Bulbils of Aerial Yam Attenuate Ethanol-Induced Hepatotoxicity in HepG2 Cells through Inhibition of Oxidative Stress by Activation of the Nuclear Factor Erythroid-2-Related Factor 2 Signaling Pathway.

Bulbil of yam (BY) extract contains various active compounds possessing many pharmacological properties. However, little is known about the effect and underlying mechanism of BY extract on ethanol-induced liver damage. The present study explored the beneficial potential of BY extract on ethanol-induced hepatotoxicity. To evaluate its effectiveness, ethanol-induced HepG2 liver cells were pretreated with BY extract. BY extract effectively rescued cells from ethanol treatment through inhibition of apoptotic cell death as well as inhibiting expression of mitogen-activated protein kinase (MAPK) proteins as stress inducers. BY extract increased the expression of typical antioxidants. Furthermore, BY extract significantly inhibited mitochondrial dysfunction and endoplasmic reticulum (ER) stress, which are major ROS-inducing factors. Finally, as an underlying mechanism of the protective effects of BY extract on ethanol-induced liver damage, it activated Nrf2 protein through translocation from the cytosol to the nucleus, which in turn activated its target oxidative stress suppressor genes. Collectively, our findings demonstrate that BY extract has potential antioxidative effects in ethanol-induced liver cells and contributes to the establishment of a treatment strategy for alcohol-derived liver injuries.

An Easy and Economical Way to Produce a Three-Dimensional Bone Phantom in a Dog with Antebrachial Deformities.

3-D surgical planning for restorative osteotomy is costly and time-consuming because surgeons need to be helped from commercial companies to get 3-D printed bones. However, practitioners can save time and keep the cost to a minimum by utilizing free software and establishing their 3-D printers locally. Surgical planning for the corrective osteotomy of antebrachial growth deformities (AGD) is challenging for several reasons (the nature of the biapical or multiapical conformational abnormalities and lack of a reference value for the specific breed). Pre-operative planning challenges include: a definite description of the position of the center of rotation of angulation (CORA) and proper positioning of the osteotomies applicable to the CORA. In the present study, we demonstrated an accurate and reproducible bone-cutting technique using patient-specific instrumentations (PSI) 3-D technology. The results of the location precision showed that, by using PSIs, the surgeons were able to accurately replicate preoperative resection planning. PSI results also indicate that PSI technology provides a smaller standard deviation than the freehand method. PSI technology performed in the distal radial angular deformity may provide good cutting accuracy. In conclusion, the PSI technology may improve bone-cutting accuracy during corrective osteotomy by providing clinically acceptable margins.

Red Ginseng Reduces Inflammatory Response via Suppression MAPK/P38 Signaling and p65 Nuclear Proteins Translocation in Rats and Raw 264.7 Macrophage.

Lipopolysaccharides (LPS) cause systemic inflammatory responses, which are characterized by high mortality and multiple signs, including metabolic disturbances, respiratory acidosis, hypotension, and vital organs disorder. Cytokines secretion and oxidative stress are the main features of the disease. Diagnosis and treatment of systemic inflammation (SI) remain a challenge. Korean Red Ginseng (RG) is one of medicinal herbs that showed a potent anti-oxidant effect. We aimed to study the protective effects of RG on systemic inflammatory response in rats and RAW 264.7 macrophage cells induced by LPS. The rats were treated with water and alcohol extracts of RG for four weeks to prevent the inflammatory response. The result showed that LPS toxin increased morbidity and mortality, and induced liver, kidney, and lung injuries manifested by deteriorated biomarkers. Hypotension, hypomagnesemia, acidosis, and oxidative stress were observed in septic rats. However, RG extracts attenuated liver, kidney, and lung enzymes and metabolites in treated groups via its anti-inflammatory and anti-oxidant properties. Furthermore, RG improved magnesium and blood pressure in the treated groups. RAW 264.7 macrophage cells exposed to LPS disturbance in translocation of p65 and MAPK/p38. Nevertheless, RG-pretreated cells did not significantly alter. In conclusion, RG reduced the rates of mortality and morbidity of treated rats - liver, kidney, and lung injuries were protected in the treated groups through the potentiation of anti-oxidant defense. RG was able to conserve mitochondrial function, inhibiting the activation of MAPK/p38 signaling and suppressing NF-κB p65 cytoplasm-nucleus transport. Further studies are needed to examine the effects on chronic conditions in animal models and human.

