More than 50 new flavonoids derived from Annonaceae are reported in the last two decades. Many genuses in Annonaceae contain flavonoids having structural novelty and broad pharmacological activities. Due to the pharmacological interest of some of these compounds, chemical investigations on this topic have grown considerably in the decades. Here the biological activities of some of these flavonoids are also briefly discussed.
Annonaceae ; chemistry ; classification ; Antineoplastic Agents, Phytogenic ; chemistry ; isolation & purification ; pharmacology ; Cell Line, Tumor ; Cell Survival ; drug effects ; Flavonoids ; chemistry ; isolation & purification ; pharmacology ; Humans ; Inhibitory Concentration 50 ; Molecular Structure ; Plants, Medicinal ; chemistry

Objective To explore a better method for treatment atrophic rhinitis.Methods 56 patients with atrophic rhinitis(96 lateral)were treated by nasal submucou pediculated bone-suberiosteal muscle flap extracted from anterior wall of sinus maxillaries.Results All patients were followed 2 to 10 years,total effective rate was 100 %, with 49 cases(87.5 %)showing prominent effect.Conclusion The grafted flap cannot be assimilated,felled off and necrosis,because the flap has rich blood supply.This methods has obvious short-term effective and stable long-term effective.No complications were found.

OBJECTIVETo determine the expression level of Smad ubiquitination regulatory factor 1 (SMURF1) gene in hepatocellular carcinoma, and to explore its role in liver cancer.

METHODSWith non-neoplastic adjacent normal tissues as controls, real-time PCR and Western blotting were used for measuring the expression of SMURF1 mRNA and protein in 89 samples of hepatocellular carcinoma. Correlations between SMURF1 expression and clinical features were explored. Following transfection of SMURF1--specific small interference RNA(siRNA), the apoptosis and proliferation of hepatic cancer cells Hep G2 were detected using flow cytometry and MTT assays .

RESULTSThe expression of SMURF1 mRNA and protein were significantly higher in hepatocellular cancer tissues compared with the paired normal tissues (P< 0.05). The expression of SMURF1 however did not correlate with any clinical features (P> 0.05). Transfection of SMURF1-specific siRNA can promote the apoptosis whilst inhibit the proliferation of Hep G2 cells.

CONCLUSIONThe expression of SMURF1 is enhanced in hepatocellular carcinoma, which may have played a role in the disease through affecting apoptosis and proliferation of hepatic cancer cells.

Female ; Hep G2 Cells ; Humans ; Liver Neoplasms ; pathology ; Male ; RNA, Messenger ; analysis ; Transforming Growth Factor beta ; physiology ; Ubiquitin-Protein Ligases ; genetics ; physiology

OBJECTIVETo investigate the effect of nano-TiO(2) intratracheal instillation on the progression of dyslipidemia and atherosclerosis in apolipoprotein E-knockout mice.

METHODSThe nano-TiO(2) was ultrasound with phosphate-buffered saline solutions (PBS) into its suspension for exposure. A total of 46 specific pathogen free (SPF) level of 11-week-old male apolipoprotein E-knockout mice were randomly divided into groups by their body weights: non-treatment group (8 mice), PBS control group (9 mice), high dose group (1.0 mg/ml, 10 mice), medium dose group (0.5 mg/ml, 10 mice), and low dose group (0.1 mg/ml, 9 mice). Except the non-treatment group, mice from other groups were intratracheally instilled with 0.05 ml each time, twice a week. After exposure of 6 weeks, viscera index, blood TC, TG, HDL-C, LDL-C, and organic lipid ratio were assessed as biomarkers. Artery and aortic root issues were assessed by histopathology.

RESULTSAfter 5 weeks exposure, mice body weights in high dose group ((29.7 ± 1.9) g) started to drop, compared to PBS control ((31.3 ± 1.9) g, t = -1.58, P < 0.05) and low dose group ((31.4 ± 1.4) g, t = -1.17, P < 0.05); after 6 weeks, high dose group ((28.8 ± 1.5) g) was lower than PBS control ((30.4 ± 1.9) g, t = -1.60, P < 0.05), non-treatment group ((30.2 ± 1.3) g, t = -1.43, P < 0.05) and low dose group ((30.6 ± 1.0) g, t = -1.83, P < 0.05). TC levels of non-treatment, PBS control, high dose group, medium dose group and low dose group were (2.92 ± 1.18), (3.12 ± 0.73), (4.19 ± 1.86), (3.46 ± 0.72) and (2.57 ± 0.64) mmol/L, respectively; TG levels were (0.39 ± 0.13), (0.39 ± 0.08), (0.60 ± 0.21), (0.55 ± 0.19) and (0.41 ± 0.11) mmol/L, respectively; HDL-C levels were (1.67 ± 0.45), (1.54 ± 0.67), (0.93 ± 0.50), (1.02 ± 0.48) and (1.31 ± 0.64) mmol/L; TG levels of high dose group were higher than that of non-treatment group (t = 1.27, P = 0.03) and low dose group (t = 1.62, P = 0.01); TG levels of medium dose group was higher than PBS control (t = 0.16, P = 0.04), and TC levels of high dose group were higher than PBS control (t = 0.22, P = 0.01), non-treatment group (t = 0.22, P = 0.04) and low dose group (t = 0.20, P = 0.03), and HDL-C levels of high dose group were lower than PBS control (t = -0.61, P = 0.04) and non-treatment group (t = -0.74, P = 0.04); organic lipid ratio of each group were (2.27 ± 0.51)%, (2.06 ± 0.53)%, (2.90 ± 0.50)%, (2.60 ± 0.23)%, (2.24 ± 0.45)%; high dose group were higher than PBS control (t = 0.85, P = 0.00), non-treatment group (t = 0.64, P = 0.03) and low dose group (t = 0.67, P = 0.01); medium dose group was higher than PBS control (t = 0.54, P = 0.02). The plaque lipid content and calcium content which showed the progression of atherosclerosis and plaque rupture were elevated in medium and high dose groups.

