Project description:Mucuna pruriens extract MPE pretreatment may have a direct protective effect on heart (other than immunological neutralization of the venom neurotoxin and phospholipase A2 by the anti-MPE antibodies) that renders the heart more resistant to the toxic action of the venom The direct protective effect probably involves functional changes to the cardiac tissue that enable the heart to resist the reduction of contractility and rate induced by the cobra venom.To explore the possibility of the direct action of MPE pretreatment on heart and to understand the molecular events involved in the protection of MPE pretreatment against the lethal action of Naja sputatrix venom, gene expression studies were carried out using microarray analysis. Rats were divided into four groups (n=6): negative control (abbreviated as ‘negative’ group), MPE pretreated group (abbreviated as ‘MPE’ group), N. sputatrix venom-challenge group (abbreviated as ‘NS’ group) and N. sputatrix venom-challenge to MPE pretreated animals group (abbreviated as ‘MPE-NS’ group). In the ‘MPE’ group, rats were injected with MPE at a dose of 21 mg/kg (i.p.), on day 0, 7 and 14, and sacrificed on day 21. In the ‘negative’ group (the untreated, control group), rats were injected with saline of the same volume and sacrificed also on day 21. Hearts were then harvested immediately. In the N. sputatrix venom-challenge group (‘NS’ group), untreated rats were challenged with 1.5 LD50 (1.25 ?g/g) of N. sputatrix venom whereas in the venom challenge to MPE pretreated animals group (the ‘MPE-NS’ group), MPE pretreated rats were challenged with 1.5 LD50 (1.25 ?g/g) of N. sputatrix venom, both on day 21. For the ‘NS’ and ‘MPE-NS’ group, the rats were observed for 24 h after venom challenged and hearts were harvested as soon as death occurred or 24 h after the venom injection, whichever occurred first.
Project description:The objective of this research is to compare the differentially expressed genes in the vascular tissues of DAPK1 wild-type (WT) and DAPK1 knockout (KO) mice after being induced with or without Ang II. WT (n=10) mice were randomly divided into two groups: WT+NS group and WT+Ang II group (n=5 for each group). KO (n=10) mice were also randomly divided into two groups: KO+NS group and KO+Ang II group (n=5 for each group). Then the vascular tissues were used to identify differentially expressed genes among different groups.
Project description:The objective of this study was to compare blank control mice (NS V) with AngII-induced hypertensive mice (AngII V). Angii-induced hypertensive mice (AngII V) and liensinine intervention group (Lien V); Different genes expressed in vascular tissue and identify new targets for reversing hypertension-induced vascular remodeling.
Project description:The goals of this study is to compare the differently expressed genes in abdominal aorta of Rab22a KO mice and Rab22a WT mice with or without Angiotensin II treatment for 14 days at the concentration of 500ng/kg/min.The mice (n=20) were randomly divided into 4 groups:WT+AngII,WT+NS,KO+AngII,KO+NS (n = 5 for each group). Mice in WT+NS and KO+NS groups were infused with saline or 500 ng/kg/min of WT+AngII and KO+AngII respectively. Then the abdominal aorta were used to identify differentially expressed genes among different groups.
Project description:Transcriptome analysis of RNAs extracted from 2 hour-TGF-b-treated or untreated LX-2 cells with or without STAT3 knockdown We prepared RNA from the following groups: NS 0h: untreated cells with control non-silencing (NS) siRNA; NS 2h: 2-hour TGF-b treated cells with control NS siRNA; siSTAT3 0h: untreated cells with STAT3 siRNA; siSTAT3 2h: 2-hour TGF-b treated cells with STAT3 siRNA. The gene expression profiles were compared, and we found 202 genes were upregulated (fold > 1.5) upon TGF-b treatment in control NS siRNA transfected LX-2 cells. Among them, 128 genes were clasified as TGF-b-induced and STAT3 -dependent genes as their response to TGF-b decreased more than 40% upon STAT3 depletion (126 genes) or fold between NS control and siSTAT3 in the absence of TGF-b was > 1.5 (2 genes). The results showed that STAT3 plays an important role in regulating TGF-b target genes.
Project description:The imbalance of intestinal flora can affect the immune function and structural integrity of the intestinal barrier, leading to the colonization and reproduction of opportunistic pathogenic bacteria in the intestine to become the dominant flora, eventually inducing enteritis. This study aimed to investigate whether fecal microbiota transplantation (FMT) could improve the gut barrier in Nile tilapia (Oreochromis niloticus). The experiment involved administering normal saline (NS group) and fecal microbiota (FMT group) (from the negative control group (C group)) to tilapia that had been treated with oxytetracycline hydrochloride (OTC) (M group) by gavage. A total of 300 male tilapia (mean body weight 596.65 ± 47.18 g) were used, with 180 of them being fed OTC (120 mg/kg body weight/day) for 7 days to induce intestinal oxidative stress, while the rest served as the control group. After confirmation of mild chronic enteritis, the tilapia were treated in different ways.
Project description:To study the pathogenicity of Salmonella Typhimurium (ST) in heterophils, a whole Salmonella genome array was used to analyze RNA isolated from Salmonella in vitro encountered with heterophils (30 min, 1 h, 2 h, and 3 h) or medium control (NS). Dual-color, direct comparisons were carried out between heterophils-encountered ST and non-encountered controls (30 min vs. NS (30M/NS), 1 h vs. NS (1HR/NS), 2 h vs. NS (2HR/NS) and 3 h vs. NS (3HR/NS)). Each comparison includes four biological replicates. Out of 4588 genes on an array, there were 605, 758, 944 and 945 genes differentially expressed in the comparisons of 30M/NS, 1HR/NS, 2HR/NS and 3HR/NS, respectively (P < 0.001, fold-change > 2). Most of the Salmonella genes associated with invasion function were found differentially expressed at 2HR/NS and 3HR/NS comparisons. These candidate genes include TypeIII-secreted protein effector sopE2, Invasion proteins (e.g. invA, invE, invG, invH), and Invasion genes tranction activator hilA. The results of continuous transcriptional changes provide important information to elucidate the pathogenicity of ST in heterophils.
Project description:The global regulator, H-NS, controls genes related to stress response, biofilm formation, and virulence expression by recognizing the curved DNA and silences gene transcription acquired from lateral gene transfer. Here, we rewired H-NS to control biofilm formation using protein engineering. One H-NS variant, H-NS K57N was obtained to reduce biofilm formation 10-fold compared to H-NS wild-type. Whole-transcriptome analysis (BW25113 hha hns / pCA24N-hns K57N vs. BW25113 hha hns / pCA24N-hns) revealed that H-NS K57N represses biofilm formation through the interactinon with other nucleoid proteins, Cnu and StpA. Remarkably, H-NS K57N enhanced the excision of defective prophage Rac while H-NS wild-type represses it, and H-NS controlled only Rac excision among E. coli prophages. These results imply that the repression of Rac excision is one of the silencing manner for foreign genes by H-NS. Also, the prophage excision not only led to the change of biofilm formation but also resulted in cell lysis through the expression of toxin protein HokD with reduced viability, which are important for cell physiology in response to the change of environmental conditions. Hence, H-NS regulatory system may be evolved easily with specialized functions in terms of biofilm formation, prophage control, and cell lysis.