scholarly journals Antiglycating Effect of Phenolics from the Chilean Currant Ribes cucullatum under Thermal Treatment

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 665
Author(s):  
Felipe Ávila ◽  
Natalia Ravello ◽  
Camila Manriquez ◽  
Felipe Jiménez-Aspee ◽  
Guillermo Schmeda-Hirschmann ◽  
...  
Keyword(s):  
Thermal Treatment ◽  
Protective Effects ◽  
Gastric Digestion ◽  
Protein Crosslinking ◽  
Dietary Polyphenols ◽  
Chromatography Analysis ◽  
Sarcoplasmic Proteins ◽  
Carboxymethyl Lysine ◽  
High Concentrations ◽  
Dose Dependent

Numerous dietary polyphenols possess antiglicating activity, but the effects of thermal treatment on this activity are mostly unknown. The effect of thermal treatment in the antiglycating activity of polyphenolic enriched extracts (PEEs) from Ribes cucullatum towards glyoxal-induced glycation of sarcoplasmic proteins was assessed. Sarcoplasmic proteins from chicken, beef, salmon, and turkey, were incubated 2 h at 60 °C with and without glyoxal and different concentrations of PEEs (0.25, 0.5, 1, and 5 mg/mL). The antiglycating activity was evaluated by: (1) Lys and Arg consumption, (2) Carboxymethyl lysine (CML) generation, and (3) lipid-derived electrophiles inhibition in a gastric digestion model. Protective effects were observed against CML generation in proteins and a decrease of electrophiles in the gastric digestion model. A dose-dependent consumption of Lys and Arg in proteins/PEEs samples, indicated the possible occurrence of quinoproteins generation from the phenolics. Protein/PEEs incubations were assessed by: (1) High pressure liquid chromatography analysis, (2) Gel electrophoresis (SDS-PAGE), and (3) Redox cycling staining of quinoproteins. Protein/PEEs incubations produced: (1) Decrease in phenolics, (2) increase of protein crosslinking, and (3) dose-dependent generation of quinoproteins. We demonstrate that phenolic compounds from R. cucullatum under thermal treatment act as antiglycating agents, but oxidative reactions occurs at high concentrations, generating protein crosslinking and quinoproteins.

Hepatic uptake of intact glutathione S-conjugate, inhibition by organic anions, and sinusoidal catabolism

1993 ◽  
Vol 265 (3) ◽  
pp. G547-G554
Author(s):  
C. A. Hinchman ◽  
A. T. Truong ◽  
N. Ballatori
Keyword(s):  
Guinea Pig ◽  
Rat Liver ◽  
Marked Decrease ◽  
Hepatic Uptake ◽  
Half Time ◽  
High Concentrations ◽  
Rat Livers ◽  
Dose Dependent ◽  
Uptake And Metabolism ◽  
Guinea Pig Liver

To identify potential mechanisms for hepatic removal of circulating glutathione (GSH) conjugates, uptake and metabolism of S-2,4-dinitrophenylglutathione (DNP-SG) were examined in isolated perfused livers from rat and guinea pig. Guinea pig livers perfused with 5 mumol of DNP-SG in a recirculating system (50 microM initial concn) rapidly cleared the conjugate from the perfusate (half time 3.7 min), whereas clearance was considerably slower in rat liver (half time 35 min). Disappearance of DNP-SG from the perfusate was accompanied by a simultaneous appearance of DNP-SG and its metabolites in bile. Addition of acivicin, an inhibitor of gamma-glutamyltransferase (gamma-GT), to the perfusate resulted in a marked decrease in DNP-SG clearance by guinea pig liver but had no effect in rat liver, suggesting that in the guinea pig this process is largely dependent on sinusoidal gamma-GT activity. However, even in the presence of acivicin, rat and guinea pig livers removed nearly one-half of the administered DNP-SG from the recirculating perfusate over 30 min. High concentrations of DNP-SG were found in bile (up to 3.7 mM), indicating that the liver is capable of transporting the intact conjugate from the circulation. When rat livers were perfused with higher concentrations of DNP-SG (100 and 250 microM), biliary excretion of DNP-SG increased dose dependently, with concentrations in bile reaching 10 mM at the higher dose. This was accompanied by a dose-dependent choleresis.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Necroptosis protects against exacerbation of acute pancreatitis

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Michittra Boonchan ◽  
Hideki Arimochi ◽  
Kunihiro Otsuka ◽  
Tomoko Kobayashi ◽  
Hisanori Uehara ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Necrotizing Pancreatitis ◽  
Neutrophil Infiltration ◽  
Dependent Manner ◽  
Protective Effects ◽  
Interacting Protein ◽  
Inflammatory Conditions ◽  
Edematous Pancreatitis ◽  
Genetic Deletion ◽  
Dose Dependent