CONCLUSIONIntratracheal instillation of nano-TiO(2) can induce dyslipidemia and accelerate the development of atherosclerosis and plaque rupture in ApoE-/-mice.

Animals ; Apolipoproteins E ; genetics ; Atherosclerosis ; blood ; chemically induced ; Dyslipidemias ; blood ; chemically induced ; Instillation, Drug ; Lipid Metabolism ; Lipids ; blood ; Male ; Mice ; Mice, Knockout ; Nanoparticles ; Specific Pathogen-Free Organisms ; Titanium ; administration & dosage ; pharmacology

To explore the anti-HSV-1 effect of silencing gD gene expression by RNA interference, five 21-nucleotide duplex small interfering RNAs(siRNAs) targeting the HSV1 gD sequence were designed and the gD-EGFP fusion gene expression vector was constructed, then co-transfected into Vero cell, and screened the effective siRNA through analyzing the intensity of the EGFP fluorescence. Finally, the anti-HSV1 effect was confirmed by plaque reduction assay, real-time PCR and daughter virus titration of HSV1 infected Vero cells transfected with siRNAs. The study demonstrated that siRNAs could effectively and specifically inhibit gD gene expression in HSV1-infected cells, but only had a little effect on HSV1 infection, so taking gD as the target of siRNA against HSV1 needs further study.
Animals ; Cercopithecus aethiops ; Genetic Vectors ; genetics ; Green Fluorescent Proteins ; genetics ; metabolism ; Herpesvirus 1, Human ; genetics ; Humans ; Polymerase Chain Reaction ; RNA Interference ; RNA, Small Interfering ; genetics ; Recombinant Fusion Proteins ; genetics ; metabolism ; Transfection ; Vero Cells ; Viral Envelope Proteins ; genetics ; metabolism

Actin-like 6A (ACTL6A), also known as BAF53A, is an SWI / SNF subunit of chromatin-remodeling factors and plays an important role in regulating stem cell function. Recent studies found that ACTL6A was involved in tumor occurrence and development. However, the mechanism of ACTL6A in cisplatin resistance is still unclear. This study investigated the biological function and molecular mechanism of ACTL6A in maintaining cancer stem cell function and cisplatin resistance. First, analysis from TCGA, GEO, and GEPIA databases showed that ACTL6A expression levels in lung adenocarcinoma (LUAD) tissues and cisplatin resistant cells were dramatically higher than that in adjacent normal tissues and cisplatin sensitive cells (P < 0. 05), and ACTL6A high expression was positively associated with a poor prognosis of LUAD. Knockdown of ACTL6A enhanced cisplatin sensitivity (P < 0. 05), reduced tumor sphere (P<0. 05), inhibited cell migration (P<0. 05), and promoted cell apoptosis (P<0. 05) in A549 cells. Western blotting showed that knockdown of ACTL6A increased the protein expression of E-cadherin, and decreased the protein expression of N-cadherin, vimentin, and twist. Moreover, knockdown of ACTL6A inhibited the expression of cancer stem cell markers, including ALDH3A1, ALDH4A1, SOX2, OCT4, and Nanog. Subsequently, Hippo / YAP signaling-related proteins were analyzed by Western blotting. The results showed the expression of beta-TRCP and YAP was decreased in A549 cell with knockdown of ACTL6A. However, phosphorylation levels at S127 and S397 of YAP were increased and inhibited translocation of YAP into the nucleus for regulating related gene expression. In summary, ACTL6A maintained the stemness of lung cancer stem cells and promoted cisplatin resistance in A549 cells by inhibiting activation of the Hippo signaling pathway.

