Effects of praziquantel isomers on the proliferation and activation of the LX-2 human hepatic stellate cell line / 中国血吸虫病防治杂志

Objective To compare the effects of levo-praziquantel (L-PZQ) and dextro-praziquantel (D-PZQ) on the proliferation and activation of the human hepatic stellate cell line LX-2 in vitro. Methods LX-2 cells were stimulated with transforming growth factor-β (TGF-β). LX-2 cell proliferation was measured using the CCK-8 assay after 24 h stimulation with 0 to 50 μg/mL concentrations of praziquantel, and the gene and protein expression of type Ⅰ collagen (collagen Ⅰ), type Ⅲ collagen (collagen Ⅲ) and α-smooth muscle actin (α-SMA) was quantified in LX-2 cells using quantitative real-time PCR (qPCR) and Western blotting assays 24 h and 48 h following stimulation with 15 μg/mL praziquantel to detect LX-2 cell activation. Results There were significant differences in the survival rate of LX-2 cells between L-PZQ and D-PZQ treatments at all concentrations (F = 6.119 and 79.180, both P values < 0.05). Either L-PZQ or D-PZQ at a concentration of < 30 μg/mL showed no remarkableeffectsonthe LX-2 cell proliferation (both P values > 0.05), and L-PZQ at a concentration of > 50 μg/mL and D-PZQ at a concentration of > 40 μg/mL inhibited the LX-2 cell proliferation (both P values < 0.05), while D-PZQ at concentrations of 40 μg/mL and 50 μg/mL showed greater inhibition on LX-2 cell proliferation than L-PZQ (t = 3.419 and 8.776, both P values < 0.05). There were significant differences in the collagen Ⅰ, collagen Ⅲ and α-SMA expression in LX-2 cells at both transcriptional (F = 21.55, 79.99 and 46.70, all P values < 0.05) and translational levels (F = 20.12, 30.29 and 32.93, all P values < 0.05) among the blank control group, TGF-β stimulation group, L-PZQ treatment group and D-PZQ treatment group. L-PZQ treatment resulted in remarkable inhibition on collagen Ⅲ and α-SMA gene expression in LX-2 cells (both P values < 0.05); however, the treatment showed no remarkable inhibition collagen Ⅰ gene expression or collagen Ⅰ, collagen Ⅲ or α-SMA protein expression in LX-2 cells (all P values > 0.05). In addition, D-PZQ treatment resulted in significant inhibition on collagen Ⅰ, collagen Ⅲ and α-SMA expression in LX-2 cells at both translational and transcriptional levels (all P values < 0.05), and D-PZQ showed higher inhibition on collagen Ⅰ, collagen Ⅲ and α-SMA gene expression in LX-2 cells than L-PZQ (all P values < 0.05). Conclusions Both L-PZQ and D-PZQ inhibit the proliferation and activation of LX-2 cells, and D-PZQ shows a higher inhibitory activity than L-PZQ.

Neonatal Exposure to Propofol Interferes with the Proliferation and Differentiation of Hippocampal Neural Stem Cells and the Neurocognitive Function of Rats in Adulthood via the Akt/p27 Signaling Pathway / 生物医学与环境科学（英文）

Objective@#Neonatal exposure to propofol has been reported to cause neurotoxicity and neurocognitive decline in adulthood; however, the underlying mechanism has not been established.@*Methods@#SD rats were exposed to propofol on postnatal day 7 (PND-7). Double-immunofluorescence staining was used to assess neurogenesis in the hippocampal dentate gyrus (DG). The expression of p-Akt and p27 were measured by western blotting. The Morris water maze, novel object recognition test, and object location test were used to evaluate neurocognitive function 2-month-old rats.@*Results@#Phosphorylation of Akt was inhibited, while p27 expression was enhanced after neonatal exposure to propofol. Propofol also inhibited proliferation of neural stem cells (NSCs) and decreased differentiation to neurons and astroglia. Moreover, the neurocognitive function in 2-month-old rats was weakened. Of significance, intra-hippocampal injection of the Akt activator, SC79, attenuated the inhibition of p-AKT and increase of p27 expression. SC79 also rescued the propofol-induced inhibition of NSC proliferation and differentiation. The propofol-induced neurocognition deficit was also partially reversed by SC79.@*Conclusion@#Taken together, these results suggest that neurogenesis is hindered by neonatal propofol exposure. Specifically, neonatal propofol exposure was shown to suppress the proliferation and differentiation of NSCs by inhibiting Akt/p27 signaling pathway.

