LncRNA TCONS_00022381 in gastric cancer and its effect on proliferation of SGC-7901 cells. Methods The expression of[] LncRNA TCONS_00022381 was determined by real-time quantitative PCR in gastric cancer samples and cell lines. The gastric cancer SGC-7901 cells were grouped into interference group, negative control group and blank group. The gastric cancer cells transfected with siRNA targeted to LncRNA TCONS_00022381 was designated as siRNA interference group, while named those transfected with scrambled siRNA as negative control group and the cells without any treatment as blank group. After transfection of 48 hours, real-time quantitative PCR was used to detect the suppression of LncRNA TCONS_00022381. The proliferation of each group was detected by MTT assay. The expression of proliferating nuclear antigen (PCNA) in each group was detected by Western blot. Results LncRNA TCONS_00022381 was up-regulated in both gastric cancer tissue samples and cell lines (P<0.05). siRNA transfection could significantly reduce the expression of LncRNA TCONS_00022381 in SGC-7901 cells(P<0.05). Compared with the negative and blank groups, the MTT assay showed that the proliferation activity and the PCNA expression were significantly down-regulated (P<0.05). Conclusion LncRNA TCONS_00022381 is highly expressed in gastric cancer and play a role in promoting the proliferation of gastric cancer cells.
2021, 38 (2): 96-99.