Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 9 de 9
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Artigo em Inglês | MEDLINE | ID: mdl-38321212

RESUMO

Cholangiocarcinoma (CCA) is a type of malignant tumor originating from the intrahepatic, periportal, or distal biliary system. The treatment means for CCA is limited, and its prognosis is poor. Spatholobi Caulis (SC) is reported to have effects on anti-inflammatory and anti-tumor, but its role in CCA is unclear. First, the potential molecular mechanism of SC for CCA treatment was explored based on network pharmacology, and the core targets were verified by molecular docking and molecular dynamics simulation. Then, we explored the inhibitory effect of SC on the malignant biological behavior of CCA in vitro and in vivo and also explored the related signaling pathways. The effect of combination therapy of SC and cisplatin (DDP) in CCA was also explored. Finally, we conducted a network pharmacological study and simple experimental verification on luteolin, one of the main components of SC. Network pharmacology analysis showed that the core targets of SC on CCA were AKT1, CASP3, MYC, TP53, and VEGFA. Molecular docking and molecular dynamics simulation indicated a good combination between the core target protein and the corresponding active ingredients. In vitro, SC inhibited proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of CCA cells. In vivo experiments, the results were consistent with in vitro experiments, and there was no significant hepatorenal toxicity of SC at our dosage. Based on KEGG enrichment analysis, we found PI3K/AKT signaling pathway might be the main signaling pathway of SC action on CCA by using AKT agonist SC79. To explore whether SC was related to the chemotherapy sensitivity of CCA, we found that SC combined with DDP could more effectively inhibit the progression of cholangiocarcinoma. Finally, we found luteolin may inhibit the proliferation and invasion of CCA cells. Our study demonstrates for the first time that SC inhibits the progression of CCA by suppressing EMT through the PI3K-AKT signaling pathway, and SC could enhance the effectiveness of cisplatin therapy for CCA.

2.
iScience ; 27(1): 108609, 2024 Jan 19.
Artigo em Inglês | MEDLINE | ID: mdl-38174316

RESUMO

Realizing camouflage by illusion and cloaking based on the metasurface has received widespread attention recently. However, existing metasurface-based illusion and cloaking devices are valid for the incident wave with a specific frequency, angle, or polarization, or exhibit a single function. Therefore, a terahertz tunable vanadium dioxide (VO2) metasurface carpet cloak is proposed for dynamic illusion and cloaking. Simulation results show that by controlling the state of the VO2, the metasurface carpet cloak can simultaneously achieve illusion and cloaking functions, working at 0.45 THz and 0.6 THz, and is effective for orthogonal circularly polarized waves with different incidence angles. That is the function, frequency, incident angle, and polarization of the metasurface carpet cloak are dynamically adjustable. Besides, the metasurface carpet cloak is robust to the incident angle and is capable of polarization angle stability. This work has potential value in the real-life application of metasurface-based illusion and cloaking devices.

3.
Eur J Pharmacol ; 959: 176090, 2023 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-37778612

RESUMO

BACKGROUND: Intestinal ischemia/reperfusion injury (IRI) is a multifactorial, complex pathophysiological process in clinical settings. In recent years, intestinal IRI has received increasing attention due to increased morbidity and mortality. To date, there are no effective treatments. Dexmedetomidine (DEX), a highly selective α2-adrenergic receptor agonist, has been demonstrated to be effective against intestinal IRI. In this systematic review and meta-analysis, we evaluated the efficacy and potential mechanisms of DEX as a treatment for intestinal IRI in animal models. METHODS: Five databases (PubMed, Embase, Web of Science, Cochrane Library, and Scopus) were searched until March 15, 2023. Using the SYRCLE risk bias tool, we assessed methodological quality. Statistical analysis was conducted using STATA 12 and R 4.2.2. We analyzed the related outcomes (mucosa damage-related indicators; inflammation-relevant markers, oxidative stress markers) relied on the fixed or random-effects models. RESULTS: There were 15 articles including 18 studies included, and 309 animals were involved in the studies. Compared to the model groups, DEX improved intestinal IRI. DEX decreased Chiu's score and serum diamine oxidase (DAO) level. DEX reduced the level of inflammation-relevant markers (interleukin (IL)-1ß, IL-6, tumor necrosis factor (TNF)-α). DEX also improved oxidative stress (decreased malondialdehyde (MDA), increased superoxide dismutase (SOD)). CONCLUSIONS: DEX's effectiveness in ameliorating intestinal IRI has been demonstrated in animal models. Antioxidation, anti-inflammation, anti-apoptotic, anti-pyroptosis, anti-ferroptosis, enhancing mitophagy, reshaping the gut microbiota, and gut barrier protection are possible mechanisms. However, in light of the heterogeneity and methodological quality of these studies, further well-designed preclinical studies are warranted before clinical implication.