Long-term oral intake of Panax ginseng improves hypomagnesemia, hyperlactatemia, base deficit, and metabolic acidosis in an alloxan-induced rabbit model.

OBJECTIVES: Panax ginseng (PG) widely used for its various pharmacological activities, including effects on diabetes and its complications. This study aims to investigate the effect of PG on mortality-related hypomagnesemia, hyperlactatemia, metabolic acidosis, and other diabetes-induced abnormalities. MATERIALS AND METHODS: Type 1 diabetes was induced by IV injection of alloxan monohydrate 110 mg/kg into New Zealand white rabbits weighing 2-2.5 kg. PG was supplied in drinking water for 20 weeks. The effects of the PG treatment on diabetes were evaluated through hematological and biochemical analysis including ELISA assays for insulin and glycated haemoglobin A1c (HBA1c) before and after PG extract was supplied. RESULTS: The serum glucose, insulin, and HBA1c levels were significantly improved after the PG treatment compared to those found before PG treatment. In addition, Mg2+, lactate, and base deficit, and acidosis was significantly enhanced in treated rabbits. Moreover, PG showed hepato- and renoprotective effect. Likewise, electrolytes, lipid and protein profile were improved. CONCLUSION: The biochemical and hematological analysis data demonstrate that the PG is effective to alleviate the diabetes serious signs.

Anti-Diabetic Effect of Cotreatment with Quercetin and Resveratrol in Streptozotocin-Induced Diabetic Rats.

Quercetin and resveratrol are known to have beneficial effects on the diabetes and diabetic complication, however, the effects of combined treatment of these compounds on diabetes are not fully revealed. Therefore, the present study was designed to investigate the combined antidiabetic action of quercetin (QE) and resveratrol (RS) in streptozotocin (STZ)-induced diabetic rats. To test the effects of co-treated with these compounds on diabetes, serum glucose, insulin, lipid profiles, oxidative stress biomarkers, and ions were determined. Additionally, the activities of hepatic glucose metabolic enzymes and histological analyses of pancreatic tissues were evaluated. 50 male Sprague-Dawley rats were divided into five groups; normal control, 50 mg/kg STZ-induced diabetic, and three (30 mg/kg QE, 10 mg/kg RS, and combined) compound-treated diabetic groups. The elevated serum blood glucose levels, insulin levels, and dyslipidemia in diabetic rats were significantly improved by QE, RS, and combined treatments. Oxidative stress and tissue injury biomarkers were dramatically inhibited by these compounds. They also shown to improve the hematological parameters which were shown to the hyperlactatemia and ketoacidosis as main causes of diabetic complications. The compounds treatment maintained the activities of hepatic glucose metabolic enzymes and structure of pancreatic ß-cells from the diabetes, and it is noteworthy that cotreatment with QE and RS showed the most preventive effect on the diabetic rats. Therefore, our study suggests that cotreatment with QE and RS has beneficial effects against diabetes. We further suggest that cotreatment with QE and RS has the potential for use as an alternative therapeutic strategy for diabetes.

Hepatoprotective effects of Nigella sativa seed extract against acetaminophen-induced oxidative stress.

