Latest ArticlesTo investigate the effects of circCSPP1 mediated autophagy on the proliferation and metastasis ability of gastric cancer cells.
The human gastric cancer cells NCI-N87 were divided into Vector group (transfected with Vector), circCSPP1 group (transfected with circCSPP1) and inhibitor group (transfected with circCSPP1 and incubated with 10 μmol·L-1 chloroquine). The MKN-45 cells were divided into sh-NC group (transfected with circCSPP1 shRNA-NC), sh-circCSPP1 group (transfected with circCSPP1 shRNA) and agonist group (transfected with circCSPP1 shRNA + 1 μmol·L-1 sirolimus). Flow cytometry was used to detect cell apoptosis. Transwell was used to detect cell migration and invasion. Western blot were used to detect the expression levels of microtubule associated protein light chain 3-Ⅱ (LC3-Ⅱ) and p62 protein.
In NCI-N87 cells: the apoptosis rates of Vector, circCSPP1 and inhibitor groups were (7.95±0.66)%, (3.93±0.62)% and (7.37±0.85)%; the number of cell migrations were 122.50±12.25, 169.40±16.09 and 109.00±8.22; the number of cell invasions were 73.38±12.33, 117.30±12.78 and 55.25±8.73; the relative expression levels of LC3-Ⅱ protein were 0.40±0.06, 1.13±0.11 and 0.44±0.08; the relative expression levels of p62 protein were 1.62±0.15, 0.21±0.08 and 1.43±0.16. The differences of above indexes were statistically significant between the circCSPP1 group and the inhibitor and Vector groups (all P<0.05). In MKN-45 cells: the cell apoptosis rates of sh-NC, sh-circCSPP1 and agonist groups were (6.81±0.68)%, (12.02±0.78)% and (5.76±1.21)%; the number of cell migrations were 191.60±21.43, 87.50±10.76 and 155.60±10.36; the number of cell invasions were 150.00±11.55, 61.63±11.39 and 154.50±17.99; the relative expression levels of LC3-Ⅱ protein were 1.08±0.05, 0.13±0.03 and 1.18±0.06; the relative expression levels of p62 protein were 0.15±0.03, 1.29±0.08 and 0.19±0.04. Compared with the sh-circCSPP1 group, the differences of above indicators in the agonist and sh-NC groups were statistically significant (all P<0.05).
circCSPP1 can improve the proliferation and metastasis ability of gastric cancer cells by inducing autophagy.
Liver fibrosis is caused by various chronic injuries and metabolic disorders. Cirrhosis is the end stage of progressive liver fibrosis, which is estimated to affect 1% - 2% of the global population and cause more than 1 million deaths worldwide every year. Activation and maintenance of hepatic stellate cells (HSCs) are the main driving factors in liver fibrosis. At the same time, the process of trans-differentiation of HSCs involves reprogramming of energy metabolism, which is a key metabolic feature necessary to promote cell growth. Current studies found that Sirtuin protein family plays an important role in the progress of liver fibrosis, and further found that in the progress of liver fibrosis, especially after HSCs activation. Energy metabolism reprogramming involves various cells, including liver cells, HSCs, and immune cells. Targeting intracellular metabolism to limit fibrosis progression is currently a research hotspot. This article reviews the regulatory role of the Sirtuin protein family in energy metabolism in HSCs.
To analyze the clinical efficacy and safety of salmeterol fluticasone propionate combined with cetirizine hydrochloride and montelukast sodium tablet in the treatment of children with cough variant asthma.
The children with cough variant asthma were divided into control group and treatment group by random number table method. The control group was treated with oral montelukast sodium chewable tablets and cetirizine hydrochloride oral solution, both 10 mg every time, qd; the treatment group was treated with salmeterol fluticasone propionate inhalation powder inhalation, 1 inhalation/time, bid on the basis of the control group. Children in both groups continued treatment for 3 weeks. The clinical efficacy, pulmonary function, airway reaction status, immune function index, inflammatory index and adverse drug reactions were compared between the two groups.
