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Antibiotic peptide-modified nanostructured titanium surface for enhancing bactericidal property

Posted by C Zhu, WW Zhang, SY Fang, et al. on 2018-01-14 23:04:54

Abstract

The infections associated with titanium-based biomaterials have been one of the most serious postoperative complications in the orthopedic surgery. Great efforts have been made to improve the antimicrobial property of titanium-based biomaterials by virtue of the surface modification strategy. From the biomimetic perspective of vegetation roots anchoring soil, alkali treatment was conducted on metallic titanium to produce a nanoroot-structured surface in the present study; then, antimicrobial peptide was anchored within the nanoroot surface by vacuum extraction and lyophilization. As a result, the obtained antibacterial peptide-leashed titanium surface showed a hierarchical structure combining the designed nanoroot topography and the anchored antibiotic peptide. Furthermore, this modified surface could steadily release for more than 10 h in a time-dependent manner. As a consequence, the elaborate antimicrobial peptide-loaded surface demonstrated a powerful antibacterial and biofilm-resistant capability against two types of Staphylococcus, without significant cytotoxicity. Specifically, Peptide-2 can kill the most planktonic and sessile bacteria for two gram-positive bacteria. Therefore, the integration of antibacterial peptide onto titanium-based implant surface may be a hopeful tool to prevent implant-associated infections in the orthopedic surgery.

Abstract

The present study involves the preparation of cubic liquid crystalline nanoparticles (cubsomes) for liver targeting to assess the potential of a formulated bioactive polysaccharide isolated from the hot aqueous extract of Ulva fasciata as an alternative natural agent with anti-hyperlipidaemic activity. Cubosomal nanoparticles were prepared by disrupting the cubic gel phase of the polysaccharide and water in the presence of a surfactant. Different lipid matrices and stabilizers were tested. All the formulations were in the nanosize range and showed sufficient negative charge to inhibit the aggregation of the cubosomes. Drug entrapment efficiencies (EEs%) were determined and in vitro release studies were performed. Transmission electron microscopy (TEM) and differential scanning calorimetry were used to analyze the loaded cubosomal nanoparticles containing glyceryl monostearate (GMO 2.25 g), poloxamer 407 (0.25 g) and 50 mg of the polysaccharide. A preclinical study comparing the cubic liquid crystalline nanoparticles containing polysaccharide to fluvastatin as a reference drug in hyperlipidaemic rats was conducted. The rats treated with the polysaccharide- loaded cubosomes showed significant decreases in total cholesterol (TC), triglycerides (TG) and total lipid (TL) compared to the untreated HL rats. In addition, oxidative stress and antioxidant biomarkers were measured in the HL rats. Compared to the untreated HL rats, the cubosome treated rats showed a significant reduction in malondialdehyde (MDA), whereas insignificant changes were detected in nitric oxide (NO), glutathione (GSH) levels and total antioxidant capacity (TAC). Further, vascular and intercellular adhesion molecules (VCAM, ICAM), and myeloperoxidase were demonstrated. A histopathological examination was conducted to study the alterations in histopathological lesions and to document the biochemical results. In conclusion, this study demonstrates the superiority of using a natural lipid regulator such as polysaccharide loaded cubosomes instead of fluvastatin.

Abstract

Background

Acute superior mesenteric venous thrombosis (ASMVT) is an abdominal vascular condition. Early recanalization is essential to successful treatment. The aim of the study was to establish rabbit models of ASMVT and assess the time course of intestinal epithelial barrier disruption.

Methods

After surgical exposure of superior mesenteric vein (Sham group), large-vessel (L-group) and small-vessel (S-group) models were established by endothelium damage, stenosis creation, and thrombin injection. At baseline, 6, 9, and 12 h, hemodynamic and serum parameters were tested. Serum from ASMVT patients diagnosed at 24, 36, 48, and 60 h from symptom onset was collected. Intestinal barrier disruption was assessed by tight junction (TJ) protein expression, morphology changes, and bacterial translocation. Mesenteric arteriospasm was measured by flow velocity and intestinal wet/dry weight ratio. The serum level of intestinal fatty acid–binding protein and endotoxin in patients was also measured as an indicator for intestinal barrier function.

