Based on LC-MS technology explored the metabolomics of Agrimonia pilosa intervening in non-small cell lung cancer A549 cells / 药学学报

The objective of this study was to analyze the effects on cell viability, apoptosis, and cell cycle of non-small cell lung cancer (NSCLC) A549 cells after intervention with Agrimonia pilosa (AP) and investigate Agrimonia pilosa anti-tumor activity in vitro. Meanwhile, liquid chromatography mass spectrometry (LC-MS) metabolomics technology was used to analyze the changes of cellular metabolites and metabolic pathways. The results of this study will provide a theoretical and experimental basis for investigating the mechanism of the effect of Agrimonia pilosa on non-small cell lung cancer A549 cells. The results showed that the cell nucleus of A549 cells crumpled and apoptosis occurred with the increase of drug concentration. The survival rate of the cells decreased, and the inhibition rate reached 21.5% and 91.74% under the low and high dose conditions, respectively. Lactate dehydrogenase (LDH) content increased (P < 0.05). Metabolomics results showed significant differences in metabolism between groups, thirty-three distinct metabolites including LysoPC(24:0/0:0), LysoPC(17:0/0:0) and PC(O-40:5) were deduced. The pathway enrichment showed that the Agrimonia pilosa plays an anti-tumor role mainly by regulating the metabolism of glycerophosphate and purine in A549 cells, in which the effect on glycerophosphate metabolism pathway was most significant. The results of combined pharmacodynamics suggested that Agrimonia pilosa might induce apoptosis and inhibit the growth of A549 cells by regulating LysoPC(24:0/0:0), LysoPC(17:0/0:0) and PC(O-40:5) metabolites in A549 cells.

Anti-injury effect of hydrogen-enriched water in a rat model of liver injury induced by aflatoxin B / 生理学报

The purpose of this study was to investigate the anti-injury effect and protective mechanism of hydrogen-enriched water in a rat model of acute liver injury induced by aflatoxin B (AFB). Healthy male Sprague-Dawley (SD) rats were randomly divided into control group, model group (AFB group) and hydrogen-enriched water treatment group (AFB+H group). The rat model of acute liver injury induced by AFB was established by single intragastric administration of AFB (2.0 mg/kg), and then the rats were treated with hydrogen-enriched water intragastrically. HE staining was used to observe the pathological changes of liver tissue. Blood samples were taken from vena cava to measure serum liver function indexes. Live tissue was sampled to detect malondialdehyde (MDA) and reduced glutathione (GSH) contents. Western blot was used to detect phosphorylation levels of MAPK signaling pathway proteins (ERK, JNK and p38 MAPK). The results showed that, compared with the AFB group, the AFB+H group exhibited increased body weights, alleviated acute liver injury, decreased activities of serum glutamic-pyruvic transaminase and glutamic oxaloacetic transaminase, as well as total bilirubin level in the serum. Meanwhile, hydrogen-enriched water decreased MDA content and increased GSH content in liver tissue. AFB-increased phosphorylation levels of ERK, JNK and p38 MAPK in liver tissue were down-regulated significantly by hydrogen-enriched water treatment. These results suggest that hydrogen-enriched water can alleviate liver injury induced by AFB, and its mechanism may be related to the reduction of oxidative stress and the inhibition of MAPK signal transduction pathway activation.

Expression of iNOS protein and gliacyte apoptosis in neonatal rats with white matter damage / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Inducible nitric oxide synthase (iNOS) is a main rate-limiting enzyme resulting in over-production of nitric oxide following hypoxia-ischemia (HI). The aim of this study was to observe the expression of iNOS protein and gliacyte apoptosis in the brains of premature rats after HI, in order to explore possible relationships of iNOS with white matter damage (WMD).</p><p><b>METHODS</b>One hundred and twelve 2-day-old premature rats were randomly subjected to right carotid ligation followed by 4 hrs hypoxic stress (WMD group) or sham operation (control group). The pups were sacrificed at 1, 3, 6, 12 hrs, and 1, 3 and 7 days after HI. Immunohistochemical technique was applied to determine the iNOS expression in periventricular white matter tissues. Gliacyte apoptosis was detected in these tissues by TUNEL.</p><p><b>RESULTS</b>Compared with the control group, iNOS expression began to increase 1 hr after HI and reached the peak 1 day after HI in the WMD group. Gliacyte apoptosis increased 1 hr after HI and peaked 1 day after HI in the WMD group compared with the control group.</p><p><b>CONCLUSIONS</b>In the neonatal rats with WMD, the expression of iNOS may be involved in the ischemic cellular events including apoptosis, and plays a role in the pathophysiological process of WMD.</p>

hTERT gene expression in children with beta-thalassemia major / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Human telomerase reverse transcriptase (hTERT) is a rate-limiting enzyme which dictates the activity of human telomerase and thus decides the life span of cells. The aim of this study was to explore the expression of hTERT in bone marrow from children with beta-thalassemia major and the relationship between the expression of hTERT and hemoglobin levels.</p><p><b>METHODS</b>Multiple allele specific polymerase chain reaction (MASPCR) was used for targeted DNA amplification and gene mutation analysis of beta-thalassemia. hTERT mRNA expression in bone marrow was examined using real-time reverse transcription polymerase chain reaction (RT-PCR) analysis in 29 children with beta-thalassemia major, in 10 children with agranulocytosis and in K562 cell line. The hemoglobin levels in peripheral blood were measured. The relationship between hTERT expression and hemoglobin levels was evaluated by the Spearman test in the beta-thalassemia major group.</p><p><b>RESULTS</b>hTERT mRNA expression significantly increased in bone marrow from children with beta-thalassemia major compared with that from children with agranulocytosis (0.2928+/- 0.0838 vs 0.0993+/- 0.0336; P<0.01), but was significantly lower than that in K562 cell line (0.8291+/- 0.0908) (P<0.01). A significantly inverse correlation was found between hTERT mRNA expression and hemoglobin levels (r=-0.841, P<0.01).</p><p><b>CONCLUSIONS</b>A low hemoglobin concentration might contribute to the up-regulation of marrow hTERT expression in children with beta-thalassemia major.</p>