Network pharmacology provides a systematic approach to understanding the treatment of ischemic heart diseases with traditional Chinese medicine.

BACKGROUND: The field of network pharmacology showed significant development. The concept of network pharmacology has many similarities to the philosophy of traditional Chinese medicine (TCM), making it suitable to understand the action mechanisms of TCM in treating complex diseases, such as ischemic heart diseases (IHDs). PURPOSE: This review summarizes the representative applications of network pharmacology in deciphering the mechanism underlying the treatment of IHDs with TCM. METHODS: In this report, we used "ischemic heart disease" OR "coronary heart disease" OR "coronary artery disease" OR "myocardial ischemia" AND ("network pharmacology" OR "systematic pharmacology") as keywords to search for publications from PubMed, the Web of Science, and Google Scholar databases and then analyzed the representative research reports that summarized and validated the active components and targets network of TCM in improving IHDs to show the advantages and deficiencies of network pharmacology applied in TCM research. RESULTS: The network pharmacology research indicated that HGF, PGF, MMP3, INSR, PI3K, MAPK1, SRC, VEGF, VEGFR-1, NO, eNOS, NO3, IL-6, TNF-α, and more are the main targets of TCM. Apigenin, 25S-macrostemonoside P, ginsenosides Re, Rb3, Rg3, SheXiang XinTongNing, colchicine, dried ginger-aconite decoction, Suxiao Xintong dropping pills, Ginseng-Danshen drug pair and Shenlian and more are the active ingredients, extracts, and formulations of TCM to ameliorate IHDs. These active compounds, extract, and formulations of TCM treat IHDs by delaying ventricular remodeling, reducing myocardial fibrosis, decreasing reactive oxygen species, regulating myocardial energy metabolism, ameliorating inflammation, mitigating apoptosis, and many other aspects. CONCLUSIONS: The network pharmacology supplies a novel research exemplification for understanding the treatment of IHDs with TCM. However, the application of network pharmacology in TCM studies is still at a superficial level. By rational combining artificial intelligence technology and network pharmacology, molecular biology, metabolomics, and other advanced theories and technologies, and systematically studying the metabolic process and the network among products, targets, and pathways of TCM from the clinical perspective may be a potential development trend in network pharmacology.

[Retracted] Long intergenic non­protein coding RNA 152 promotes multiple myeloma progression by negatively regulating microRNA­497.

Following the publication of this paper, an interested reader drew the authors' attention to the fact that several of the tumour images shown in Fig. 6B were strikingly similar to images that had appeared in another paper by different authors published at around the same time. The authors also admitted that the in vivo experiments reported in this study had been performed by a third party. Consequently, owing to a lack of confidence in the presented data, the authors requested that this paper be retracted from the Journal. The Editor was in agreement that the paper should be retracted. All authors agree with the retraction of this article, and the Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 40: 3763­3771, 2018; DOI: 10.3892/or.2018.6721].

microRNA­577 inhibits cell proliferation and invasion in non­small cell lung cancer by directly targeting homeobox A1.

An increasing number of studies have indicated that the dysregulation of microRNAs (miRNAs/miR) is closely associated with non­small cell lung cancer (NSCLC) development and progression by acting as tumor suppressors or oncogenes. Therefore, an in­depth understanding of the biological roles of miRNAs in NSCLC may provide novel therapeutic methods for the treatment of patients with this disease. In the present study, reverse transcription­quantitative polymerase chain reaction was used to detect miR­577 expression in NSCLC tissues and cell lines. Cell Counting Kit­8 and Transwell invasion assays were performed to determine the effects of miR­577 on NSCLC cell proliferation and invasion. Luciferase reporter assays were used to demonstrate the relationship between miR­577 and homeobox A1 (HOXA1) in NSCLC cells. The results revealed that miR­577 was markedly downregulated in NSCLC tissues and cell lines. Additionally, restoration of miR­577 expression significantly decreased the proliferation and invasion of NSCLC cells. Furthermore, miR­577 negatively regulated HOXA1 expression in NSCLC cells by directly binding to its 3'­untranslated region. HOXA1 was significantly upregulated in NSCLC tissues, and its upregulation was inversely correlated with miR­577. Notably, restored HOXA1 expression abrogated the reduced proliferation and invasion of NSCLC cells caused by miR­577 overexpression. Taken together, these results indicated that miR­577 may have served tumor suppressive roles in NSCLC by directly targeting HOXA1. Therefore, this miRNA may be developed as a potential therapeutic target for the therapy of patients with NSCLC.