In the treatment group, 50 cases were enrolled, 1 case was lost, and 49 cases were finally included in the statistical analysis. In the control group, 52 cases were enrolled, 3 cases were lost, and finally 49 cases were included in the statistical analysis. After treatment, the total effective rate of the control group and the treatment group were 77.55% (38 cases/49 cases) and 93.88% (46 cases/49 cases), respectively, and the difference were statistically significant (P<0.05). After treatment, the maximum expiratory flow were (4.68±0.56) and (5.07±0.62) L·s-1 in the control and treatment groups; the vital capacity were (0.98±0.05) and (1.02±0.07) L; the forced expiratory volume in the first second were (75.72±7.24)% and (80.03±8.36)%; the forced vital capacity were (75.49±7.68)% and (79.97±6.72)%; the initial airway resistance were (7.33±0.75) and (7.01±0.73) cm H2O·L-1·s-1; the minimum induced cumulative dose were (1.89±0.14) and (2.01 ± 0.25) mg·L-1; the 35th percentile of specific airway conduction decrease were (5.24±0.52)% and (5.59±0.68)%. There were statistically significant differences in the above indexes between the treatment group and the control group (P<0.05, P<0.01, P<0.001). The adverse drug reactions of the control group and the treatment group were headache, palpitation and sleep difficulty, and the incidence of the total adverse drug reactions of the treatment group and the control group were 6.12% (3 cases /49 cases) and 12.24% (6 cases /49 cases), respectively, with no statistical significance (P>0.05).
Salmeterol fluticasone propionate, cetirizine hydrochloride and montelukast sodium tablet are effective and safe in the treatment of children with cough variant asthma.
To analyze the clinical characteristics and distribution of pathogens in adult acute empyema.
Adult patients with acute empyema were divided into the control group (patients with community-acquired empyema) and the treatment group (patients with hospital-acquired empyema) according to cohort method. The general data, clinical manifestations, laboratory examinations, imaging data, antimicrobial drugs use, invasive treatment and outcomes of the two groups were collected and compared.
There were 59 cases in the treatment group and 102 cases in the control group. Compared with the control group, the proportion of lung abscess in the treatment group was lower (1.69% vs 10.78%, P<0.05), the proportion of pneumothorax, positive rates of pus culture and mixed infection were higher (47.46% vs 18.63%, 55.93% vs 24.51%, 27.12% vs 1.96%, all P<0.05). In the control group, 27 strains of pathogens were isolated, predominantly Gram-positive cocci (74.07%), with Streptococcus anginosus group being the most common (44.44%). In the treatment group, 52 strains were isolated, predominantly Gram-negative bacilli (67.31%), with Pseudomonas aeruginosa being the most common (21.15%). Streptococcus anginosus group was sensitive to penicilins and cephalosporins, while the multidrug resistance rate of Gram-negative bacilli was high, with Pseudomonas aeruginosa showing a 69.23% resistance to meropenem. Six patients in total died, all from the treatment group and receiving non-surgical treatment, due to malignant tumors or hospital-acquired pneumonia.
In adult acute empyema, non-parapneumonic empyema is common, and there were significant differences in the pathogenic distribution between community-acquired empyema and hospital-acquired empyema.
To observe the efficacy and safety of snake venom hemocoagulase injection combined with tranexamic acid injection and omeprazole sodium injection in the treatment of emergency patients with acute upper gastrointestinal bleeding.
Patients with acute upper gastrointestinal bleeding were divided into control group and treatment group according to the cohort method. Patients in the control group were administered with tranexamic acid injection 500 mg (iv; qd) combined with omeprazole sodium for injection 40 mg (bid); the treatment group was given snake venom hemocoagulase injection 0.5-1.5 kU (once in the morning and once in the evening) on the basis of the control group. All patients were treated for 3 d. The total effective rate, coagulation function [platelet (PLT), activated partial thromboplastin time (APTT), fibrinogen (Fib), plasma prothrombin time (PT)], hemodynamics [plasma viscosity (PV), erythrocyte sedimentation rate (ESR), whole blood high shear viscosity (WBVH) and hematocrit (HCT)], inflammatory stress response [C-reactive protein (CRP), cortisol (Cor) and neutrophil to lymphocyte ratio (NLR)], and adverse drug reactions were compared between two groups.
A total of 120 patients were enrolled in this trial, including 58 in the control group and 62 in the treatment group. After treatment, the effective rates of the control group and the treatment group were 79.31% (46 cases/58 cases) and 95.16% (59 cases / 62 cases), respectively, with statistical difference (P<0.05). After treatment, the PLT levels in the control and treatment groups were (170.18±10.86) and (180.18±9.83)×109·L-1, respectively; APTT values were (47.39±4.52) and (44.68±4.62), respectively; Fib levels were (2.98±0.33) and (3.21±0.28) g·L-1, respectively; PT values were (19.21±3.76) and (17.01±2.62) seconds, respectively; PV levels were (1.98±0.36) and (2.38±0.43) MPa·s, respectively; ESR values were (53.69±4.52)% and (59.89±14.62)%, respectively; WBVH levels were (7.08±0.23) and (7.98±0.28) MPa·s, respectively; HCT levels were (49.21±5.62) and (52.01±8.62) L·L-1, respectively; CRP levels were (8.63±1.36) and (6.38±0.93) mg·L-1, respectively; Cor values were (323.69±14.82) and (315.86±14.62) mmol·L-1, respectively; NLP levels were 4.08±0.43 and 2.98±0.48. All these differences were statistically significant (P<0.05). During the trial, the adverse drug reactions in the control group were mainly stomach distension, dizziness, headache and diarrhea, and the adverse drug reactions in the treatment group were mainly stomach distension, dizziness, headache and diarrhea. The total incidences of adverse drug reactions in the control group and the treatment group were 10.34% (6 cases / 58 cases) and 12.90% (8 cases / 62 cases), respectively, with no statistically significant difference (P>0.05).