OBJECTIVE: To investigate the protective effects of Nigella sativa seed extract (NSSE) against acetaminophen (APAP)-induced hepatotoxicity in TIB-73 cells and rats. METHODS: Toxicity in TIB-73 cells was induced with 10 µmol/L APAP and the protective effects of NSSE were evaluated at 25, 50, 75, 100 µg/mL. For in vivo examination, a total of 30 rats were equally divided into five experimental groups; normal control (vehicle), APAP (800 mg/kg body weight single IP injection) as a hepatotoxic control, and three APAP and NS pretreated (2 weeks) groups (APAP + NSSE 100 mg; APAP + NSSE 300 mg and APAP + NSSE 900 mg/kg). RESULTS: TIB-73 cell viability was drastically decreased by (49.0 ± 1.9)% after the 10 µmol/LAPAP treatment, which also increased reactive oxygen species production. Co-treatment with NSSE at 25, 50, 75, and 100 µg/mL significantly improved cell viability and suppressed reactive oxygen species generation. In vivo, the APAP induced alterations in blood lactate levels, pH, anionic gap, and ion levels (HCO3(-), Mg(2+) and K(+)), which tended to normalize with the NSSE pretreatment. The NSSE also significantly decreased elevated serum levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase induced by APAP, which correlated with decreased levels of hepatic lipid peroxidation (malondialdehyde), increased superoxide dismutase levels, and reduced glutathione concentrations. Improved hepatic histology was also found in the treatment groups other than APAP group. CONCLUSIONS: The in vitro and in vivo findings of this study demonstrated that the NSSE has protective effects against APAP-induced hepatotoxicity and metabolic disturbances by improving antioxidant activities and suppressing both lipid peroxidation and ROS generation.

Antidiabetic Effects of Yam (Dioscorea batatas) and Its Active Constituent, Allantoin, in a Rat Model of Streptozotocin-Induced Diabetes.

The objective of this study was to investigate the therapeutic efficacies of crude yam (Dioscorea batatas) powder (PY), water extract of yam (EY), and allantoin (the active constituent of yam) in streptozotocin (STZ)-induced diabetic rats with respect to glucose, insulin, glucagon-like peptide-1 (GLP-1), C-peptide, glycated hemoglobin (HbAlc), lipid metabolism, and oxidative stress. For this purpose, 50 rats were divided into five groups: normal control (NC), diabetic control (STZ), and STZ plus treatment groups (STZ + PY, STZ + EY, and STZ + allantoin). After treatment for one-month, there was a decrease in blood glucose: 385 ± 7 in STZ, 231 ± 3 in STZ + PY, 214 ± 11 in STZ + EY, and 243 ± 6 mg/dL in STZ + allantoin, respectively. There were significant statistical differences (p < 0.001) compared to STZ (100%): 60% in STZ + PY, 55% in STZ + EY, and 63% in STZ + allantoin. With groups in the same order, there were significant decreases (p < 0.001) in HbAlc (100% as 24.4 ± 0.6 ng/mL, 78%, 75%, and 77%), total cholesterol (100% as 122 ± 3 mg/dL, 70%, 67%, and 69%), and low-density lipoprotein (100% as 29 ± 1 mg/dL, 45%, 48%, and 38%). There were also significant increases (p < 0.001) in insulin (100% as 0.22 ± 0.00 ng/mL, 173%, 209%, and 177%), GLP-1 (100% as 18.4 ± 0.7 pmol/mL, 160%, 166%, and 162%), and C-peptide (100% as 2.56 ± 0.10 ng/mL, 129%, 132%, and 130%). The treatment effectively ameliorated antioxidant stress as shown by a significant decrease (p < 0.001) in malondialdehyde (100% as 7.25 ± 0.11 nmol/mL, 87%, 86%, and 85%) together with increases (p < 0.01) in superoxide dismutase (100% as 167 ± 6 IU/mL, 147%, 159%, and 145%) and reduced glutathione (100% as 167 ± 6 nmol/mL, 123%, 141%, and 140%). The results indicate that yam and allantoin have antidiabetic effects by modulating antioxidant activities, lipid profiles and by promoting the release of GLP-1, thereby improving the function of ß-cells maintaining normal insulin and glucose levels.

Relationships between blood Mg2+ and energy metabolites/enzymes after acute exhaustive swimming exercise in rats.