The correlation between serum uric acid levels in the third trimester of pregnancy and adverse pregnancy outcomes / 中华内科杂志

Objective:To investigate the associations between serum uric acid levels during the third trimester of pregnancy and risks of adverse pregnancy outcomes.Methods:In this retrospective study, a cohort of 7 995 pregnant women who were hospitalized for childbirth from January 2014 to January 2019 were collected to compare pregnancy outcomes between subjects with or without hyperuricemia (HUA). A smooth curve analysis was used to evaluate the relationship between uric acid levels and preterm delivery, low birth weight and smaller than gestational age. Logistic regression analyses were performed to identify risk factors for adverse pregnancy outcomes, and the interaction of the factors.Results:During the third trimester of pregnancy, the uric acid levels of about 10% pregnant women were over 420 μmol/L. In those with HUA, the median neonatal birth weight was 2 590 (1 790, 3 410) g, the probability of premature birth was 49.81%, and the incidence of small than gestational age was 20.41%. These were significantly different from the women without HUA (the median neonatal birth weight: 3300 (2850, 3640) g; the probability of premature birth 23.09%; the incidence of small than gestational age 6.55%, respectively) (All P<0.001). Maternal uric acid levels were negatively correlated with neonatal birth weight, and positively correlated with the risk of smaller than gestational age. It has a U-shaped association with the probability of premature birth, and the lowest probability of premature birth was at 200-400 μmol/L of the uric acid. Risks of low birth weight (adjusted β=-5.22, 95% CI-6.46—-3.99) and smaller than gestational age (adjusted OR=1.03, 95% CI 1.02-1.04) were increased in the function of uric acid levels. High uric acid, hypertension, oligoamnios and preeclampsia were important risk factors for the adverse pregnancy outcomes. The risk of preterm delivery and low birth weight enhanced when hyperuricemia combined with hypertension and preeclampsia. Conclusions:Serum uric acid level can be used as one of reliable markers for predicting adverse pregnancy outcomes, which might provide theoretical basis for clinical intervention in practice.

Progress of researches on the actions of praziquantel against hepatic fibrosis / 中国血吸虫病防治杂志

Praziquantel not only has broad-spectrum anti-trematode and anti-tapeworm effects, but also has pharmacological effects such as regulating inflammatory response and anti-fibrosis. Hereby, the anti-fibrosis effect of praziquantel and its mechanism were reviewed in order to provide theoretical basis for the treatment of liver fibrosis.

Risk factors for hypoglycemia in preterm infants with a gestational age of ≤32 weeks / 中国当代儿科杂志