Snake venom hemocoagulase injection combined with tranexamic acid injection and omeprazole sodium for injection has significant curative effect on emergency patients with acute upper gastrointestinal bleeding, with low adverse drug reactions.
To investigate the inhibitory effect of deoxyelephantopin on non-small cell lung cancer (NSCLC) and its potential mechanism.
Human lung adenocarcinoma H1975 cells were randomly divided into control group (routine culture), experimental-L group (1.0 μmol·L-1 deoxyelephantopin), experimental-M group (2.0 μmol·L-1 deoxyelephantopin), experimental-H group (5.20 μmol·L-1 deoxyelephantopin), Vector group (transfected Vector plasmid +5.20 μmol·L-1 deoxyelephantopin), epidermal growth factor receptor (EGFR) group (transfected with EGFR plasmid+5.20 μmol·L-1 deoxyelephantopin). 5-ethynyl-2′-deoxyuridine(EdU) assay was used to detected cell proliferation; cell apoptosis were detected by TdT mediated dUDP nick end labeling(Tunel)and flow cytometry; Western blot assay was used to detect the proteins expression; and Transwell assay was used to detect cell migration and invasion.
The proliferation rates of cells in the control group and experimental-L, -M, -H groups were (40.64±2.70)%, (29.78±3.28)%, (23.59±1.98)% and (15.72±1.01)%, respectively; the rates of TUNEL-positive cells were (4.63±0.57)%, (10.18±0.88)%, (15.96±0.79)% and (24.73±3.70)%, respectively; the relative expression levels of phosphorylated epidermal growth factor receptor (p-EGFR) protein were 0.87±0.10, 0.60±0.05, 0.49±0.04 and 0.33±0.04, respectively. Comparisons between the experimental-L, -M, -H groups and the control group, as well as comparisons among the experimental-L, -M, -H groups, revealed statistically significant differences (all P<0.05). The relative expression levels of p-EGFR/EGFR protein in the control group, experimental-H group, Vector group, and EGFR group were 0.76±0.10, 0.49±0.07, 0.47±0.05 and 0.71±0.10, respectively; apoptosis rates were (4.11±0.39)%, (26.33±2.29)%, (25.40±1.58)% and (12.68±1.73)%, respectively; the number of migrating cells was 147.78±12.69, 87.11±9.65, 93.89±9.67 and 124.00±14.10, respectively. Statistical analysis showed significant differences in the above indices between the experimental-H group and the control group, as well as between the EGFR group and the Vector group (all P<0.05).
Deoxyelephantopin can degrade EGFR, inhibit related signaling pathways, inhibit proliferation and metastasis of lung cancer cells, and induce apoptosis.
To investigate the effects of microRNA-425-5p (miR-425-5p) targeting fibroblast growth factor 9 (FGF9) on the proliferation, glucose metabolism and olaparib resistance of ovarian cancer cells.
Human ovarian cancer cell line SKOV3 were divided into control group (normal culture), NC inhibitor group (transfected empty vector miR-NC), miR-425-5p inhibitor group (transfected miR-425-5p inhibitor), si-NC group (transfected si-NC on the basis of miR-425-5p inhibitor group), si-FGF9 group (transfected si-FGF9 on the basis of miR-425-5p inhibitor group). Quantitative real time polymerase chain reaction was used to detect the expression levels of miR-425-5p and FGF9 in cells. The cell proliferation rate was detected by 5-ethynyl-2′-deoxyuridine (EdU) assay. Lactic acid production and glucose absorption were measured by lactic acid metabolism and glucose detection kit. The survival rate of cells in each group was detected by cell counting kit-8 assay. Western blot was used to detect signal transducer and activator of transcription 3/sirtuin 3 (STAT3/SITR3) signaling pathway related protein expression levels in each group.