Assuntos
Dexmedetomidina , Traumatismo por Reperfusão , Ratos , Animais , Dexmedetomidina/farmacologia , Dexmedetomidina/uso terapêutico , Ratos Sprague-Dawley , Agonistas de Receptores Adrenérgicos alfa 2/uso terapêutico , Traumatismo por Reperfusão/patologia , Inflamação/tratamento farmacológico , Isquemia/tratamento farmacológico
4.
Am J Chin Med ; 51(6): 1501-1526, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37530507

RESUMO

Inflammatory bowel disease (IBD) is a group of chronic inflammatory disorders that include Crohn's disease (CD) and ulcerative colitis (UC). Today, IBD has no successful treatment. As a result, it is of paramount importance to develop novel therapeutic agents for IBD prevention and treatment. Astragalus membranaceus (AMS) is a traditional Chinese medicine found in the AMS root. Modern pharmacological studies indicate that AMS and its constituents exhibit multiple bioactivities, such as anti-inflammatory, anti-oxidant, immune regulatory, anticancer, hypolipidemic, hypoglycemic, hepatoprotective, expectorant, and diuretic effects. AMS and its active constituents, which have been reported to be effective in IBD treatment, are believed to be viable candidate drugs for IBD treatment. These underlying mechanisms are associated with anti-inflammation, anti-oxidation, immunomodulation, intestinal epithelial repair, gut microbiota homeostasis, and improved energy metabolism. In this review, we summarize the efficacy and underlying mechanisms involved in IBD treatment with AMS and its active constituents in preclinical studies.


Assuntos
Colite Ulcerativa , Doenças Inflamatórias Intestinais , Humanos , Astragalus propinquus , Doenças Inflamatórias Intestinais/tratamento farmacológico , Colite Ulcerativa/tratamento farmacológico , Anti-Inflamatórios/uso terapêutico , Antioxidantes
5.
Kaohsiung J Med Sci ; 38(9): 826-838, 2022 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-35748489

RESUMO

To investigate the effect of long noncoding RNA (LINC01419)/miR-485-5p/LSM4 on the malignant behavior of hepatocellular carcinoma (HCC) cells. The expressions of LINC01419, miR-485-5p, and LSM4 were determined in HCC at the cellular and clinical levels, and cell biological behavior was evaluated. The relationships between LINC01419, miR-485-5p, and LSM4 were predicted and verified. Additionally, the subcellular localization of LINC01419 in HCC cells was analyzed. Finally, an animal experiment was conducted to confirm the effect of LINC01419 silencing on tumor growth. in HCC tissues and cells, LINC01419 and LSM4 were increasingly expressed, but miR-485-5p was decreasingly expressed. LINC01419 negatively regulated miR-485-5p- and miR-485-5p-targeted LSM4. LINC01419 was localized in the cytoplasm of HCC cells. Downregulation of miR-485-5p or upregulation of LSM4 reversed the inhibition of HCC cell malignant behavior by LINC01419 interference. LINC01419 sponges miR-485-5p to upregulate LSM4 expression, thereby facilitating the biological behavior of HCC cells.


Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , MicroRNAs , RNA Longo não Codificante , Animais , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/patologia , MicroRNAs/genética , MicroRNAs/metabolismo , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo
6.
J Gastrointest Surg ; 26(4): 802-812, 2022 04.
Artigo em Inglês | MEDLINE | ID: mdl-34647226

RESUMO

BACKGROUND: Long noncoding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) is an oncogenic lncRNA that has been reported in many cancers, but the role of SNHG3 in cholangiocarcinoma (CCA) remains largely unknown. Bioinformatic analysis revealed a regulatory relationship among SNHG3, miR-3173-5p, and ERG. miR-3173-5p is a tumour suppressive miRNA, while ERG is an oncogene. In the present study, we focused on the regulatory effects and molecular mechanisms of SNHG3 in CCA. METHOD: The expression of SNHG3 and miR-3173-5p was evaluated using qRT-PCR analysis. Knockdown of SNHG3 was achieved by shRNA. Cell viability was assessed by MTT assay. Migration and invasion were determined by Transwell assay. Flow cytometry was used to assess cell apoptosis. Western blots were applied to quantify protein levels. Furthermore, using RNA pulldown and dual luciferase assays, the interactions between SNHG3 and miR-3173-5p and between miR-3173-5p and ERG in CCA cells were validated. RESULTS: SNHG3 was significantly upregulated in CCA cells compared with normal human intrahepatic biliary epithelial cells. Knockdown of SNHG3 inhibited the proliferation and migration of CCA cells. Mechanistically, SNHG3-sponged miR-3173-5p, thus releasing the repression of ERG by miR-3173-5p. Rescue experiments showed that the miR-3173-5p/ERG axis mediated the oncogenic effect of SNHG3. CONCLUSION: Taken together, our data suggest that SNHG3 is a pleiotropic oncogenic lncRNA in CCA. Knockdown of SNHG3 expression suppressed malignant phenotypes in CCA cells via the miR-3173-5p/ERG axis.


