Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add more filters










Database
Language
Publication year range
1.
Eur Rev Med Pharmacol Sci ; 24(16): 8251-8262, 2020 08.
Article in English | MEDLINE | ID: mdl-32894531

ABSTRACT

OBJECTIVE: Intervertebral disc (IVD) degeneration (IDD) is a well-known consequence of low back pain, as characterized by aberrant cell proliferation and apoptosis of nucleus pulposus (NP) cells. In the present study, we aimed to investigate the effect of lncRNA small nucleolar RNA host gene 6 (SNHG6) on deregulated functions of degenerative NP cells. MATERIALS AND METHODS: After the establishment of rat IDD models, the mRNA and protein levels of collagen-I (Col-I) and collagen II (Col-II), and mRNA level of SNHG6 were detected by using reverse transcription quantitative Real Time-PCR (RT-qPCR) and Western blot. We further investigated the role and molecular mechanisms of SNHG6 by overexpressing or silencing it in degenerative NP cells. Cell proliferation was measured by MTT assay and EdU staning, and apoptosis was measured by flow cytometry. The target of SNHG6 was identified by starBase and Dual-Luciferase reporter assay. RESULTS: Upregulation of SNHG6 was found in IDD NP cells than in normal cells, associated with higher level of Col-I and lower level of Col-II. Overexpression of SNHG6 inhibited cell proliferation and enhanced apoptosis, accompanied by increased expression of Bax, caspase-3, and p21, as well as decreased expression of Bcl-2, which was in reverse to the treatment of SNHG6 silencing. Moreover, miR-101-3p was indicated as a target of SNHG6, and inhibition of miR-101-3p reversed the effects on proliferation and apoptosis induced by SNHG6. CONCLUSIONS: SNHG6 suppressed cell proliferation and induced apoptosis by increasing expression of Bax, caspase-3, p21 and decreasing Bcl-2 through targeting miR-101-3p, which suggested that SNHG6 could be a potential target in the treatment of IDD.


Subject(s)
Apoptosis , MicroRNAs/metabolism , Nucleus Pulposus/metabolism , RNA, Long Noncoding/metabolism , Animals , Cell Proliferation , MicroRNAs/genetics , Nucleus Pulposus/pathology , RNA, Long Noncoding/genetics , Rats , Rats, Wistar
2.
Eur Rev Med Pharmacol Sci ; 21(23): 5370-5377, 2017 Dec.
Article in English | MEDLINE | ID: mdl-29243778

ABSTRACT

OBJECTIVE: To observe the reversal effect of apatinib on the resistance to cisplatin (DDP) of A549/cisplatin (A549/DDP) cells and its relevant mechanism. MATERIALS AND METHODS: A549/DDP cells were treated with the control method, apatinib alone, DDP alone and DDP combined with apatinib. The cell proliferation was detected by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and the cell clone formation assay. The cell apoptosis was detected by Hoechst 33258 staining and annexin V and propidium iodide (PI) double labeling. The changes in apoptotic proteins, multidrug resistance protein 1 (MDR1) and extracellular signal-regulated kinase (ERK) signaling pathway proteins in each group after treatment were detected by Western blotting. RESULTS: MTT assay results showed that compared with A549 cells, A549/DDP cells had obvious resistance to DDP. MTT assay and cell clone formation assay revealed that the tumor inhibition rate of the sub-lethal dose of apatinib (10 µM) combined with DDP was higher than that of DDP alone. The apoptosis detection results indicated that the proportion of apoptotic cells in the apatinib (10 µM) combined with DDP group was significantly increased. Western blotting results revealed that compared with that in parental A549 cells, the expression level of MDR1 in A549/DDP cells was significantly increased, and the ERK signaling pathway was activated. In the apatinib combined with DDP group, the levels of cleaved caspase-3, cleaved caspase-9 and B-cell lymphoma-2 (Bcl-2)-associated X (BAX) proteins were significantly upregulated, while the level of Bcl-2 proteins was downregulated. Apatinib could inhibit the expression of MDR1 and the activity of the ERK signaling pathway in a dose-dependent manner. CONCLUSIONS: Apatinib can restore the sensitivity of A549/DDP cells to DDP by down-regulating the expression level of MDR1 and inhibiting the activity of the ERK signaling pathway.


