Oxidative magnetization of biochar at relatively low pyrolysis temperature for efficient removal of different types of pollutants.

A novel oxidative magnetization, involving phosphomolybdic acid and Fe(NO3)3 co-promoted pyrolysis, was established to manufacture highly adsorptive magnetic biochars for adsorbing aqueous tetracycline, methylene blue, and Cr6+. The modification of phosphomolybdic acid greatly boosted the formation of γ-Fe2O3 and oxygen containing groups with enhancement of specific surface area and pore volume at 400 °C. Importantly, γ-Fe2O3 was stably fixed on surface in quasi-nanoscale. The oxidized magnetic biochar displayed 631.53, 158.45, 155.13 mg/g adsorption capabilities for tetracycline, methylene blue, and Cr6+ with 22.79 emu/g saturation magnetization, respectively. Oxygen containing groups and quasi-nanoscale γ-Fe2O3 served as key adsorption sites for these pollutants. A general oxidative magnetization was established for manufacturing high-performance magnetic biochar through phosphomolybdic acid/Fe(NO3)3 co-promoted pyrolysis at relatively low temperature.

Lactobacillus rhamnosus TR08 Improves Dyslipidemia in Mice Fed with a High Fat Diet by Regulating the Intestinal Microbiota, Reducing Systemic Inflammatory Response, and Promoting Sphingomholipid Metabolism.

Dysbiosis is a crucial manifestation of dyslipidemia; however, oral supplementation of probiotic modulates the intestinal commensal composition. The protective mechanism of probiotics against hyperlipidemia is still under investigation. To elucidate the hypolipidemic effect of Lactobacillus rhamnosus TR08 through the analysis of gut microbiota and lipid metabolomics, we investigated changes in gut microbiota and lipid metabolomic phenotypes in mice by real time quantitative PCR and untargeted metabolomics analysis. High fat diet-induced dyslipidemia mice were orally administered with TR08 for 8 weeks. The proinflammatory cytokines (interleukin-2 and interferon-γ) levels in spleen and aortic wall injury in the mice fed with a high-fat diet were inhibited after treatment with TR08 at 1 × 108 CFU per day per mouse. TR08 also reshaped the gut microbiota with increases of the relative abundances of Bifidobacterium and Bacteroides, reduced the abundance of the pro-pathogen bacterial Enterococcus, increased the serum level of short chain fatty acids (SCFAs) contents, and promoted sphingomholipid metabolic pathway. The results indicated that TR08 could improve the intestinal microbiota of mice to increase the production of SCFAs, and then play the anti-inflammation induced by hyperlipidemia and reduce the inflammatory injury of blood vessel wall. Therefore, TR08 can potentially be used as a hypolipidemic effect probiotic in further interventions.

Superoxide anions modulate the performance of apelin in the paraventricular nucleus on sympathetic activity and blood pressure in spontaneously hypertensive rats.

The present study was designed to determine how apelin in paraventricular nucleus (PVN) modulates the renal sympathetic nerve activity (RSNA), arterial blood pressure (ABP), mean arterial pressure (MAP), and heart rate (HR), and whether superoxide anions regulate the performance of PVN apelin in spontaneously hypertensive rats (SHRs). Acute experiment was carried out with 13-week-old male Wistar-Kyoto rats (WKY) and SHRs under anaesthesia. RSNA, ABP, MAP and HR after PVN microinjection were measured. Apelin microinjection into PVN increased RSNA, ABP, MAP and HR in WKY rats and SHRs, more obviously in SHRs. APJ antagonist F13A decreased the RSNA, ABP, MAP and HR in SHRs, and inhibited the effects of apelin. Apelin and APJ mRNA levels were higher in the PVN in SHRs. PVN microinjection of superoxide anion scavengers tempol and tiron, or NAD(P)H oxidase inhibitor apocynin, decreased the RSNA, ABP, MAP and HR in SHRs, and inhibited the effects of apelin, but the superoxide dismutase (SOD) inhibitor diethyldithiocarbamic acid (DETC) potentiated the effects of apelin. NAD(P)H oxidase activity and superoxide anion levels in PVN were increased by apelin, but decreased by APJ antagonist F13A. The apelin-induced increases in NAD(P)H oxidase activity and superoxide anion level were abolished by pre-treatment with F13A. These results indicate that apelin in PVN increases the sympathetic outflow and blood pressure via activating APJ receptor. The enhanced activity of endogenous apelin and APJ receptor in PVN contributes to sympathetic activation in hypertension, and the superoxide anion is involved in these apelin-mediated processes in PVN.

High glucose induces podocyte epithelial­to­mesenchymal transition by demethylation­mediated enhancement of MMP9 expression.