AbstractThe sensing of various extrinsic stimuli triggers the receptor-interacting protein kinase-3 (RIPK3)-mediated signaling pathway, which leads to mixed-lineage kinase-like (MLKL) phosphorylation followed by necroptosis. Although necroptosis is a form of cell death and is involved in inflammatory conditions, the roles of necroptosis in acute pancreatitis (AP) remain unclear. In the current study, we administered caerulein to Ripk3- or Mlkl-deficient mice (Ripk3−/− or Mlkl−/− mice, respectively) and assessed the roles of necroptosis in AP. We found that Ripk3−/− mice had significantly more severe pancreatic edema and inflammation associated with macrophage and neutrophil infiltration than control mice. Consistently, Mlkl−/− mice were more susceptible to caerulein-induced AP, which occurred in a time- and dose-dependent manner, than control mice. Mlkl−/− mice exhibit weight loss, edematous pancreatitis, necrotizing pancreatitis, and acinar cell dedifferentiation in response to tissue damage. Genetic deletion of Mlkl resulted in downregulation of the antiapoptotic genes Bclxl and Cflar in association with increases in the numbers of apoptotic cells, as detected by TUNEL assay. These findings suggest that RIPK3 and MLKL-mediated necroptosis exerts protective effects in AP and caution against the use of necroptosis inhibitors for AP treatment.

Long Noncoding RNA SPRY4-IT1 Modulates Ketamine-Induced Neurotoxicity in Human Embryonic Stem Cell-Derived Neurons through EZH2

2021 ◽  
pp. 1-9
Author(s):  
Jingyuan Huang ◽  
Yan Xu ◽  
Fang Wang ◽  
Haili Wang ◽  
Lu Li ◽  
...  
Keyword(s):  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Embryonic Stem ◽  
Protective Effects ◽  
Tyrosine Kinase Signaling ◽  
Ezh2 Expression ◽  
Induced Neurons ◽  
Neurite Degeneration ◽  
Dose Dependent

<b><i>Objective:</i></b> This study aimed to investigate whether long noncoding RNA sprouty receptor tyrosine kinase signaling antagonist 4-intronic transcript 1 (SPRY4-IT1) is involved in the regulation of ketamine-induced neurotoxicity. <b><i>Methods:</i></b> Human embryonic stem cells (hESCs) were induced into neurons in vitro and treated with ketamine. Apoptosis and neurite degeneration assays were used to determine ketamine-induced neurotoxicity and qRT-PCR to determine SPRY4-IT1 expression. SPRY4-IT1 was downregulated in hESC-induced neurons to examine its regulation on ketamine-induced neurotoxicity. The correlation between enhancer of zeste homolog 2 (EZH2) and SPRY4-IT1 was also examined. EZH2 was upregulated in SPRY4-IT1-downregualted hESC-induced neurons to further examine its participation in SPRY4-IT1-mediated ketamine neurotoxicity. <b><i>Results:</i></b> Ketamine-induced dose-dependent apoptosis, neurite degeneration, and SPRY4-IT1 upregulation in hESC-induced neurons. Lentivirus-mediated SPRY4-IT1 downregulation protected ketamine neurotoxicity. EZH2 expression was positively correlated with SPRY4-IT1 in hESC-induced neurons. EZH2 overexpression markedly reversed the protective effects of SPRY4-IT1 knockdown on ketamine neurotoxicity. <b><i>Conclusions:</i></b> SPRY4-IT1 is involved in anesthesia-induced neurotoxicity, possibly through the regulation on EZH2 gene.

scholarly journals Anthracycline-induced cytotoxicity in the GL261 glioma model system

2021 ◽  
Author(s):  
Amber M. Tavener ◽  
Megan C. Phelps ◽  
Richard L. Daniels
Keyword(s):  
Cell Viability ◽  
Tumor Cells ◽  
Flow Cytometric Analysis ◽  
Annexin V ◽  
Chemotherapeutic Agents ◽  
Cytotoxic Effects ◽  
High Concentrations ◽  
Induced Apoptosis ◽  
Dose Dependent ◽  
Gl261 Glioma