Subject(s)
Antineoplastic Agents/pharmacology , Carcinoma, Non-Small-Cell Lung/drug therapy , Cisplatin/pharmacology , Drug Resistance, Neoplasm , Lung Neoplasms/drug therapy , MAP Kinase Signaling System/drug effects , Pyridines/pharmacology , A549 Cells , ATP Binding Cassette Transporter, Subfamily B/analysis , Carcinoma, Non-Small-Cell Lung/pathology , Caspase 9/analysis , Cell Line, Tumor , Drug Resistance, Neoplasm/drug effects , Humans
3.
QJM ; 110(7): 453-457, 2017 Jul 01.
Article in English | MEDLINE | ID: mdl-28158768

ABSTRACT

BACKGROUND: Sepsis will induce stroke, new-onset atrial fibrillation (AF) increase ischemic stroke (IS) in in-hospitalization and long-term period after sepsis. Physicians must alert this condition and given suitable treatment. AIM: The associated of IS and new-onset AF in septicemia survivors after discharge have to be evaluated. DESIGN: The inpatient data was used of the Taiwan National Health Insurance Database (NHIRD) in 2010. We identified patients suffered their first occurrence of septicemia (International Classification of Disease, Ninth Revision, Clinical Modification [ICD-9-CM] is 038, 003.1, 036.1) and excluded less than 18 years old. Patients had AF (ICD-9-CM to 427.3×) during the same admission or after septicemia hospitalization discharged were defined as new-onset AF. The outcome was IS happened after septicemia discharge (ICD-9-CM as 433-437). METHODS: The factors related to IS after septicemia survival were established using multivariate logistic regression with forward stepwise selection. RESULTS: There were 1286 new-onset AF and 1026 IS happened after septicemia discharge. The crude odds ratio (OR) were 3.88 (95% confidence interval [C.I.]: 1.69-8.89) and 1.62 (95% C.I.: 1.14-2.3) in middle-aged and elderly septicemia survivors with new-onset AF induced IS. The risk of IS after septicemia survivors was noticed adjusted OR 1.74 (95% C.I.: 1.26-2.41) for new-onset AF. CONCLUSION: The middle-aged and elderly septicemia survivors suffered from new-onset AF had increased incidence of IS within three months. New-onset AF was a mediator factor of IS in septicemia survivors of Asian population.


Subject(s)
Atrial Fibrillation/complications , Atrial Fibrillation/epidemiology , Patient Discharge , Sepsis/complications , Stroke/epidemiology , Aged , Aged, 80 and over , Comorbidity , Databases, Factual , Female , Follow-Up Studies , Humans , Incidence , Logistic Models , Male , Middle Aged , Multivariate Analysis , Risk Factors , Stroke/etiology , Survivors/statistics & numerical data , Taiwan/epidemiology
4.
Int Orthop ; 20(2): 100-2, 1996.
Article in English | MEDLINE | ID: mdl-8739702

ABSTRACT

Total knee replacement has been carried out in the 4 knees of 2 patients for spontaneous bony ankylosis. Minimally constrained prostheses were used because the ligaments were usually intact and the patellofemoral and tibiofemoral joint lines could be re-established. The approach and repair was by a V-Y quadricepsplasty. Satisfactory results were obtained.


Subject(s)
Ankylosis/surgery , Knee Prosthesis , Adult , Ankylosis/diagnostic imaging , Ankylosis/physiopathology , Female , Humans , Knee Prosthesis/instrumentation , Knee Prosthesis/methods , Male , Middle Aged , Pain Measurement , Prosthesis Design , Radiography , Range of Motion, Articular
SELECTION OF CITATIONS
SEARCH DETAIL
...