To analyze the preventive effect of potassium citrate sustained-release tablets on stent mural calculi after ureteral lithotripsy for upper urinary tract calculi and influence on urinary calcium ion and urinary oxalic acid concentration.

The patients with upper urinary tract calculi who underwent ureteral lithotripsy were randomly divided into control group and treatment group. Both groups of patients received routine dietary guidance and health education after surgery. The control group received routine anti-infection, pain relief and stone removal treatment after surgery, while the treatment group received oral potassium citrate sustained-release tablets on the basis of the control group after surgery (1.08 g per time, 3 times a day) continuously until the ureteral stent tube was removed. The ureteral stent tube was removed at 4 or 8 weeks after surgery based on the patient’s recovery status, and the occurrence of stent mural calculi was observed, and 24-hour urine samples were collected from patients during follow-up at 4 weeks after surgery to detect urine pH, levels of uric acid, oxalic acid and citric acid and concentrations of calcium and phosphorus ions. The differences in occurrence of ureteral stent calculi and urine detection indicators were compared between the two groups.

In treatment group, 42 cases were enrolled but 2 cases were lost to follow-up, and 40 cases were finally included for statistical analysis. In control group, 43 patients were included but 3 patients were lost to follow-up, thus 40 patients were enrolled for statistical analysis. Ureteral stents were removed at 4 weeks or 8 weeks after surgery in both groups. The treatment group had a total of 64 ureteral stent tubes retained, and the incidence rate of stent mural calculi was 1.56% (1 case/64 cases). The control group had a total of 62 ureteral stent tubes retained, and the incidence rate of stent mural calculi was 11.29% (7 cases/62 cases, P<0.05). At 4 weeks after surgery, the calcium ion concentrations in treatment group and control group were (2.63±0.66) and (3.45±1.02) mmol·L^-1, oxalic acid levels were (0.41±0.04) and (0.52±0.07) mmol·L^-1, phosphorus ion concentrations were (12.36±2.38) and (16.01±2.16) mmol·L^-1, uric acid levels were (2.02±0.17) and (2.43±0.23) mmol·L^-1, urine pH values were 6.85±0.34 and 6.24±0.34, urine citric acid levels were (1.61±0.22) and (1.39±0.17) mmol·L^-1, respectively (all P<0.05). The adverse drug reactions in treatment group during medication included nausea and diarrhea, with a total incidence rate of 10.00% (4 cases/40 cases). No adverse drug reactions were observed in the control group.

Potassium citrate sustained-release tablets can reduce the incidence rate of stent mural calculi after ureteral lithotripsy for upper urinary tract calculi, and lower the concentrations of urinary calcium ion and oxalic acid.

To observe the clinical efficacy and safety of ferulic acid piperazine tablets combined with continuous renal replacement therapy in the treatment of children with acute renal failure.

Children with acute renal failure were randomly divided into control group and treatment group. Both groups were given basic treatment, based on which, the control group was given continuous renal replacement therapy; the treatment group was given piperazine ferulate tablets 100 mg per time, orally, tid, on the basis of control group. Two groups were treated for 2 weeks. The clinical efficacy, renal function, levels of renal injury markers and safety were compared between the two groups.

Treatment group was enrolled 85 cases, 2 cases dropped out, and 83 cases were finally included in the statistical analysis. Control group was enrolled 84 cases, 3 cases dropped out, and 81 cases were finally included in the statistical analysis. After treatment, the total effective rates of treatment and control groups were 92.77% (77 cases/83 cases) and 81.48% (66 cases / 81 cases) with statistically significant difference (P<0.05). After treatment, the serum creatinine levels of treatment and control groups were (120.35±17.12) and (148.12±20.03) μmoL·L^-1; the blood urea nitrogen levels were (12.29±2.14) and (15.64±3.01) μmoL·L^-1; the β2-microglobulin levels were (1.87±0.25) and (2.14±0.39) mg·L^-1; the 24-h urinary protein quantification were (0.94±0.31) and (1.24±0.47) g·24 h^-1; N-acetyl-β-D-glucosidase contents were (17.03±2.98) and (20.36±3.51) U·L^-1; the renal injury molecule 1 contents were (1.62±0.27) and (2.09±0.32) μg·L^-1; the neutrophil gelatinase-associated lipid transport protein contents were (50.36±8.13) and (59.23±10.14) μg·L^-1, respectively, and the differences were all statistically significant (all P<0.05). The adverse drug reactions of treatment group were nausea, vomiting and abdominal distension, while those in the control group were dizziness, nausea and vomiting. The total incidences of adverse drug reactions in the treatment and control groups were 7.23% and 4.94% without significant difference (P>0.05).

Ferulic acid piperazine tablets combined with continuous renal replacement therapy have definitive clinical efficacy in the treatment of children with acute renal failure, which can significantly improve the renal function of children, reduce renal injury, without increasing the incidence of adverse drug reactions.

