OBJECTIVE:To verify the effect of Weichangkang capsule(WCK) on the function of gastrointestinal tract.MET-HODS:The effects on movement of charcoal powder in mice and secretion of digestive enzyme and absorption of D-xylopyranose into serum in rats were studied.RESULTS:WCK capsule markedly increased the movement of charcoal powder in mice,secretion of digestive enzyme and absorption of D-xylopyranose into serum in rats.CONCLUSION:WCK capsule could obviously improve the dysfunction of gastrointestinal tract.

Objective To study the effecet of oxidized low-density lipoprotein(Ox-LDL) on endothelium-dependent relaxation and mechanism of susceptibility to atherosclerosis(AS) in hyperlipdemic male patients.(Methods)LDL isolated from 13 normal patients and 29 hyperlipidemic patients were modified by CuSO_4.The amount of malondialdehyde(MDA) was measured by TBARS.The amount of lysophosphatidylcholine(LPC) was determined by the Bartlett.Endothelium-dependent relaxation was produced by acetylcholine.Results After LDL from normal and hyperlipidemic patients were modified by CuSO_4,the amount of MDA was increased(P

Objective To describe the characteristics of the symptoms of hospitalized patients with liver cirrhosis and to provide guidelines for clinical symptom management,alleviating the symptom distress of patients.Methods By convenient sampling,125 patients with liver cirrhosis were recruited into this study.The Memorial Symptom Assessment Scale (MSAS) combined with self-designed entries were used to measure the characteristics of symptom experience in the subjects.Results Patients with liver cirrhosis experienced a number of symptoms including fatigue,abdominal distension,pain,drowsiness,loss of weight,loss of appetite,poor sleep,feeling sad,dry mouth,anxiety.The incidences of 19 symptoms were higher than 50％.Symptoms occurred frequently and constantly ranged from 0.8％ to 44.0％,the symptoms occurred with moderate to severe ranged from 1.6％ to 61.6％,and symptom distress was from 0 to 22.4％.The score of PSYCH subscale,PHYS subscale,and the Global Distress Index was (1.02±0.51),(1.03±0.36) and (1.13±0.41) respectively.The total score of MSAS was (0.80±0.29),self-designed entry was (1.00±0.55).Conclusions Hospitalized patients with liver cirrhosis suffer from an array of symptoms,common symptoms in patients with liver cirrhosis in hospital,the degree of symptom in frequency,severity and distress are differcnt.Patients' overall symptoms level is relatively low,but the degree of psychological dis-tress is higher.Medical staffs must strengthen the psychological nursing intervention for patients,using multi-dimensional instrument to do systematic assessment,making sure effective symptom management.

Objective:To investigate the effect and mechanism of Acyl-CoA: lysocardiolipin acyltransferase 1 (ALCAT1) on hepatocyte steatosis and oxidative stress in fatty liver cell model.Methods:A fatty liver cell model was established and induced by free fatty acids (FFA). The expression of ALCAT1 in fatty liver cell model was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. The empty siRNA plasmid and ALCAT1 siRNA plasmid were constructed. For the fatty liver cell model group, human normal hepatocytes (L-02 cells) were transfected with empty siRNA plasmid for 24 hours, and then cultured with FFA for 24 hours. For the ALCAT1 interfering group, L-02 cells were transfected with ALCAT1 siRNA plasmid for 24 hours, and then cultured with FFA for 24 hours. And L-02 cells cultured in common medium were used as as blank control group. Lipid droplet deposition and mitochondrial morphology were observed under transmission electron microscopy. The expression levels of autophagy-associated proteins (microtubule-associated protein 1 light chain 3 (LC3)-Ⅱ and Beclin1) and key proteins of autophagy signal pathway (mammalian target of rapamycin (mTOR) and serine/threonine kinase (AKT)) were measured by Western blotting. The expression levels of oxidative stress products (malondialdehyde, 4-hydroxynonenal (4-HNE) and reactive oxygen species (ROS)) and inflammatory factors (interleukin-6(IL-6) and tumor necrosis factor (TNF)-α) were detected by enzyme-linked immunosorbent assay (ELISA) kits. Independent