Abnormal expression of matrix metalloproteinase 9 (MMP9) is correlated with podocyte epithelial-to---mesenchymal transition (EMT) in diabetic nephropathy (DN). However, the mechanisms underlying this process are not well defined. Site­specific demethylation may sustain high expression levels of target genes. In the present study, in order to investigate the association between DNA demethylation of MMP9 promoter and podocyte EMT in DN, human podocytes were cultured in high­glucose (HG) medium and a rat model of DN was established by intraperitoneal injection of streptozotocin (STZ) to determine whether site­specific demethylation of the MMP9 promoter was involved in regulating podocyte EMT in DN. The MTT assay was used to assess the effects of HG culture on the growth of podocytes, and the demethylation status of the MMP9 promoter was assessed by bisulfite sequencing polymerase chain reaction. mRNA and protein expression levels of MMP9, α­smooth muscle actin (α­SMA), podocalyxin and fibronectin­1 in podocytes were assessed by reverse transcription­quantitative PCR (RT­qPCR) and western blot analyses. The results demonstrated that HG treatment up regulated the expression of MMP9, α­SMA and fibronectin­1, but down regulated the expression of podocalyxin in podocytes. The MMP9 promoter region was revealed to contain a variety of demethylated CpG sites, and HG treatment reduced the rate of MMP9 promotermethylation, which, in turn, enhanced its promoter activity. In summary, these data suggested that demethylation of the MMP9 promoter may serve an important role in podocyte EMT in DN. The demethylation status of the MMP9 promoter maybe used as an important prognostic marker of DN in clinic.

CFTR protects against vascular inflammation and atherogenesis in apolipoprotein E-deficient mice.

Atherosclerosis is a chronic inflammatory disease of the vascular wall. Dysfunction of cystic fibrosis transmembrane conductance regulator (CFTR) has been shown to result in inflammatory responses in cystic fibrosis (CF) patients. However, little is known about the role of CFTR in vascular inflammation and atherogenesis. Our results showed that CFTR was dominantly expressed in macrophages of atherosclerotic plaque and reduced in aorta and aortic sinus from atherosclerotic apolipoprotein E-deficient (apoE-/-) mice. In vivo administration of adenovirus encoding CFTR (Ad-CFTR) with apoE-/- mice fed on high-fat diet (HFD) improved plaque stability by decreasing lipid accumulation and necrotic area and increasing smooth muscle cell content and collagen. The Ad-CFTR-treated mice also displayed reduced proinflammatory cytokines levels in aorta and peritoneal macrophages, whereas the anti-inflammatory M2 macrophage markers were increased. Confocal microscopy revealed that the infiltration of T lymphocytes, neutrophils, and macrophages in aortic sinus was markedly attenuated in Ad-CFTR-treated apoE-/- mice. Moreover, in vitro experiments showed that overexpression of CFTR inhibited ox-LDL-induced the migration of peritoneal macrophages. Finally, it was observed that CFTR up-regulation suppressed NFκB and MAPKs activity induced by ox-LDL. Inhibition of JNK or ERK abrogated CFTR down-regulation induced NFκB activation, whereas NFκB inhibitor had no effect on JNK or ERK activation. Taken together, these results demonstrate that CFTR prevents inflammation and atherogenesis via inhibition of NFκB and MAPKs activation. Our data suggest that CFTR may present a potential therapeutic target for the treatment of vascular inflammation and development of atherosclerotic disease.

Role of PI3K/Akt signaling in the protective effect of magnesium sulfate against ischemia-perfusion injury of small intestine in rats.

BACKGROUND: The protective effects of magnesium sulfate against ischemia-reperfusion injury of the small intestine in Sprague-Dawley (SD) rats have been confirmed in our previous research. However, its exact mechanism is unclear. This study was to evaluate the role of PI3K/Akt signal pathway in the protective effect of magnesium sulfate against ischemia-reperfusion injury of the small intestine in SD rats. METHODS: Rat model of intestinal ischemia-reperfusion injury was used. The SD rats were divided into four groups randomly: sham operation group, ischemia-reperfusion group, magnesium sulfate group and magnesium sulfate plus LY294002 (an inhibitor of PI3K) group. The pathological changes of intestinal mucosa were examined; the activity of diamine oxidase (DAO) in plasma, the plasma contents of malondialdehyde (MDA), and apoptosis rate of the intestinal mucosal cells were determined and compared. The expression of p-Akt was detected by Western blotting. RESULTS: There were more evident pathological changes of the intestinal mucosa (higher Chiu's score, P < 0.05), enhanced DAO activity (P < 0.05), elevated contents of MDA (P < 0.05), higher apoptosis rate (P < 0.05), and lower level of p-Akt (P < 0.05) in the ischemia-reperfusion group compared with the sham operation group. There were less evident pathological changes of the intestinal mucosa (lower Chiu's score, P < 0.05), lower DAO activity (P < 0.05), lower contents of MDA (P < 0.05), and lower apoptosis rate (P < 0.05), but higher level of p-Akt (P < 0.05) in the magnesium sulfate group compared with the ischemia-reperfusion group. There were more evident pathological changes of the intestinal mucosa (higher Chiu's score, P < 0.05), higher contents of MDA (P < 0.05), higher DAO activity (P < 0.05) and higher apoptosis rate (P < 0.05), and lower level of p-Akt (P < 0.05) in the magnesium sulfate plus LY294002 group compared with the magnesium sulfate group. CONCLUSIONS: Activation of PI3K/Akt signal pathway results in the reduction of cell apoptosis, which likely accounts for the protective effect of magnesium sulfate against intestinal ischemia-reperfusion injury.