To explore the specific mechanism of the gastric protective effect of salvianolic acid B (Sal B) on precancerous lesions of the stomach (PLGC) in rats by regulating the microRNA (miR)-106b-5p/B-cell translocation gene 3 (BTG3) molecular axis.

Except for the NC group, the rat models of PLGC were established. The rats were randomly divided into the NC group (without any treatment, intragastric administration of normal saline), the model group (after successful modeling, intragastric administration of normal saline), the experimental group (intragastric administration of Sal B based on the model group), the NC mimic group (based on the experimental group, injection of NC mimic plasmid via the tail vein), the miR-106b-5p mimic group (based on the experimental group, injection of miR-106b-5p mimic plasmid via the tail vein), the pcDNA3.1-NC group (based on the miR-106b-5p mimic group, intraperitoneal injection of pcDNA3.1-NC plasmid) and the pcDNA3.1-BTG3 group (based on the miR-106b-5p mimic group, intraperitoneal injection of pcDNA3.1-BTG3 plasmid). Quantitative real-time polymerase chain reaction experiments were carried out to detect the mRNA expression levels of miR-106b-5p, BTG3 and inflammatory factors in the gastric mucosa tissues. Enzyme-linked immunosorbent assays were performed to detect the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and gastrin-17 (G-17) in the serum. Western blot experiments were used to detect the levels of proteins related to the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and mucin 2 (MUC2) in the gastric mucosa tissues.

The relative expression levels of miR-106b-5p in the NC group, the model group and the experimental group were 1.00±0.08, 1.76±0.35 and 1.33±0.26, respectively, and the relative expression levels of BTG3 mRNA were 1.00±0.05, 0.39±0.06 and 0.81±0.15, respectively. There were statistically significant differences in the above-mentioned indicators between the model group and the NC group, as well as between the experimental group and the model group (all P<0.05). The levels of SOD in the NC group, the model group, the experimental group, the NC mimic group, the miR-106b-5p mimic group, the pcDNA3.1-NC group and the pcDNA3.1-BTG3 group were (197.81±47.15), (118.54±20.49), (172.29±34.34), (176.78±35.57), (127.65±21.23), (119.41±20.50) and (158.28±31.07) U·mL^-1, respectively; the levels of MDA were (3.44±0.67), (8.08±1.32), (3.92±0.75), (3.84±0.70), (6.50±1.21), (6.34±1.17) and (4.22±0.79) nmol·mL^-1, respectively; the levels of G-17 were (221.57±40.26), (155.62±28.43), (201.13±37.35), (194.85±35.24), (162.72±31.65), (160.04±29.37) and (189.32±32.15) pg·mL^-1, respectively; the levels of PI3K were 1.00±0.14, 1.81±0.36, 1.23±0.21, 1.19±0.20, 1.65±0.32, 1.70±0.35 and 1.38±0.28, respectively; the ratios of phosphorylated AKT/AKT were 1.00±0.09, 1.94±0.39, 1.27±0.23, 1.21±0.18, 1.77±0.37, 1.73±0.33 and 1.42±0.26, respectively. There were statistically significant differences in the above-mentioned indicators between the miR-106b-5p mimic group and the NC mimic group, and between the pcDNA3.1-BTG3 group and the pcDNA3.1-NC group (all P<0.05).

Sal B may exert a gastric protective effect by down-regulating the targeted negative regulation of BTG3 expression by miR-106b-5p, inhibiting the activation of the PI3K/AKT signaling pathway, thereby alleviating the oxidative stress and inflammatory response in PLGC rats and improving the condition of the gastric mucosa.

To observe the clinical efficacy and safety of agomelatine combined with paroxetine tablets in patients with depression and insomnia, and its effects on neurotransmitter levels and sleep.

The patients with depression and insomnia were divided into control group and treatment group, according to random number table. Control group was treated with paroxetine tablets 20 mg, oral, treatment course was 8 weeks. Treatment group was treated with agomelatine 25 mg and paroxetine tablets 20 mg, once a day, treatment course was 8 weeks. The Hamilton depression rating scale (HAMD), Montreal cognitive assessment scale (MoCA), neurotransmitters [norepinephrine (NE), 5-hydroxytryptamine (5-HT), dopamine (DA)], Pittsburgh sleep quality index (PSQI) and incidence of adverse drug reactions between two groups were compared.