sample t test was used for statistical analysis. Results:The mRNA and protein expression levels of ALCAT1 of the fatty liver cell model group were both higher than that of negative control group (9.26±0.83 vs. 1.02±0.12, 0.35±0.02 vs. 0.17±0.01), and the differences were statistically significant ( t=9.82 and 6.83, both P<0.05). The results of electron microscopy indicated that the deposition of lipid droplets of the fatty liver cell model group and ALCAT1 interfering group were both higher than that of blank control group (17.67±3.52 and 7.67±0.33 vs. 4.33±0.33), the quantity of lipid droplets deposition of ALCAT1 interfering group was lower than that of fatty liver cell model group (7.67±0.33 vs. 17.67±3.52), and the differences were statistically significant ( t=3.76, 7.07 and 2.82, all P<0.05). The degree of mitochondria swelling of fatty liver cell model group was higher than that of blank control group and the degree of mitochondria swelling of ALCAT1 interfering group was lower than that of fatty liver cell model group. The results of Western blotting showed that the expression level of LC3-Ⅱof the fatty liver cell model group was higher than that of the blank control group (0.43±0.01 vs. 0.28±0.02), and the difference was statistically significant ( t=7.32, P<0.05). However there was no significant difference in the expression level of Beclin1 between fatty live cell model group and blank control group (0.93±0.05 vs. 0.98±0.05, P>0.05). The expression levels of LC3-Ⅱ and Beclin1 of the ALCAT1 interfering group were both higher than those of the fatty liver cell model group and blank control group (0.95±0.04 vs. 0.42±0.01 and 0.28±0.02, 2.07±0.06 vs. 0.93±0.05 and 0.98±0.05), and the differences were statistically significant ( t=13.30, 15.63, 14.05 and 13.02, all P<0.05). The expression levels of mTOR of the fatty liver cell model group and ALCAT1 interfering group were both lower than that of the blank control group (1.44±0.02 and 0.74±0.01 vs. 1.93±0.10), the expression level of mTOR of the ALCAT1 interfering group was lower than that of the fatty liver cell model group (0.74±0.01 vs. 1.44±0.02), and the differences were statistically significant ( t=4.83, 12.04 and 32.14, all P<0.05). The expression levels of phosphorylated AKT of the fatty liver cell model group and ALCAT1 interfering group were both lower than that of the blank control group (0.14±0.01 and 0.07±0.01 vs. 0.28±0.01), while the expression level of phosphorylated AKT of the ALCAT1 interfering group was lower than that of the fatty liver cell model group (0.07±0.01 vs. 0.14±0.01), and the differences were statistically significant ( t=8.59, 14.10 and 5.96, all P<0.05). The results of ELISA indicated that the expression levels of ROS, malondialdehyde, 4-HNE, IL-6 and TNF-α of the fatty liver cell model group and the ALCAT1 interfering group were all higher than those of the blank control group ((11.44±0.30) and (5.84±0.36) g/L vs. (1.72±0.38) g/L; (19.94±2.47) and (11.95±1.55) μmol/L vs. (1.47±0.18) μmol/L; (5.00±0.43) and (2.99±0.37) ng/L vs. (1.46±0.23) ng/L; (203.40±5.16) and (92.07±11.98) ng/L vs. (23.32±3.33) ng/L; (123.70±8.38) and (67.42±4.88) ng/L vs. (47.18±4.57) ng/L), and the differences were all statistically significant ( t=19.86, 7.86, 7.45, 6.74, 7.22, 3.49, 29.34, 5.53, 8.02 and 3.03, all P<0.05). While the expression levels of ROS, 4-HNE, IL-6 and TNF-α of the ALCAT1 interfering group were all lower than those of the fatty liver cell model group ((5.84±0.36) g/L vs. (11.44±0.30) g/L, (2.99±0.37) ng/L vs. (5.00±0.43) ng/L, (92.07±11.98) ng/L vs. (203.40±5.16) ng/L and (67.42±4.88) ng/L vs. (123.70±8.38) ng/L), and all the differences were statistically significant ( t=11.99, 3.51, 8.54 and 5.81, all P<0.05). There was no statistically significant difference in the expression of malondialdehyde between ALCAT1 interfering group and fatty liver cell model group ((11.95±1.55) μmol/L vs. (19.94±2.47) μmol/L, P>0.05). Conclusions:The expression of ALCAT1 is up-regulated in fatty liver cell model. Knockdown of ALCAT1 can inhibit the expression of mTOR pathway proteins, activate autophagy, alleviate hepatocyte steatosis, oxidative stress and inflammatory response.