Role of miR-214 in modulating proliferation and invasion of human colon cancer SW620 cells.

This study investigated the role of miR-214 in modulating proliferation and invasion of human colon cancer SW620 cells. Fifty-five patients with colon cancer who were treated in China-Japan Union Hospital of Jilin University from March 2014 to March 2015 were enrolled into this study. Their cancer and corresponding paracancerous tissues were collected and the expression levels of miR-214 were determined by RT-qPCR. A miR-214 expression vector was constructed. SW620 cells were transfected with the miR-214 expression vector and a blank vector. Cells transfected with the miR-214 expression vector were assigned to the miR-214 positive group and cells transfected with the blank vector were assigned to the miR-214 negative group. Cell proliferation, invasion and apoptosis were assessed by MTT assay, Transwell migration assay and TUNEL apoptosis assay, respectively. The RT-qPCR results showed that the expression level of miR-214 in colon cancer tissue, as well as in miR-214 negative cells, was significantly lower than that in paracancerous tissue (P<0.05 for both). In cell comparison, the expression level of miR-214 in the miR-214 positive group was significantly higher than that in the miR-214 negative group (0.483±0.001 vs. 0.172±0.001; P<0.05). The proliferation level of SW620 cells in the miR-214 positive group was lower than that in the miR-214 negative group (P<0.05). The Transwell migration assay indicated that there were less cells penetrating the membrane in the miR-214 positive group than in the miR-214 negative group (P<0.05). In addition, The apoptosis rate of cells in the miR-214 negative group was significantly lower than that in the miR-214 positive group (P<0.05). Finally, the low expression of miR-214 was found in colon cancer, indicating that miR-214 is a cancer suppressor playing an opposing role in colon cancer onset and progression. Therefore, miR-214 can promote apoptosis of colon cancer cells SW620 by inhibiting their proliferation and invasion.

Long intergenic non­protein coding RNA 152 promotes multiple myeloma progression by negatively regulating microRNA­497.

Long intergenic non­protein coding RNA 152 (LINC00152, also known as cytoskeleton regulator RNA) is reportedly involved in the development and progression of various types of human malignancy. However, the functional role of LINC00152 in multiple myeloma (MM) and the underlying molecular mechanisms have remained elusive. The present study aimed to investigate the role of LINC00152 in the genesis of MM and the potential molecular mechanisms. It was identified that the expression of LINC00152 was significantly upregulated in plasma cells from patients with MM vs. healthy subjects, and that a high expression of LINC00152 was correlated with a shorter overall survival in patients with MM. Functional assays demonstrated that knockdown of LINC00152 by transfecting MM cells with LINC00152­specific short hairpin RNA expression plasmids significantly inhibited cell proliferation by inducing cell cycle arrest at the G0/G1 phase. Furthermore, knockdown of LINC00152 promoted caspase­3/9 activity and apoptosis in MM cells. In addition, knockdown of LINC00152 significantly attenuated tumor growth in mice bearing a myeloma xenograft. A luciferase reporter assay indicated that microRNA (miR)­497 is a direct target of LINC00152, and its expression levels were inversely correlated with those of LINC00152 in MM tissues. Furthermore, repression of miR­497 partly abrogated the inhibitory effects of LINC00152 knockdown on MM cells. Collectively, the results indicated that LINC00152 has an oncogenic effect in MM by targeting miR­497, and may be a novel diagnostic marker and therapeutic target for MM.

Analyse clinique du traitement du plasmodium falciparum a l'artesunate

Depuis le mois de decembre 1992; les auteurs ont traite 30 malades atteints de paludisme a plasmodium falciparum par l'artesunate en perfusion; en comparaison avec un autre groupe de malades qui; cette fois; ont ete traites par du quinimax en perfusion egalement. De part et d'autre ces groupes de malades ont supporte le traitement pendant 3 jours. Les malades soumis a l'artesunate ont eu chacun une dose totale de 240 mg. Ceux soumis au quinimax ont eu chacun 2400 mg au total. Le temps moyen de l'artesunate pour faire baisser la temperature et eliminer le plasmodium est plus court et plus rapide que celui du quinimax. Le taux de recidive avec l'artesunate est tres faible et les effets secondaires sont pratiquement rares. Il est vrai que c'est un nouveau medicament; mais nos observations montrent deja qu'il est d'une tres bonne qualite; tres efficace comme antipaludeen; et que les praticiens peuvent l'utiliser sans crainte pour le moment