Magnesium (Mg) plays a central role in neuronal activity, cardiac excitability, neuromuscular transmission, muscular contraction, vasomotor tone, and blood pressure, all of which are significantly related to physical performance. To date, the available data about detection of blood total Mg (tMg; free-ionized, protein-bound, and anion-complex forms) are inconsistent, and there is limited information on blood free-ionized Mg (Mg(2+)) in relation to physical exercise. The aim of this study was to determine the biochemical changes related to energy metabolism after acute exhaustive swimming exercise (AESE) in rats in an attempt to correlate the role of blood Mg(2+) with metabolites/enzymes related to energy production. After AESE, blood Mg(2+), tMg, K(+), partial pressure of carbon dioxide, lactate, total protein (T-PRO), high-density lipoprotein (HDL), creatinine (CRE), blood urea nitrogen (BUN), uric acid (UA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alanine phosphatase (ALP), lactate dehydrogenase (LDH), and creatinine kinase (CK) were significantly increased, whereas pH, partial pressure of oxygen, oxygen saturation, the Mg(2+)/tMg and Ca(2+)/Mg(2+) ratios, HCO3 (-), glucose, triglyceride (TG), and low-density lipoprotein (LDL) were significantly decreased. During AESE, lactate, T-PRO, albumin, AST, ALP, LDH, CK, CRE, BUN, and UA showed significant positive correlations with changes in blood Mg(2+), while glucose, TG, and LDL correlated to Mg(2+) in a negative manner. In conclusion, AESE induced increases in both blood Mg(2+) and tMg, accompanied by changes in blood metabolites and enzymes related to energy metabolism due to increased metabolic demands and mechanical damages.

Fluoxetine-induced apoptosis in hepatocellular carcinoma cells.

BACKGROUND: In addition to being used to treat mental disorders, a serious complication of cancer, antidepressants have been reported to improve cancer patient immunity, inhibit cell growth and have an antitumor effect on various cancer cell lines. We investigated the apoptotic effect of fluoxetine against the Hep3B human hepatocellular carcinoma cell line. MATERIALS AND METHODS: After treatments of Hep3B cells with fluoxetine, we measured cell viability, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and activation of mitogen-activated protein kinases (MAPK). RESULTS: Fluoxetine reduced the viability of cancer cells, induced loss of MMP and formation of ROS, reduced expression of extracellular signal-regulated kinase 1/2 and increased expression of c-JUN N-terminal kinase and p38 MAPK. N-Acetylcysteine, an oxidant-scavenger, and 1,2-bis (o-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), an intracellular Ca(2+) chelator, prevented fluoxetine-induced modulation of MAPK. CONCLUSION: Fluoxetine appears to exhibit an apoptotic effect against Hep3B cells through the loss of MMP, formation of ROS and modulation of MAPK activities.

A study on hemodynamic characteristics at the stenosed blood vessel using computational fluid dynamics simulations.

In this study, we have used computational fluid dynamics to investigate the blood flow in the stenosed blood vessels. The numerical simulation using commercial software ADINA 8.6 were solved about the stenosed blood vessel according to the percent of stenosis and Reynolds number. The blood flow in the normal and stenosed blood vessel was grasped for the validity of the model. The characteristic of the pulsatile flow changed through the steady state flow and analysis of the pulsatile flow according to the time was grasped. The computational model with the characteristics of the fluid-structure interaction is introduced to investigate the wall shear stress, pressure distribution and axial flow velocity. The results show that axial flow velocity and wall shear stress in the region of stenosis was increased by increasing percent of stenosis and Reynolds number. Also, we can know that in the stenosed blood vessel the possibility of the generation of the aneurysm was increased by increasing Reynolds number and percent of stenosis.

NAADP mediates insulin-stimulated glucose uptake and insulin sensitization by PPARγ in adipocytes.