Assuntos
Neoplasias dos Ductos Biliares , Colangiocarcinoma , MicroRNAs , RNA Longo não Codificante/genética , Apoptose , Neoplasias dos Ductos Biliares/patologia , Ductos Biliares Intra-Hepáticos/patologia , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Colangiocarcinoma/genética , Colangiocarcinoma/patologia , Regulação Neoplásica da Expressão Gênica , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , Fenótipo , RNA Longo não Codificante/metabolismo , Regulador Transcricional ERG/genética , Regulador Transcricional ERG/metabolismo
7.
Mol Med Rep ; 24(1)2021 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33982784

RESUMO

Following the publication of the above article, the authors have realized that the Funding section of the Declarations on p. 7 was written incorrectly: The text here should have appeared as follows: 'This work was supported by the Research Fund Subsidy Project of Hunan Provincial Committee on Health Commission (grant no. 20200179) and Xiang Wei Medical Administration Medical Office Memorandum (2019) No. 118 and the Research Fund of Hunan Provincial Department of Education (grant no. 20C1163)'. The authors regret their oversight in providing this incorrect information in the Funding section of their paper. They thank the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and apologize to the readership of the Journal and to the inappropriately credited funding bodies in question for any inconvenience caused. [the original article was published in Molecular Medicine Reports 23: 343, 2021; DOI: 10.3892/mmr.2021.11982].

8.
Mol Med Rep ; 23(5)2021 05.
Artigo em Inglês | MEDLINE | ID: mdl-33760124

RESUMO

Glycyrrhizin (GA) is the most essential active ingredient in licorice root, and has a wide range of biological and pharmacological activities. The present study aimed to conduct a detailed analysis of the effects of GA on liver cancer (LC) cell proliferation and the Warburg effect. Hexokinase­2 (HK2) is a glycolytic enzyme that catalyzes the Warburg effect. To this end, the LC HepG2 cell line was transfected with small interfering RNA­HK2 or pCDNA3.1­HK2, followed by GA treatment. A Cell Counting Kit­8 assay and EdU staining were employed to evaluate the proliferation rate of LC cells. The expression levels of HK2 and the phosphorylation level of AKT were measured by reverse transcription­quantitative PCR and western blotting, respectively. Furthermore, the glucose uptake capacity and lactic acid content were assessed by kits, and the glycolysis level was evaluated by assessing the extracellular acidification rate (ECAR) and the oxygen consumption rate (OCR). A pronounced increase in the OCR, and decreases in the cell proliferation, glucose uptake capacity, lactic acid content, ECAR and HK2 expression were detected in LC cells subjected to GA treatment or HK2­knockdown. Conversely, overexpression of HK2 reversed these trends, indicating that glycyrrhizin may inhibit LC cell proliferation and the Warburg effect through suppression of HK2. In addition, it was revealed that the PI3K/AKT signaling pathway was associated with LC cell proliferation and the Warburg effect; notably, treatment of LC cells with the AKT agonist SC79 induced elevation of the ECAR, cell proliferation, glucose uptake capacity, lactic acid content, phosphorylated­AKT and HK2 expression, and suppressed the OCR. In conclusion, GA may inhibit the Warburg effect and cell proliferation in LC by suppressing HK2 through blockade of the PI3K/AKT signaling pathway.


Assuntos
Ácido Glicirrízico/farmacologia , Hexoquinase/genética , Neoplasias Hepáticas/tratamento farmacológico , Apoptose/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Glicólise/efeitos dos fármacos , Células Hep G2 , Humanos , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Fosfatidilinositol 3-Quinases/genética , Transdução de Sinais/efeitos dos fármacos , Efeito Warburg em Oncologia/efeitos dos fármacos
9.
IEEE Trans Neural Netw Learn Syst ; 31(8): 2980-2992, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31536017

RESUMO

This article aims to solve the Moore-Penrose inverse of time-varying full-rank matrices in the presence of various noises in real time. For this purpose, two varying-parameter zeroing neural networks (VPZNNs) are proposed. Specifically, VPZNN-R and VPZNN-L models, which are based on a new design formula, are designed to solve the right and left Moore-Penrose inversion problems of time-varying full-rank matrices, respectively. The two VPZNN models are activated by two novel varying-parameter nonlinear activation functions. Detailed theoretical derivations are presented to show the desired finite-time convergence and outstanding robustness of the proposed VPZNN models under various kinds of noises. In addition, existing neural models, such as the original ZNN (OZNN) and the integration-enhanced ZNN (IEZNN), are compared with the VPZNN models. Simulation observations verify the advantages of the VPZNN models over the OZNN and IEZNN models in terms of convergence and robustness. The potential of the VPZNN models for robotic applications is then illustrated by an example of robot path tracking.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...