The proliferation rate were (84.11±14.76)%, (36.12±6.95)%, (34.32±6.62)% and (77.37±12.83)% in the NC inhibitor group, miR-425-5p inhibitor group, si-NC group and si-FGF9 group, respectively; the relative lactic acid production were 1.02±0.13, 0.71±0.09, 0.74±0.09 and 0.89±0.10, respectively; the relative glucose absorption values were 0.99±0.14, 0.68±0.08, 0.70±0.09 and 0.91±0.11, respectively; the survival rates under 40 μmol·L-1 olaparib were (59.86±9.55)%, (41.08±7.72)%, (40.25±7.02)% and (55.71±7.68)%, respectively; the relative expression levels of STAT3 protein were 1.01±0.17, 0.68±0.10, 0.66±0.09 and 0.88±0.12, respectively; the relative expression levels of SITR3 protein were 0.98±0.17, 1.84±0.28,1.85±0.29 and 1.23±0.20, respectively. The above indexes of miR-425-5p inhibitor group were compared with those of NC inhibitor group, and those of si-FGF9 group were compared with those of si-NC inhibitor group, and the differences were statistically significant (P<0.01, P<0.001).
Silting miR-425-5p can inhibit the proliferation and glucose metabolism of ovarian cancer cells, and reduce the resistance of cells to olaparib, which may be achieved by up-regulating FGF9 level and inhibiting STAT3/SIRT3 signaling pathway.
To investigate the effects and mechanism of wogonoside on the malignant biological behavior of pancreatic cancer SW1990 cells.
Human pancreatic cancer cells SW1990 were cultured in vitro and randomly divided into control group (normal culture), miR-NC group (transfected with miR-NC), miR-573 group (transfected with miR-573 mimics), anti-miR-NC group (transfected with miR-NC + 20 μmol·L-1 wogonoside), anti-miR-573 group (transfected with anti-miR-573 + 20 μmol·L-1 wogonoside) and experimental -L, -M, -H groups (given 5, 10 and 20 μmol·L-1 wogonoside, respectively). The ability of cell proliferation, migration and invasion were detected by methyl thiazolyl tetrazolium assay, plate cloning assay, scratch assay and Transwell assay, respectively; the expression level of microRNA (miR-573) was detected by real-time fluorescence quantitative polymerase chain reaction; Western blot were used to detect the expression levels of E-cadherin and N-cadherin protein.
The inhibition rates of experimental-H group, control group, miR-NC group, miR-573 group, anti-miR-NC group and anti-miR-573 group were (65.37±5.17)%, 0, (6.13±0.58)%, (51.94±4.99)%, (67.74±4.38)% and (28.23±2.47)%, respectively; the scratch healing rates were (27.33±2.52)%, (73.47±6.56)%, (74.27±6.86)%, (36.42±3.14)%, (25.91±2.53)% and (61.49±5.11)%, respectively; the number of invading cells were 58.05±5.46, 124.21±10.25, 126.77±11.89, 64.74±5.63, 56.65±4.79 and 103.94±10.68, respectively; the relative expression levels of miR-573 were 3.11±0.26, 1.00±0.00, 1.00±0.00, 3.96±0.37, 1.00±0.00 and 0.35±0.03, respectively; the relative expression levels of E-cadherin protein were 0.56±0.04, 0.16±0.02, 0.15±0.02, 0.50±0.04, 0.58±0.04 and 0.28±0.03, respectively; the relative expression levels of N-cadherin protein were 0.24±0.02, 0.66±0.04, 0.68±0.05, 0.31±0.03, 0.23±0.02 and 0.55±0.05, respectively. The differences of above indexes were statistically significant between the experimental -H group and the control group, between the miR-573 group and the miR-NC group, and between the anti-miR-573 group and the anti-miR-NC group (all P<0.05).
Wogonoside can decrease the proliferation, migration and invasion of pancreatic cancer cells by up-regulating the expression of miR-573, decreasing the expression of N-cadherin and increasing the expression of E-cadherin.
To observe the intervention effects of Radix Angelica Sinensis and Radix Hedysari ultrafiltration (RAS-RH) on the NOD-like receptor thermal protein domain associated protein 3/cysteinyl aspartate specific proteinase-1/gasdermin D (NLRP3/Caspase-1/GSDMD) signaling pathway and radiation-induced heart disease (RIHD).