Results

Severe acidosis and lacticemia were observed in both the groups. The L-group experienced greater hemodynamic alteration than the S-group. Intestinal barrier disruption was detected by significantly decreased TJ protein expression, histology and ultrastructure injury of TJ, increased permeability, and bacterial translocation, at 9 h in the S-group and 12 h in the L-group. Secondary mesenteric arteriospasm occurred at the same time of complete intestinal barrier disruption and could be a significant cause of bowel necrosis. Significant increased level of intestinal fatty acid–binding protein and endotoxin was found in patients at 48 h in the S-group type and 60 h in the L-group type.

Conclusions

The ASMVT animal models of both the types were first established. The loss of intestinal barrier function occurred at 6 h in the S-group model and 9 h in the L-group model. For clinical patients, the time window extended to 36 h in the S-group type and 48 h in the L-group type.

Keywords:

Mesenteric venous thrombosis; Intestinal epithelial barrier; Acute ischemic injury; Therapeutic time window

Coagonist of GLP-1 and glucagon decreases liver inflammation and atherosclerosis in dyslipidemic condition

Posted by V Patel, A Joharapurkar, S Kshirsagar, et al. on 2018-01-14 18:49:27

Abstract

Dyslipidemia enhances progression of atherosclerosis. Coagonist of GLP-1 and glucagon are under clinical investigation for the treatment of obesity and diabetes. Earlier, we have observed that coagonist reduced circulating and hepatic lipids, independent of its anorexic effects. Here, we investigated the role of coagonist of GLP-1 and glucagon receptors in complications of diet-induced dyslipidemia in hamsters and humanized double transgenic mice. Hamsters fed on high fat high cholesterol diet were treated for 8 weeks with coagonist of GLP-1 and glucagon receptors (75 and 150?ug/kg). Pair-fed control was maintained. Cholesterol fed transgenic mice overexpressing hApoB100 and hCETP with coagonist (300 ug/kg) for 4 weeks. After the completion of treatment, biochemical estimations were done. Coagonist treatment reduced triglycerides in plasma, liver and aorta, plasma cholesterol and hepatic triglyceride secretion rate. Expressions of HMG-CoA reductase and SBREBP-1C were reduced and expressions of LDLR, CYP7A1, ABCA1 and ABCB11 were increased in liver, due to coagonist treatment. Coagonist treatment increased bile flow rate and biliary cholesterol excretion. IL-6 and TNF-beta were reduced in plasma and expression of TNF-beta, MCP-1, MMP-9 and TIMP-1 decreased in liver. Treatment with coagonist reduced oxidative stress in liver and aorta. Energy expenditure was increased and respiratory quotient was reduced by coagonist treatment. These changes were correlated with reduced hepatic inflammation and lipids in liver and aorta in coagonist treated hamsters. Coagonist treatment also reduced lipids in cholesterol-fed transgenic mice. These changes were independent of glycaemia and anorexia observed after coagonist treatment. Long term treatment with coagonist of GLP-1 and glucagon receptor ameliorated diet-induced dyslipidemia and atherosclerosis by regulating bile homeostasis, liver inflammation and energy expenditure.

Abstract

A Chinese perfluorooctane sulfonate (PFOS) substitute frequently detected in the environment, 6:2 chlorinated polyfluorinated ether sulfonate (F-53B), has a similar structure to PFOS and it is proposed to cause thyroid dysfunction. To further confirm this hypothesis, the effects of F-53B on the thyroid endocrine system and underlying mechanisms were investigated in vitro and in vivo using rat pituitary GH3 cells and developing zebrafish, respectively. In GH3 cells, F-53B enhanced cell proliferation in a dose-dependent manner, indicative of thyroid receptor agonistic activity. In zebrafish larvae, F-53B exposure induced significant developmental inhibition and increased thyroxine (T4) but not 3,5,3-triiodothyronine (T3) levels accompanied by a decrease in thyroglobulin (TG) protein and transcript levels of most genes involved in the hypothalamic-pituitary-thyroid (HPT) axis. Interestingly, T4 levels remained significantly increased while TG protein and gene transcription levels were markedly upregulated after depuration. Molecular docking studies revealed that F-53B binds to transthyretin (TTR) by forming hydrogen bonds with Lys123 and Lys115, thereby interfering with thyroid hormone homeostasis. Our collective in vitro, in vivo and in silico studies provide novel evidence that F-53B disrupts the thyroid endocrine system at environmentally relevant concentrations, which cannot be recovered after depuration. Given the persistence of F-53B in the environment, the long-term consequences of thyroid hormone disruption by this chemical warrant further investigation.

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