OBJECTIVE@#To investigate the risk factors for hypoglycemia after birth in preterm infants with a gestational age of ≤32 weeks.@*METHODS@#A retrospective analysis was performed for 86 neonates with hypoglycemia and a gestational age of ≤32 weeks who were admitted to the neonatal intensive care unit from January 2017 to June 2020 (hypoglycemia group). A total of 172 preterm infants with normal blood glucose who were hospitalized during the same period were randomly enrolled as the control group. Univariate analysis and multivariate logistic regression analysis were used to screen out the risk factors for hypoglycemia in preterm infants.@*RESULTS@#There were 515 preterm infants during the study, among whom 86 (16.7%) had hypoglycemia. Compared with the control group, the hypoglycemia group had significantly higher percentages of small for gestational age (SGA), cesarean section, maternal hypertension, and antenatal steroid administration (P<0.05), but significantly lower birth weight and rate of intravenous glucose use before blood glucose test (P<0.05). SGA (OR=4.311, 95%CI: 1.285-14.462, P<0.05), maternal hypertension (OR=2.469, 95%CI: 1.310-4.652, P<0.05), and antenatal steroid administration (OR=6.337, 95%CI: 1.430-28.095, P<0.05) were risk factors for hypoglycemia in preterm infants, while intravenous glucose use (OR=0.318, 95%CI: 0.171-0.591, P<0.05) was a protective factor against hypoglycemia in preterm infants.@*CONCLUSIONS@#SGA, maternal hypertension, and antenatal steroid administration may increase the risk of early hypoglycemia in preterm infants with a gestational age of ≤32 weeks, and intravenous glucose use is recommended as soon as possible after birth for preterm infants with a gestational age of ≤32 weeks to reduce the incidence rate of hypoglycemia.

Effect of boifilm cleaning agents and muctienzyme cheaning agents in the cleaning of tubular in thstruments / 现代临床护理

Objective To investigate the effect of biofilm cleaning agents and multienzyme cleaning agents in the cleaning of tubular instruments. Methods About 200 pieces of intramedullary nail used in tibial fracture and intramedullary nailing were selected and divided into multienzyme cleaning group and biomembrane cleaning group according to the order of recovery. According to the random number table method, each group had 100 pieces. The biofilm cleaning group was cleaned with biological membrane cleaning agent, and the multienzyme cleaning group was cleaned with multienzyme cleaning agent. The cleaning effect of luminal instruments was observed by means of microscopy, dipstick test and ATP bioluminescence assay. Result The cleaning quality and biofilm removal effect of the biofilm cleaning group were better than those of the multienzyme cleaning group (P<0.05). Conclusion Cleaning the luminal instruments with biomembrane cleaning agent can improve the cleaning quality and prevent the formation of bacterial biofilm.

Association between maternal pre-pregnancy body mass index and adverse outcomes of late preterm infants / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the association between maternal pre-pregnancy body mass index (BMI) and adverse outcomes of late preterm infants (LPI).</p><p><b>METHODS</b>A total of 367 LPI who were born from January 2011 to December 2015 and admitted to the neonatal ward were enrolled. The BMI criteria for Chinese population were used to analyze the factors for maternal pre-pregnancy BMI and its association with adverse outcomes of LPI (1 minute Apgar score ≤7, delivery room resuscitation, hospitalization days after birth >7 days, and ventilation duration ≥6 hours).</p><p><b>RESULTS</b>Of all LPIs, there were 64 LPI (17.4%) in the low maternal pre-pregnancy BMI group, 243 LPI (66.2%) in the normal maternal pre-pregnancy BMI group, and 60 LPI (16.4%) in the high maternal pre-pregnancy BMI group. Low pre-pregnancy BMI was the risk factor for 1 minute Apgar score ≤7 (OR=3.243, 95% CI: 1.102-9.546) and need for delivery room resuscitation (OR=3.492, 95%CI: 1.090-11.190), and high pre-pregnancy BMI was the risk factor for hospitalization days after birth >7 days (OR=1.992, 95%CI: 1.024-3.874).</p><p><b>CONCLUSIONS</b>Abnormal maternal pre-pregnancy BMI has adverse effects on the outcomes of LPI. In order to reduce these adverse outcomes BMI should be controlled within the normal range in pregnant women.</p>

