To study the mechanisms of total flavonoid from Glycyrrhizae Radix et Rhizoma (TFGR) and its ingredient isoliquiritigenin (ISL) on their regulation of M2 phenotype polarization of macrophages. IL-4 (60 μg x L(-1)) induced RAW264.7 cells for 6 h to establish the M2 macrophage model. TFGR and ISL restrained breast cancer cells migration with the aid of M2 macrophages in vitro. TFGR and ISL inhibited gene and protein expression of Arg-1, up-regulated gene of HO-1 and protein expression of iNOS, enhanced the expression of microRNA 155 and its target gene SHIP1, meanwhile down-regulated.the phosphorylation of STAT3 and STAT6. So TFGR and ISL were the bioactive fraction and ingredient in Glycyrrhizae Radix et Rhizoma to reverse M2 phenotype macrophages polarization. TFGR and ISL inhibited the promotion of M2 macrophages to breast cancer cells migration in vitro, STAT signal pathways and miR155 were partly involved.
Animals ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Polarity ; drug effects ; Chalcones ; pharmacology ; Flavonoids ; pharmacology ; Glycyrrhiza ; chemistry ; Interleukin-4 ; genetics ; metabolism ; Macrophages ; cytology ; drug effects ; metabolism ; Mice ; RAW 264.7 Cells ; Rhizome ; chemistry

Objective This report describes the mechanism of Ginsenoside Re to resist Exercise-induced fatigue based on the observation of effects on MDA content and SOD activity.Methods Thirty male SD rats were divided into 3 groups randomly:Ginsenoside Re group,model group and control group,10 rats in each group.Rats in Ginsenoside Re group were given gastric gavage of Ginsenoside Re once a day,while rats in model and control groups were given the same volume of normal saline.One hour after administration,rats of Ginsenoside Re groups and Model groups received medium-intensity treadmill exercise for 20 minutes at the speed of 15m/min,with a slope of 0 degree,and after 40-mimute break repeated it for another 20minutes.Fourteen days later,MDA content and SOD activity have been tested.Results MDA content in the serum,liver tissue and muscle tissue of Ginsenoside Re group was obviously lower than that in the model group (P

Aim To investigate the changes of serum metabolism after the treatment of DOA and DOO on myocardial ischemia reperfusion ( MI/R ) injury in rats, and to explore the pathogenesis of MI/R injury and drug action mechanism. Method The serum samples of Sham group, Model group, DOA group and DOO group of rats were acquired, gas phase time of flight mass spectrometry ( GC-TOF-MS) was applied to analyze the metabolic profiles of the samples. After da-ta preprocessing, they were processed into SIMCA 14. 1 software for multivariate statistical analysis. Results By principal components analysis ( PCA ) , partial least squares analysis ( PLS-DA) and orthogonal partial least squares analysis ( OPLS-DA ) , the Model group and Sham group were obviously separated, the drug in-tervention group and Model group were separated and close to Sham group. The therapeutic effect of DOO and DOA on MI/R injury in rats was proved. The ex-perimental results identified 13 endogenous biomark-ers, which were related to the glucose metabolism,lipid metabolism and amino acid metabolism pathway. Con-clusion DOA and DOO may protect the MI/R injured rats by regulating the glucose metabolism, lipid metab-olism and amino acid metabolism pathway.

Animals ; Comet Assay ; DNA Damage ; drug effects ; Lymphocytes ; drug effects ; Male ; Organometallic Compounds ; toxicity ; Rats

OBJECTIVETo study the effects of oxymatrine (OM) on the expressions of pro-collagen I (PC I), pro-collagen II (PC III), fibronectin (FN), matrix metalloproteinase-1 (MMP-1) mRNA of fibroblasts from keloid (KFb), hyperplastic scar (HFb), and normal skin (NFb), and to compare with hydrocortisone (HC).

METHODSThe primary KFb, HFb and NFb were derived from patients and cultured in vitro using tissue block culture method. The fibroblasts were treated with 500 microg/mL OM, 2 microg/mL HC, or without any medicine (as the control). The mRNA expressions of PC I, PC III, FN, MMP-1 of the fibroblasts were detected using RT-PCR.

RESULTSUnder the normal condition, when compared with NFb, the mRNA expressions of PC I of KFb and HFb increased by 31.7% and 34.2% (both P < 0.05). Besides, the mRNA expression of PC III of KFb increased by 44.9% (P < 0.01). OM down-regulated the mRNA expressions of FN and PC I of HFb by 18.8% and 23.6% respectively (both P < 0.05). HC decreased the mRNA expressions of FN and PC I of HFb by 26.8% and 43.6% respectively (P < 0.05, P < 0.01). Meantime, OM up-regulated the mRNA expression of MMP-1 of KFb by 21.8% (P < 0.05).