Insulin stimulates glucose uptake through the membrane translocation of GLUT4 and GLUT1. Peroxisome proliferator-activated receptor γ (PPARγ) enhances insulin sensitivity. Here, we demonstrate that insulin stimulates GLUT4 and GLUT1 translocation, and glucose uptake, by activating the signaling pathway involving nicotinic acid adenine dinucleotide phosphate (NAADP), a calcium mobilizer, in adipocytes. We also demonstrate that PPARγ mediates insulin sensitization by enhancing NAADP production through upregulation of CD38, the only enzyme identified for NAADP synthesis. Insulin produced NAADP by both CD38-dependent and -independent pathways, whereas PPARγ produced NAADP by CD38-dependent pathway. Blocking the NAADP signaling pathway abrogated both insulin-stimulated and PPARγ-induced GLUT4 and GLUT1 translocation, thereby inhibiting glucose uptake. CD38 knockout partially inhibited insulin-stimulated glucose uptake. However, CD38 knockout completely blocked PPARγ-induced glucose uptake in adipocytes and PPARγ-mediated amelioration of glucose tolerance in diabetic mice. These results demonstrated that the NAADP signaling pathway is a critical molecular target for PPARγ-mediated insulin sensitization.

Reactive oxygen species mediated ginsenoside Rg3- and Rh2-induced apoptosis in hepatoma cells through mitochondrial signaling pathways.

Panax ginseng (P. ginseng) has anti-cancer effects in several cancer models. Ginsenosides are the main bioactive components in P. ginseng. Korean red ginseng (KRG) extract can potently kill various cancer cells and ginsenosides Rg3 (GRg3) and Rh2 (GRh2) are the primary ginsenosides in KRG. This study was carried out to examine whether KRG and its primary ginsenosides (GRg3 and GRh2) affect apoptosis of human hepatocellular carcinoma cells (Hep3B). KRG, GRg3 and GRh2 have obvious cytotoxic and apoptotic effects in Hep3B cells as evidenced by a decrease in cell viability and mitochondria membrane potential, but an increase in LDH release. In the mitochondria-mediated apoptosis pathway, KRG, GRg3 and GRh2 have the ability to stimulate the release of mitochondrial cytochrome c, activation of caspase-3 and Bax protein, inhibition of Bcl-2 protein and production of intracellular reactive oxygen species in Hep3B cells. These results suggest that KRG, GRg3 and GRh2 may induce apoptosis by direct activation of the mitochondrial pathway.

Silver-loaded biomimetic hydroxyapatite grafted poly(epsilon-caprolactone) composite nanofibers: a cytotoxicity study.

We report on poly(epsilon-caprolactone) (PCL) containing biomimetic hydroxyapatite (HA) and hydroxyapatite-silver (HA-Ag) composite nanofibers prepared via an electrospinning process for the biomedical applications. The morphology, structure and thermal properties of the PCL, PCL/HA and PCL/HA-Ag composite nanofibers were characterized by scanning electron microscopy (SEM), transmission electron microscopy (TEM), energy dispersive X-ray (EDX) spectroscopy, X-ray diffraction (XRD) and thermogravimetry (TGA). SEM images revealed that the nanofibers were well-oriented and incorporated the HA-Ag nanoparticles well. The adhesion, viability and proliferation properties of composite nanofibers and differentiation of osteoblast were carried out to study the in vitro cell compatibility of the PCL/HA/HA-Ag composite nanofibers. Our results showed that pristine PCL and PCL/HA composite nanofibers scaffold can be utilized for the bone regeneration applications, however, PCL/HA-Ag composite nanofibers results in mild cytotoxic effect to human cells.

Korean red ginseng and its primary ginsenosides inhibit ethanol-induced oxidative injury by suppression of the MAPK pathway in TIB-73 cells.

ETHNOPHARMACOLOGICAL RELEVANCE: Panax ginseng (P. ginseng) is one of the most widely used medicinal plants due to its wide spectrum of medicinal effects. Among the currently available Panax ginseng products, Korea red ginseng (KRG) has been shown to exhibit a variety of antioxidative and hepatoprotective action. AIM OF THE STUDY: Our aim was to investigate the effects of KRG and its primary ginsenosides (Rg3 and Rh2) on EtOH-induced injury to mouse hepatocytes (TIB-73). MATERIALS AND METHODS: We investigated the effects of KRG and its primary ginsenoside on EtOH-induced injury to TIB-73 cells and evaluated MAPKs signals as a possible mechanism of action. Hepatocytic injury was evaluated by biochemical assays as cell viability, lactate dehydrogenase (LDH), aspartate aminotransferase (AST), ROS and mitochondria membrane potential (MMP) level in TIB-73 cells. The levels of MAPK activation were analyzed by Western blots. RESULTS: The results showed that exposure of EtOH to TIB-73 cells led to cell death and membrane damage, accompanied by a decrease in cell viability, MMP, and Mg(2+) concentrations, but an increase in LDH, AST, ROS and MAPK activation. KRG and its primary ginsenosides reduced EtOH-induced generation of ROS and the activation of ERK and JNK, and increased Mg(2+) concentrations. CONCLUSION: These results suggest that KRG and its primary ginsenosides inhibit EtOH-induced oxidative injury by suppression of the MAPK pathway in TIB-73 cells.