Involvement of the mitochondrion-dependent and the endoplasmic reticulum stress-signaling pathways in isoliquiritigenin-induced apoptosis of HeLa cell / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>Isoliquiritigenin (ISL), a licorice chalconoid, is considered to be a bioactive agent with chemopreventive potential. This study investigates the mechanisms involved in ISL-induced apoptosis in human cervical carcinoma HeLa cells.</p><p><b>METHODS</b>Cell viability was evaluated using a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay. Apoptosis was determined by flow cytometry using an Annexin V-FITC Apoptosis Detection Kit. The intracellular ROS levels were assessed using a 2, 7-dichlorofluorescein probe assay. The mitochondrial membrane potential was measured with the dual-emission potential-sensitive probe 5, 5', 6, 6'-tetra-chloro-1, 1', 3, 3'-tetraethyl-imidacarbocyanine iodide (JC-1). The degradation of poly-ADP-ribose polymerase (PARP) protein, the phosphorylation of PKR-like ER kinase (PERK), the phosphorylation of the α-subunit of eukaryotic initiation factor 2 (eIF2α), the expression of the 78 kD glucose-regulated protein (GRP 78), and the activation of caspase-12 were analyzed via western blot analysis.</p><p><b>RESULTS</b>ISL significantly inhibited the proliferation, the increase in ROS levels and apoptotic rates of HeLa cells in a concentration-dependent manner. Moreover, ISL induced mitochondrial dysfunction, caspase activation, and PARP cleavage, which displayed features of mitochondria dependent on apoptotic signals. Besides, exposure of HeLa cells to ISL triggered endoplasmic reticulum (ER) stress, as indicated by the increase in p-eIF2α and GRP78 expression, ER stress-dependent apoptosis is caused by the activation of ER-specific caspase-12.</p><p><b>CONCLUSION</b>The findings from our study suggest that ISL-induced oxidative stress causes HeLa cell apoptosis via the mitochondrion-dependent and the ER stress-triggered signaling pathways.</p>

The mechanism of alteronol inhibiting the proliferation of human promyelocytic leukemia HL-60 cells / 药学学报

This study is to investigate the mechanism of human promyelocytic leukemia HL-60 cells proliferation induced by alteronol in vitro. Human promyelocytic leukemia HL-60 cells cultured in vitro were treated with different concentrations of alteronol. Inhibition rate was detected by SRB assay. Cellular morphological changes were observed by Hoechst and AO/EB (acridine orange/ethidium bromide dye) staining. The apoptosis rate was determined by Annexin V-FITC/PI assay. Cell cycle distribution was determined by flow cytometry. Western blotting analysis was carried out to determine the cell cycle related proteins. The proliferation of HL-60 cells treated with alteronol was inhibited in a concentration-dependent manner. Based on cell viability assay, observation on cell morphology and apoptosis rate, it confirmed that alteronol played an obvious role in proliferation inhibition of human promyelocytic leukemia HL-60 cells, but it did not induce apoptosis in human promyelocytic leukemia HL-60 cells in different concentrations groups. Alteronol could effectively inhibit the proliferation of human promyelocytic leukemia HL-60 cells inducing cell cycle arrest at G1 phase, as well as, alteration expression of cell cycle proteins level of CyclinD1 and pRb.

The mechanism of alteronol inhibiting the proliferation of human promyelocytic leukemia HL-60 cells / 药学学报

This study is to investigate the mechanism of human promyelocytic leukemia HL-60 cells proliferation induced by alteronol in vitro. Human promyelocytic leukemia HL-60 cells cultured in vitro were treated with different concentrations of alteronol. Inhibition rate was detected by SRB assay. Cellular morphological changes were observed by Hoechst and AO/EB (acridine orange/ethidium bromide dye) staining. The apoptosis rate was determined by Annexin V-FITC/PI assay. Cell cycle distribution was determined by flow cytometry. Western blotting analysis was carried out to determine the cell cycle related proteins. The proliferation of HL-60 cells treated with alteronol was inhibited in a concentration-dependent manner. Based on cell viability assay, observation on cell morphology and apoptosis rate, it confirmed that alteronol played an obvious role in proliferation inhibition of human promyelocytic leukemia HL-60 cells, but it did not induce apoptosis in human promyelocytic leukemia HL-60 cells in different concentrations groups. Alteronol could effectively inhibit the proliferation of human promyelocytic leukemia HL-60 cells inducing cell cycle arrest at G1 phase, as well as, alteration expression of cell cycle proteins level of CyclinD1 and pRb.