ABSTRACT
Influenza is a severe respiratory infectious disease caused by influenza viruses. Due to the widespread prevalence, high morbidity and high mutation rate of influenza viruses, current anti-influenza drugs are not efficient and abundant. Development of novel anti-influenza virus agents is necessary and urgent nowadays. It is meaningful to investigate novel anti-influenza virus agents from traditional Chinese medicines, which is a great heritage and invaluable source for drug development. Though it is difficult to describe the mechanisms of traditional Chinese medicines clearly and comprehensively because of their characteristics of "multiple components and multiple targets", with more in-depth studies, many chemical constituents and action mechanisms of traditional Chinese medicines have been gradually reported nowadays. Most Chinese medicinal herbs could indirectly suppress influenza viruses and alleviate inflammation response via the regulation of cellular immune function of the host. However, studies on the traditional Chinese medicines that directly act on and target the influenza viruses are more complicated. Some of the traditional Chinese prescriptions, single traditional Chinese medicines and isolated compounds as well as their targets for the direct anti-influenza virus effects have been reported, including the familiar targets of hemagglutinin, neuraminidase, RNA polymerase, nucleoprotein complex and viral RNA, etc. This review summarizes the traditional Chinese prescriptions, single traditional Chinese medicines and isolated compounds, which show direct anti-influenza virus effects, in terms of their targets, so as to provide a reference for future studies.
ABSTRACT
OBJECTIVES@#To investigate the effect of Procyanidins (OPCs) on the autophagy of laryngeal cancer cell line TU686 and to explore the effect of OPCs on the chemosensitivity of laryngeal cancer cells to DDP in terms of autophagy and apoptosis.@*METHODS@#CCK-8 was used to detected the effect of different concentrations of OPC and DDP on TU686 cell viability. Experimental grouping: Both kinds of cells were divided into CON group, DDP group, OPC group and MIX group. Annexin-V-FITC/PI double staining of flow cytometry was used to detect the effect of each experimental group on the apoptosis. Cell immunofluorescence staining was used to detect the formation of autophagy. Western blot was used to detect the expression of autophagy-related and apoptosis-related proteins. Autophagy inhibitors (3-MA) were used to study the effect of autophagy on apoptosis.@*RESULTS@#The results of CCK-8 showed that TU686 cells were inhibited by OPC and DDP in a concentration-dependent manner for 24 hours. LC3-Ⅱ protein staining showed that compared with CON group, DDP group and OPC group, MIX group significantly induced autophagy formation in TU686 cells (<0.05). Flow cytometry showed that compared with CON group, apoptosis of TU686 cells was induced in DDP group, OPC group and MIX group. And the effect of MIX on apoptosis was significantly higher than that of OPC and DDP groups (<0.05). After pretreatment with 3-MA, the apoptotic effect of OPC group and MIX group on TU686 cells was significantly decreased (<0.05). Western blot results showed that the expression of LC3-Ⅱ and Caspase-3 in DDP, OPC and MIX groups was significantly higher than that in CON group (<0.05). In MIX group, the expression of LC3-Ⅱ and Caspase-3 also had significant difference (<0.05) compared with single drug group. After using 3-MA to inhibit autophagy, the expression of LC3-Ⅱ was significantly decreased (<0.05), and the expression of Caspase-3 was decreased along with LC3-Ⅱ, but the decrease of Caspase-3 expression was only significant in OPC and MIX group (<0.05).@*CONCLUSIONS@#OPC can induce autophagy in laryngeal carcinoma TU686 cells and promote its apoptosis, which in turn enhances sensitivity of laryngeal cancer cells to cisplatin chemotherapy.
Subject(s)
Humans , Antineoplastic Agents , Apoptosis , Apoptosis Regulatory Proteins , Autophagy , Cell Line, Tumor , Cisplatin , Pharmacology , Drug Resistance, Neoplasm , Laryngeal Neoplasms , Drug Therapy , Proanthocyanidins , PharmacologyABSTRACT
<p><b>UNLABELLED</b>To screen and analyze the apoptosis- and proliferation-related genes in human nasopharyngeal carcinoma (NPC).</p><p><b>METHODS</b>According to gene ontology classification, the abnormal expressions of the genes related to cell apoptosis and proliferation were identified in the NPC gene chip data. The cell apoptosis- and proliferation-related genes expressed in each of the 3 stages, as defined by the tree model for the pathogenesis and progression of NPC, were screened, and with literature review, their distribution in the tree model were analyzed.</p><p><b>RESULTS</b>Nineteen genes related to cell apoptosis were found in NPC, among which 9 were down-regulated (such as DNASE1L3) and located in the chromosome deletion regions, and 10 were up-regulated (such as DEDD) in the chromosome amplification regions. Twenty-one cell proliferation-related genes were identified, including 8 down-regulated genes (such as TUSC2) in the chromosome deletion regions and 13 up-regulated ones (such as EMP1) in the chromosome amplification regions. In the chromosome deletion regions, the down-regulated cell apoptosis-related genes participated mostly in inducing and regulating cell apoptosis, and the up-regulated cell proliferation-related genes in the chromosome amplification regions were mostly associated with the positive regulation of cell proliferation.</p><p><b>CONCLUSION</b>NPC occurs possibly through two pathways by inhibiting cell apoptosis or by promoting excessive cell proliferation.</p>