CONCLUSIONSOM suppressed the synthesis of extracellular matrix (ECM) possibly through down-regulating the mRNA expressions of PC I and FN. Compared with HC, OM could promote the degradation of ECM through inducing the MMP-1 mRNA expressions of KFb. Therefore, OM could be potentially used in treatment of hypertrophic scar and keloid.

Alkaloids ; pharmacology ; Cells, Cultured ; Cicatrix ; metabolism ; pathology ; Extracellular Matrix ; metabolism ; pathology ; Fibroblasts ; drug effects ; metabolism ; pathology ; Fibronectins ; metabolism ; Humans ; Keloid ; metabolism ; pathology ; Matrix Metalloproteinase 1 ; metabolism ; Procollagen ; metabolism ; Quinolizines ; pharmacology

Objective: To investigate epidemiological characteristics of hospitalized children with burn injury in the author′s affiliation, so as to provide theoretical basis for developing prevention strategies of children with burn injury. Methods: Medical records of 384 and 596 hospitalized children with burn injury, aged 0 to 12-year-old, were collected respectively from January 2001 to December 2005 and January 2011 to December 2015. Percentage of children with burn injury to total hospitalized patients with burn injury in the same period of time, age, causes of injury, gender, injury month, residence, condition of first aid measures conforming to medical standard, time of admission post injury, burn degree, and operation condition of children with burn injury were analyzed. Data were processed with Mann-Whitney U test and Chi-square test. Results: From January 2001 to December 2005 and January 2011 to December 2015, percentages of children with burn injury to total hospitalized patients with burn injury in the same period of time were respectively 23.6% (384/1 626) and 25.4% (596/2 346) , with no statistically significant difference (χ²=1.653, P>0.05). Age of all children with burn injury was 1.0 (1.0, 2.0) year old from January 2011 to December 2015, obviously lower than that from January 2001 to December 2005[1.0 (1.0, 3.0) year old, Z=-3.257, P<0.01]. Ages of children with burn caused by hot liquid and electrical burn from January 2011 to December 2015 were obviously lower than those from January 2001 to December 2005 (with Z values respectively -4.248 and -2.040, P<0.05 or P<0.01). Compared with that from January 2001 to December 2005, age of children with burn caused by flame from January 2011 to December 2015 increased, with no statistically significant difference (Z=1.852, P>0.05). There was no statistically significant difference in gender of children with burn injury between the two periods of time (χ²=1.374, P>0.05). Burn injury of children in the two periods of time mainly occurred in Spring, and season of burn injury between the two periods of time was similar (χ²=1.177, P>0.05). There was statistically significant difference in residence of children with burn injury between the two periods of time (χ²=15.513, P<0.01). The number of children with burn injury of first aid measures conforming to medical standard and admission within 6 h post injury from January 2011 to December 2015 was obviously more than that from January 2001 to December 2005 (with χ² values respectively 7.434 and 43.961, P values below 0.01). Burn degrees of children with burn injury mainly were moderate in the two periods of time, and there was no statistically significant difference in burn degree and condition of operation between the two periods of time (with χ² values respectively 5.731 and 1.583, P values above 0.05). Conclusions Burn of children is a social problem. We should make great efforts on popularization of prevention and treatment about burn of children, especially children with younger age in rural areas. We should publicize standard first aid measures of burn of children and advocate admission of burn of children within 6 h post burn injury for treatment.

Background: Synaptic plasticity contributes to nociceptive signal transmission and modulation, with calcium/ calmodulin-dependent protein kinase II (CaMK II) playing a fundamental role in neural plasticity. This research was conducted to investigate the role of CaMK II in the transmission and regulation of nociceptive information within the nucleus accumbens (NAc) of naïve and morphine-tolerant rats. Methods: Randall Selitto and hot-plate tests were utilized to measure the hindpaw withdrawal latencies (HWLs) in response to noxious mechanical and thermal stimuli. To induce chronic morphine tolerance, rats received intraperitoneal morphine injection twice per day for seven days. CaMK II expression and activity were assessed using western blotting. Results: Intra-NAc microinjection of autocamtide-2-related inhibitory peptide (AIP) induced an increase in HWLs in naïve rats in response to noxious thermal and mechanical stimuli. Moreover, the expression of the phosphorylated CaMK II (p-CaMK II) was significantly decreased as determined by western blotting. Chronic intraperitoneal injection of morphine resulted in significant morphine tolerance in rats on Day 7, and an increase of p-CaMK II expression in NAc in morphine-tolerant rats was observed. Furthermore, intra-NAc administration of AIP elicited significant antinociceptive responses in morphine-tolerant rats. In addition, compared with naïve rats, AIP induced stronger thermal antinociceptive effects of the same dose in rats exhibiting morphine tolerance. Conclusions This study shows that CaMK II in the NAc is involved in the transmission and regulation of nociception in naïve and morphine-tolerant rats.