Autophagy induced by resveratrol prevents human prion protein-mediated neurotoxicity.

Our previous study revealed that resveratrol blocks prion protein peptide PrP(106-126)-induced neurotoxicity. However, the mechanism of resveratrol-mediated neuroprotection in prion diseases is not clear. Resveratrol initiates neuroprotective effects via the activation of autophagy, which protects organelles, cells, and organisms against misfolded protein-disorders, including Alzheimer's disease and Parkinson's disease via regulation of mitochondrial homeostasis. Thus, we focused on elucidating the mechanisms responsible for resveratrol-mediated neuroprotection related to mitochondrial homeostasis as a result of autophagy activation. Resveratrol prevented PrP(106-126)-induced neuronal cell death by activating autophagy. Moreover, resveratrol-induced autophagy prevented the PrP(106-126)-induced reduction in mitochondrial potential and translocation of Bax to the mitochondria and cytochrome c release. Our results indicate that treatment with resveratrol appears to protect against neurotoxicity caused by prion protein peptides and the neuroprotection is induced by resveratrol-mediated autophagy signals.

Bactericidal activity and in vitro cytotoxicity assessment of hydroxyapatite containing gold nanoparticles.

Hydroxyapatite (HA) containing gold (Au) nanoparticles was synthesized for the biomedical applications. The morphology, structure and thermal properties of the HA containing Au nanoparticles were characterized by field emission scanning electron microscopy (FE-SEM), transmission electron microscopy (TEM), energy dispersive X-ray (EDX) spectroscopy, X-ray diffraction (XRD), Fouriertransform infrared spectroscopy (FT-IR) and thermogravimetry (TGA). XRD patterns clearly revealed the formation of HA-Au composite nanoparticles. TEM observation showed that the Au nanoparticles had an average size of 5 nm and were incorporated into HA powder very well. Bactericidal activity of HA-Au with Au nanoparticles immobilized in HA was investigated. The adhesion, viability and proliferation properties of HA containing Au nanoparticles and the differentiation of osteoblast were studied for in vitro cell compatibility of the HA containing Au nanoparticles. Our results showed that HA containing Au nanoparticles were cytotoxic to the human osteoblastic cells.

Human osteoblast cytotoxicity study of electrospun polyurethane/calcium chloride ultrafine nanofibers.

This work was focused on preparation and characterization of the polyurethane nanofibers containing calcium chloride (CaCl2) prepared via electrospinning process for the bionanotechnological applications. The morphological, structural characterizations and thermal properties of the polyurethane/CaCl2 nanofibers were determined by using scanning electron microscopy (SEM), field-emission scanning electron microscopy (FE-SEM), energy dispersive X-ray spectroscopy (EDX), Fourier transform-infrared (FT-IR) spectroscopy and thermogravimetry (TGA). SEM images revealed that these composite nanofibers were well-oriented and had good incorporation of CaCl2. The morphological feature of the cells attached on polyurethane/CaCl2 nanofibers scaffold was confirmed by SEM. The in vitro cell compatibility of the polyurethane/CaCl2 composite nanofibers was studied. This study demonstrated the non-toxic effect of electrospun polyurethane/CaCl2 composite nanofibers. Based on this, we propose a mechanism for the cell attachment.

Taurine prevents hypertension and increases exercise capacity in rats with fructose-induced hypertension.