Aim To evaluate the effect of ZST93 on the proliferation in human chronic myeloid leukemia(CML)cells(K562)and explore the possible mechanism.Methods MTT assay, cell growth curve and inverted microscope were used to investigate the effect of ZST93 on proliferation of K562 cells.Cell transfection and Western blot were performed to detect the autophagy, while PI staining, Annexin V-FITC/PI and flow cytometry were conducted to determine cell apoptosis and its anticancer mechanism.Results ZST93 could significantly inhibit the proliferation of K562(IC50=2.59 μmol·L-1)and induce cell cycle arrest at G1-phase in a dose- and time-dependent manner.Also, through leading to accumulation of GFP-LC3, transition into LC3- II from LC3- 1 , and decrease of p62 expression, ZST93 induced autophagy initiation and autophagic flux.Furthermore, ZST93 induced extrinsic apoptotic pathway by activating caspase-8, and further promoted the cleavage of apoptosis related proteins including caspase-9, caspase-3 and PAR P.Moreover, Z-DEYD-FMK, the specific inhibitor of caspase-3 , could dramatically reduce the apoptosis induced by ZST93.Taken together, ZST93 could effec tively inhibit CML cells, arrest eell cycle at G,-phase, induce cell apoptosis anrl initiate autophagy.Conclusions The potential mechanism may he related to the regulation of autophagy intiation/caspase-8/caspase-3 signaling pathway, which provides a new idea and theoretical basis for the treatment of CML.

Background: Human infections with zoonotic coronaviruses (CoVs), including severe acute respiratory syndrome (SARS)-CoV and Middle East respiratory syndrome (MERS)-CoV, have raised great public health concern globally. Here, we report a novel bat-origin CoV causing severe and fatal pneumonia in humans. Methods: We collected clinical data and bronchoalveolar lavage (BAL) specimens from five patients with severe pneumonia from Jin Yin-tan Hospital, Wuhan, Hubei province, China. Nucleic acids of the BAL were extracted and subjected to next-generation sequencing. Virus isolation was carried out, and maximum-likelihood phylogenetic trees were constructed. Results: Five patients hospitalized from December 18 to December 29, 2019 presented with fever, cough, and dyspnea accompanied by complications of acute respiratory distress syndrome. Chest radiography revealed diffuse opacities and consolidation. One of these patients died. Sequence results revealed the presence of a previously unknown β-CoV strain in all five patients, with 99.8–99.9% nucleotide identities among the isolates. These isolates showed 79.0% nucleotide identity with the sequence of SARS-CoV (GenBank NC_004718) and 51.8% identity with the sequence of MERS-CoV (GenBank NC_019843). The virus is phylogenetically closest to a bat SARS-like CoV (SL-ZC45, GenBank MG772933) with 87.6–87.7% nucleotide identity, but is in a separate clade. Moreover, these viruses have a single intact open reading frame gene 8, as a further indicator of bat-origin CoVs. However, the amino acid sequence of the tentative receptor-binding domain resembles that of SARS-CoV, indicating that these viruses might use the same receptor. Conclusion: A novel bat-borne CoV was identified that is associated with severe and fatal respiratory disease in humans.

BACKGROUND: Human infections with zoonotic coronaviruses (CoVs), including severe acute respiratory syndrome (SARS)-CoV and Middle East respiratory syndrome (MERS)-CoV, have raised great public health concern globally. Here, we report a novel bat-origin CoV causing severe and fatal pneumonia in humans. METHODS: We collected clinical data and bronchoalveolar lavage (BAL) specimens from five patients with severe pneumonia from Wuhan Jinyintan Hospital, Hubei province, China. Nucleic acids of the BAL were extracted and subjected to next-generation sequencing. Virus isolation was carried out, and maximum-likelihood phylogenetic trees were constructed. RESULTS: Five patients hospitalized from December 18 to December 29, 2019 presented with fever, cough, and dyspnea accompanied by complications of acute respiratory distress syndrome. Chest radiography revealed diffuse opacities and consolidation. One of these patients died. Sequence results revealed the presence of a previously unknown β-CoV strain in all five patients, with 99.8% to 99.9% nucleotide identities among the isolates. These isolates showed 79.0% nucleotide identity with the sequence of SARS-CoV (GenBank NC_004718) and 51.8% identity with the sequence of MERS-CoV (GenBank NC_019843). The virus is phylogenetically closest to a bat SARS-like CoV (SL-ZC45, GenBank MG772933) with 87.6% to 87.7% nucleotide identity, but is in a separate clade. Moreover, these viruses have a single intact open reading frame gene 8, as a further indicator of bat-origin CoVs. However, the amino acid sequence of the tentative receptor-binding domain resembles that of SARS-CoV, indicating that these viruses might use the same receptor. CONCLUSION A novel bat-borne CoV was identified that is associated with severe and fatal respiratory disease in humans.
Adult ; Aged ; Betacoronavirus ; genetics ; isolation & purification ; Coronavirus Infections ; diagnostic imaging ; therapy ; virology ; Female ; Humans ; Male ; Middle Aged ; Pandemics ; Pneumonia, Viral ; diagnostic imaging ; therapy ; virology ; Tomography, X-Ray ; Treatment Outcome