Objective To investigate the effects of miR-181b-5p on cells proliferation and apoptosis in acute myeloid leukemia (AML) by targeting paired box 9 (PAX9). Methods The relationship between expression level of PAX9 and prognosis in AML patients was analyzed by gene expression profiling interactive analysis (GEPIA) database and The Cancer Genome Atlas (TCGA) database. Kasumi-1 and AML5 cells were transfected with empty vector (Vector group) or PAX9 (PAX9 group). The proliferation activity was detected by CCK-8 assay, and cells cycle and apoptosis were detected by flow cytometry. Expressions of cyclin-dependent kinase 2 (CDK2), cyclin B1 (CCNB1), B-cell lymphoma 2 (Bcl2) and Bcl2-associated X protein (BAX) were detected by Western blot analysis. The targeted microRNA (miRNA) by PAX9 was predicted by bioinformatics analysis, and the targeted effect was verified by luciferase reporter assay. The level of PAX9 mRNA was detected by real-time quantitative PCR, and expression of PAX9 protein was detected by Western blot analysis. Kasumi-1 and AML5 cells were transfected with miR-NC (miR-NC group) or miR-181b-5p (miR-181b-5p group). The cells were further transfected with PAX9 (miR-181b-5p combined with PAX9 group) in miR-181b-5p group. The proliferation, cycle and apoptosis of cells were detected by the above methods.Results GEPIA and TCGA databases showed that the expression of PAX9 was down-regulated in AML patients, which was correlated with poor prognosis. In Kasumi-1 and AML5 cells, compared with Vector group, proliferation activity of cells, percentage of cells in S phase, and expressions of CDK2, CCNB1 and Bcl2 proteins were decreased, while percentage of cells in G0/G1 phase, apoptosis rate and the expression of BAX protein were increased in PAX9 group. It was confirmed by double luciferase reporter assay that PAX9 was the target gene of miR-181b-5p. Compared with miR-NC group, proliferation activity of cells, percentage of cells in S phase, and expressions of CDK2, CCNB1 and Bcl2 proteins were increased, while percentage of cells in G0/G1 phase, apoptosis rate and the expression of BAX protein were decreased in miR-181b-5p group. Compared with miR-181b-5p group, proliferation activity of cells, percentage of cells in S phase, and expressions of CDK2, CCNB1 and Bcl2 proteins were decreased, while percentage of cells in G0/G1 phase, apoptosis rate and the expression of BAX protein were increased in miR-181b-5p combined with PAX9 group. Conclusion The miR-181b-5p can promote the proliferation of AML cells and delay apoptosis by inhibiting PAX9.
Humans ; Apoptosis/genetics* ; bcl-2-Associated X Protein ; Cell Line, Tumor ; Cell Proliferation/genetics* ; Leukemia, Myeloid, Acute/pathology* ; Luciferases ; MicroRNAs/metabolism* ; PAX9 Transcription Factor/genetics*