A model was constructed using a single whole-body X-ray irradiation at a dose of 8 Gy. SPF-grade male Wistar rats were randomly divided into the normal group, the model group (X-ray 8 Gy), the experimental-L group (X-ray 8 Gy+25 mg·kg-1·d-1 RAS-RH by gavage) and the experimental-H group (X-ray 8 Gy+50 mg·kg-1·d-1 RAS-RH by gavage), with ten rats in each group. 2 h after the last administration, cardiac function was evaluated using echocardiography; serum levels of inflammatory factors, including interleukin-18 (IL-18), IL-1β and tumor necrosis factor-alpha (TNF-α) were measured using enzyme-linked immunosorbent; relative protein expression levels of NLRP3, Caspase-1, GSDMD, IL-18 and IL-1β in myocardial tissue were detected using Western blotting.
The left ventricular ejection fraction (LVEF) in experimental-L group, experimental-H group, normal group and model group were (66.61±1.04)%, (71.89±0.69)%, (81.45±1.34)% and (47.62±1.67)%; the serum levels of IL-18 were (171.21±3.92), (145.60±3.37), (125.51±2.94) and (201.80±4.05) ng·mL-1; the IL-1β levels were (43.03±0.68), (41.12±1.01), (36.12±0.98) and (51.19±0.85) ng·mL-1; the TNF-α levels were (484.96±3.35), (441.24±3.94), (381.32±4.16) and (566.51±4.98) ng·mL-1; the relative expression levels of NLRP3 protein in myocardial tissue were 0.54±0.02, 0.34±0.02, 0.20±0.02 and 0.75±0.03; the relative expression levels of Caspase-1 protein were 0.52±0.02, 0.44±0.02, 0.36±0.02 and 0.65±0.03; the relative expression levels of GSDMD-NT protein were 0.53±0.02, 0.42±0.01, 0.33±0.02 and 0.73±0.03; the relative expression levels of IL-18 protein were 0.50±0.02, 0.42±0.01, 0.13±0.01 and 0.63±0.02; the relative expression levels of IL-1β protein were 0.59±0.02, 0.42±0.02, 0.27±0.02 and 0.79±0.03, respectively. The indicators in the model group were significantly different compared to the normal group, and the indicators in the experimental-L and experimental-H groups were significantly different from the model group, with statistical significance (all P<0.05).
RAS-RH may improve RIHD by regulating the NLRP3/Caspase-1/GSDMD signaling pathway.
To investigate the effect of ulinastatin on epithelial-mesenchymal transition (EMT) of bladder cancer T24 cells.
Bladder cancer T24 cells were randomly divided into blank, control, experimental, combined groups. The cells in the blank group were cultured normally; and the cells in the control group were treated with RPMI-1640 medium containing 0.75 μmol·L-1 KYA1797K; the cells in the experimental group were treated with RPMI-1640 medium containing 5.00 μmol·L-1 ulinastatin and the cells in the combined group were treated with RPMI-1640 medium containing 5.00 μmol·L-1 ulinastatin and 0.75 μmol·L-1 KYA1797K. The treatment time was 48 hours. The cell viability was detected by methyl thiazolyl tetrazolium (MTT) assay. Transwell assay was used to detect the invasion and migration ability of cells. The protein expression levels of epithelial-mesenchymal transition related proteins, wingless-type MMTV integration site family 3α (Wnt3α) and β-catenin were detected by Western blotting.
The survival rates of the blank group, control group, experimental group and combined group were (100.00±0.00)%, (73.28±6.37)%, (76.98±5.82)% and (40.36±3.21)%, respectively; the numbers of invasive cells were 66.83±8.18, 33.33±3.27, 38.67±4.32 and 11.33±1.21, respectively; the migration number were 79.33±6.38, 53.00±6.26, 52.33±3.14 and 28.33±5.28, respectively; the relative expression levels of E-cadherin protein were 0.23±0.08, 0.51±0.02, 0.58±0.05 and 0.82±0.03, respectively; the relative expression levels of Vimentin protein were 0.78±0.03, 0.55±0.02, 0.58±0.06 and 0.27±0.06, respectively; the relative expression levels of N-cadherin were 0.83±0.08, 0.59±0.02, 0.62±0.02 and 0.31±0.09, respectively; the relative expression levels of Wnt3α protein were 0.85±0.09, 0.28±0.13, 0.29±0.05 and 0.12±0.01, respectively; the relative expression levels of β-catenin were 0.81±0.05, 0.25±0.07, 0.22±0.03 and 0.08±0.02, respectively. The above indexes in the control group and experimental group were significantly different from those in the blank group and combined group (all P<0.05).
Ulinastatin can inhibit the epithelial-mesenchymal transition of bladder cancer T24 cells, and its mechanism may be related to the inhibition of Wnt signaling pathway.