Treatment group was enrolled 60 cases; control group was enrolled 60 cases. After 8 weeks of treatment, the HAMD in treatment group and control group were (17.33±1.54) and (21.19±1.87) scores; MoCA were (29.01±0.19) and (28.52±0.21) scores; NE levels were (65.56±4.63) and (53.74±4.52) ng·mL^-1; 5-HT levels were (165.82±7.17) and (149.63±8.48) ng·mL^-1; DA levels were (582.73±17.52) and (543.85±20.38) ng·mL^-1, sleep latency were (1.09±0.12) and (1.53±0.15) scores; sleep efficiency were (1.12±0.17) and (1.58±0.20) scores; hypnotic drug were (1.01±0.13) and (1.42±0.15) scores; subjective sleep quality were (1.14±0.10) and (1.62±0.16) scorse; sleep persistence were (1.16±0.11) and (1.55±0.13) scores; the score for sleep disorders were (1.07±0.14) and (1.52±0.17) scores; daytime functional disorders were (0.99±0.16) and (1.51±0.18) scores, all with statistically significant difference (all P<0.05). The adverse drug reactions in treatment group and control group were 11.67% and 8.33%, with no statistically significant differences (P>0.05).

Administration of agomelatine and paroxetine tablets to patients with depression and insomnia can improve depressive symptoms, cognitive function, sleep conditions, regulate the expression of neurotransmitters such as NE and 5-HT, and has good safety.

To investigate the inhibition of NG108-15 cells proliferation by Xanthohumol (XN) and its effects on reactive oxygen species (ROS), extracellular signal-regulated kinase (ERK) pathway and cell cycle.

NG108-15 cells were divided into control group (conventional culture), experimental-L group, experimental-M group, experimental-H group (20, 40, and 60 μmol·L^-1 XN), NAC combined with XN experimental group [10 μmol·L^-1 N-acetylcysteine (NAC)+40 μmol·L^-1 XN] and ERK inhabitor combined with XN experimental group (20 μmol·L^-1 ERK inhibitor PD98059+40 μmol·L^-1 XN). Cell proliferation capacity was detected by cell counting kit 8 (CCK-8) and trypan blue staining assay; ROS levels were detected by ROS kit; cell cycle and apoptosis levels were detected by flow cytometry; protein relative expression levels of ERK, p-ERK and Caspase 3 were detected by Western blot.

The cell proliferation activities of the control group and the experimental-L group, experimental-M group and experimental-H group were (99.89±1.52)%, (87.57±6.23)%, (51.96±3.08)% and (37.11±1.57)%, respectively; the cell death rates were (4.65±1.57)%, (15.54±1.94)%, (41.06±2.77)% and (65.22±5.81)%, respectively; the average fluorescence intensities of ROS in the control group, the experimental-M group and the NAC combined with XN experimental group were 176.51±25.17, 716.48±95.15 and 543.80±48.91. The relative expression levels of p-ERK protein in the control group, the experimental-M group, and the ERK inhibitor combined with XN experimental group were 0.54±0.04, 1.13±0.18 and 0.31±0.33; the proportions of G2 phase cells were (15.56±1.43)%, (20.31±2.17)% and (16.14±0.81)%, respectively. Compared with the control group, the above indicators in the experimental-L, -M, -H groups showed statistically significant differences (all P<0.001). Compared with the experimental-M group, the control group and the NAC combined with XN experimental group showed statistically significant differences (P<0.05, P<0.01, P<0.001). Compared with the experimental-M group, the ERK inhibitor combined with XN experimental group showed statistically significant differences (P<0.05, P<0.01, P<0.001).

Xanthohumol demonstrates potent inhibition of NG108-15 cells proliferation, with its molecular mechanism likely involving G2/M phase cell cycle arrest through ROS upregulation and activation of the ERK signaling pathway.

To investigate the regulatory mechanism of plantamajoside (PMS) on the growth and metastasis of non-small cell lung cancer (NSCLC).