BACKGROUND: Fructose-induced hypertension was used to test the hypothesis that taurine supplementation and/or exercise can prevent hypertension and increase exercise capacity. METHODS: Five groups of 15 Sprague-Dawley rats were allocated and designated as control, high fructose-fed (fructose), high fructose-fed plus exercise (FE), high fructose-fed plus 2% taurine supplement (FT) and high fructose-fed plus 2% taurine supplement and exercise (FET) groups. Noninvasive systolic blood pressure (SBP) was recorded weekly and invasive arterial blood pressure (ABP) was recorded at the end of the 4-week trial. Three consecutive swimming tests were performed in the selected rats from each group and the plasma biomarkers were measured in the remaining rats. RESULTS: Noninvasive SBP differed significantly (P < 0.001) from week 3, both noninvasive and invasive ABP increased significantly (P < 0.001), and exercise capacity significantly decreased (P < 0.001) in the fructose group compared with the control group. The individual effects of swimming and taurine supplementation were incapable of preventing the development of hypertension and SBP significantly (P < 0.001) increased in the FE and FT groups; exercise capacity in those groups remained similar to control. The combined effects of exercise and taurine alleviated hypertension and significantly increased exercise capacity in the FET group. Insulin resistance increased significantly and plasma nitric oxide (NO) decreased significantly in the F, FE, and FT groups. Both parameters remained similar to control values in the FET group with an increasing antioxidant activity. CONCLUSION: Taurine supplementation in combination with exercise prevents hypertension and increases exercise capacity by possibly antioxidation and maintaining NO concentrations.

Preparation of polyamide-6/chitosan composite nanofibers by a single solvent system via electrospinning for biomedical applications.

This work was focused on preparation and characterizations of chitosan blended polyamide-6 nanofibers by a new single solvent system via electrospinning process for human osteoblastic (HOB) cell culture applications. The morphological, structural and thermal properties of the polyamide-6/chitosan nanofibers were analyzed by using field-emission scanning electron microscopy (FE-SEM), X-ray diffraction (XRD), Fourier transform-infrared (FT-IR) spectroscopy, Raman spectroscopy, differential scanning calorimetry (DSC) and thermogravimetry (TGA). SEM images revealed that the nanofibers were well-oriented and had good incorporation of chitosan. FT-IR results indicated that the amino groups of chitosan existed in the blended nanofibers. TGA analysis revealed that the onset degradation temperature was decreased with increasing chitosan content in the blended nanofibers. The morphological features of the cells attached on nanofibers were confirmed by SEM. The adhesion, viability and proliferation properties of osteoblast cells on the polyamide-6/chitosan blended nanofibers were analyzed by in vitro cell compatibility test.

Myocardial calcification and hypertension following chronic renal failure and ameliorative effects of furosemide and captopril.

OBJECTIVES: The aim of this study was to prevent metastatic myocardial calcification and hypertension following chronic renal failure (CRF). METHODS: A total of 50 male Sprague-Dawley rats were allocated to one of five groups: the control group (sham), the NxNT group (nephrectomized rats receiving no treatment), the NxFuro group (nephrectomized rats treated with furosemide), the NxCap group (nephrectomized rats treated with captopril) and the NxFuroCap group (nephrectomized rats treated with furosemide and captopril). Surgery (5/6 nephrectomy) was performed to induce CRF. Oral treatment with furosemide (20 mg/kg) and/or captopril (0.05 mg/kg) was given twice daily for 5 weeks. Parameters were studied after 5 weeks. RESULTS: In the NxNT group, arterial blood pressure was significantly increased compared with the controls. Monotherapy with furosemide or captopril and both in combination maintained blood pressure to near or below control. Myocardial and remnant-kidney calcification was detected in NxNT rats, but calcification was absent in the NxFuroCap rats. Cardiac hypertrophy and fibrosis was observed in the NxNT group but not in treatment groups. Both plasma inorganic phosphate and Ca(2+) significantly increased in the NxNT group, but the difference was not significant in the treatment groups. CONCLUSION: Furosemide, either alone or in combination with captopril, is capable to prevent myocardial calcification, cardiac hypertrophy and hypertension, maintaining blood Ca(2+) and phosphate levels by slowing CRF.