A549 cells were divided into control group (normal culture), model group (40 μg·mL^-1 PMS), NC inhibitor group (40 μg·mL^-1 PMS+NC inhibitor), miR-525-5p inhibitor group (40 μg·mL^-1 PMS+miR-525-5p inhibitor), sh-NC group (40 μg·mL^-1 PMS+miR-525-5p inhibitor+sh-NC) and sh-ubiquitin conjugating enzyme E2C (UBE2C) group (40 μg·mL^-1 PMS+miR-525-5p inhibitor+sh-UBE2C). Transwell assay was used to evaluate the invasion ability of A549 cells after different treatments. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay was used to evaluate the apoptosis of A549 cells after different treatments. At the animal level, mice were injected with A549 cell suspension (5×10⁶/100 μL) to construct the NSCLC model. They were randomly divided into model-M group, PMS group (50 mg·kg^-1 PMS), miR-525-5p inhibitor-M group (50 mg·kg^-1 PMS+miR-525-5p inhibitor) and sh-UBE2C-M group (50 mg·kg^-1 PMS+miR-525-5p inhibitor+sh-UBE2C). All groups were treated for 5 days with once a day. The size of the transplanted tumor was measured with a ruler every 7 days, and the transplanted tumor was removed and weighed on the 28th day. The number of Transwell invasions in control group, model group, NC inhibitor group, miR-525-5p inhibitor group, sh-NC group and sh-UBE2C group were 173.62±23.46, 82.05±14.17, 84.69±13.82, 143.48±19.81, 139.57±18.24 and 105.93±16.25, respectively; the apoptosis rates were (22.65±4.01)%, (53.34±8.93)%, (51.46±8.81)%, (37.52±5.86)%, (34.83±5.27)% and (48.75±6.19)%, respectively. Compared in model group and control group, compared in miR-525-5p inhibitor group and NC inhibitor group, compared in sh-UBE2C group and sh-NC group, there were significant differences in the number of Transwell invasion and apoptosis rates (all P<0.05). At the animal level, 28 d tumor volumes of model-M group, PMS group, miR-525-5p inhibitor-M group and sh-UBE2C-M group were (966.30±176.53), (495.70±52.40), (841.10±121.25) and (623.80±105.85) mm³, respectively; the tumor weight on day 28 were (1.43±0.52), (0.75±0.21), (1.32±0.43) and (0.85±0.26) g, respectively. Differences of the tumor volume and weight between PMS group and model-M group, sh-UBE2C-M group and miR-525-5p inhibitor-M group were statistically significant at the 28th day (P<0.01, P<0.001).

PMS can significantly inhibit the growth and metastasis of NSCLC by regulating the miR-525-5p/UBE2C axis.

To investigate the effects of Cepharanthine on apoptosis, energy metabolism and angiogenesis of breast cancer cells by regulating the microRNA (miR)-378c/Golgi transport 1A protein (GOLT1A) axis.

MDA-MB-231 cells in the logarithmic growth phase were divided into the following groups: Control group (no treatment), NC inhibitor group (transfected with miR-378c inhibitor negative control), miR-378c inhibitor group (transfected with miR-378c inhibitor), si-NC group (transfected with si-NC plasmid), si-GOLT1A group (transfected with si-GOLT1A plasmid), Cepharanthine group (20 μmol·L^-1 Cepharanthine), Cepharanthine combined with miR-378c inhibitor group (Cepharanthine group with miR-378c inhibitor transfection) and miR-378c inhibitor combined with si-GOLT1A group (Cepharanthine group with co-transfection of miR-378c inhibitor and si-GOLT1A plasmid). Real-time fluorescence quantitative polymerase chain reaction was used to detect the relative expression levels of miR-378c, GOLT1A, vascular endothelial growth factor A (VEGFA) and thrombospondin-1 (THBS1); kits were used to detect energy metabolism indicators; immunofluorescence was used to detect VEGFA and THBS1 expression levels.

The relative expression levels of miR-378c in the control group and Cepharanthine group were 1.00±0.14 and 3.26±0.48, respectively; the relative expression levels of GOLT1A mRNA were 1.00±0.15 and 0.43±0.07, respectively. The glutamine concentrations in the control group, Cepharanthine group, Cepharanthine combined with miR-378c inhibitor group and miR-378c inhibitor combined with si-GOLT1A group were (22.03±3.14), (8.27±1.94), (17.25±2.86) and (13.11±2.28) nmol·10^-7 cells, respectively; the acetyl coenzyme A concentrations were (11.32±2.06), (5.71±1.19), (9.62±1.85) and (6.67±1.63) nmol·10^-6 cells, respectively; the succinate concentrations were (53.67±6.92), (21.24±3.87), (39.82±4.39) and (30.36±4.21) nmol·mg^-1·Pr^-1, respectively; the ATP production values were (2.32±0.42), (0.96±0.12), (1.91±0.33) and (1.16±0.26) mmol·mg^-1·Pr^-1, respectively; the relative expression levels of VEGFA mRNA were 1.00±0.14, 0.56±0.10, 0.84±0.13 and 0.69±0.10, respectively; the relative expression levels of THBS1 mRNA were 1.00±0.12, 3.43±0.57, 2.04±0.36 and 3.10±0.52, respectively; the relative fluorescence intensities of VEGFA were 1.00±0.11, 0.37±0.05, 0.76±0.09 and 0.48±0.06, respectively; and the relative fluorescence intensities of THBS1 were 1.00±0.09, 3.71±0.62, 1.88±0.31 and 2.55±0.37, respectively. All the above indicators showed significant differences between the control group and the Cepharanthine group, the Cepharanthine group and the Cepharanthine combined with miR-378c inhibitor group, the Cepharanthine combined with miR-378c inhibitor group and the miR-378c inhibitor combined with si-GOLT1A group (P<0.05, P<0.01, P<0.001).

Cepharanthine can promote apoptosis and inhibit energy metabolism and angiogenesis in breast cancer cells, which may be related to its regulation of the miR-378c/GOLT1A axis.