AbstractGlioblastoma (GBM) is a lethal astrocyte-derived tumor that is currently treated with a multi-modal approach of surgical resection, radiotherapy, and temozolomide-based chemotherapy. Alternatives to current therapies are urgently needed as its prognosis remains poor. Anthracyclines are a class of compounds that show great potential as GBM chemotherapeutic agents and are widely used to treat solid tumors outside the central nervous system. Here we investigate the cytotoxic effects of doxorubicin and other anthracyclines on GL261 glioma tumor cells in anticipation of novel anthracycline-based CNS therapies. Three methods were used to quantify dose-dependent effects of anthracyclines on adherent GL261 tumor cells, a murine cell-based model of GBM. MTT assays quantified anthracycline effects on cell viability, comet assays examined doxorubicin genotoxicity, and flow cytometry with Annexin V/PI staining characterized doxorubicin-induced apoptosis and necrosis. Dose-dependent reductions in GL261 cell viability were found in cells treated with doxorubicin (EC50 = 4.9 μM), epirubicin (EC50 = 5.9 μM), and idarubicin (EC50 = 4.4 μM). Comet assays showed DNA damage following doxorubicin treatments, peaking at concentrations of 1.0 μM and declining after 25 μM. Lastly, flow cytometric analysis of doxorubicin-treated cells showed dose-dependent induction of apoptosis (EC50 = 5.2 μM). Together, these results characterized the cytotoxic effects of anthracyclines on GL261 glioma cells. We found dose-dependent apoptotic induction; however at high concentrations we find that cell death is likely necrotic. Our results support the continued exploration of anthracyclines as compounds with significant potential for improved GBM treatments.

scholarly journals Farnesol-Loaded Liposomes Protect the Epidermis and Dermis from PM2.5-Induced Cutaneous Injury

2021 ◽  
Vol 22 (11) ◽  
pp. 6076
Author(s):  
Yu-Chiuan Wu ◽  
Wei-Yun Chen ◽  
Chun-Yin Chen ◽  
Sheng I. Lee ◽  
Yu-Wen Wang ◽  
...  
Keyword(s):  
Chronic Inflammation ◽  
Water Solubility ◽  
Antibacterial Properties ◽  
Hair Follicles ◽  
Protective Effects ◽  
Cutaneous Injury ◽  
Anti Inflammatory ◽  
High Concentrations ◽  
Acute And Chronic Inflammation

Particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5) increases oxidative stress through free radical generation and incomplete volatilization. In addition to affecting the respiratory system, PM2.5 causes aging- and inflammation-related damage to skin. Farnesol (Farn), a natural benzyl semiterpene, possesses anti-inflammatory, antioxidative, and antibacterial properties. However, because of its poor water solubility and cytotoxicity at high concentrations, the biomedical applications of Farn have been limited. This study examined the deleterious effects of PM2.5 on the epidermis and dermis. In addition, Farn-encapsulated liposomes (Lipo-Farn) and gelatin/HA/xanthan gel containing Lipo-Farn were prepared and applied in vivo to repair and alleviate PM2.5-induced damage and inflammation in skin. The prepared Lipo-Farn was 342 ± 90 nm in diameter with an encapsulation rate of 69%; the encapsulation significantly reduced the cytotoxicity of Farn. Lipo-Farn exhibited a slow-release rate of 35% after 192 h of incubation. The half-maximal inhibitory concentration of PM2.5 was approximately 850 μg/mL, and ≥400 μg/mL PM2.5 significantly increased IL-6 production in skin fibroblasts. Severe impairment in the epidermis and hair follicles and moderate impairment in the dermis were found in the groups treated with post-PM2.5 and continuous subcutaneous injection of PM2.5. Acute and chronic inflammation was observed in the skin in both experimental categories in vivo. Treatment with 4 mM Lipo-Farn largely repaired PM2.5-induced injury in the epidermis and dermis, restored injured hair follicles, and alleviated acute and chronic inflammation induced by PM2.5 in rat skin. In addition, treatment with 4 mM pure Farn and 2 mM Lipo-Farn exerted moderate reparative and anti-inflammatory effects on impaired skin. The findings of the current study indicate the therapeutic and protective effects of Lipo-Farn against various injuries caused by PM2.5 in the pilosebaceous units, epidermis, and dermis of skin.

scholarly journals Effects of Propentofylline on Hypoxia—Hypoglycemia-Induced Calcium Accumulation in Gerbil Hippocampal Slices

1992 ◽  
Vol 12 (2) ◽  
pp. 301-305 ◽  
Author(s):  
Fumito Kadoya ◽  
Akira Mitani ◽  
Tatsuru Arai ◽  
Kiyoshi Kataoka
Keyword(s):  
Cerebral Ischemia ◽  
Intracellular Calcium ◽  
Neuronal Damage ◽  
Hippocampal Slices ◽  
Dependent Manner ◽  
Protective Effects ◽  
Calcium Accumulation ◽  
Xanthine Derivative ◽  
Acute Increase ◽  
Dose Dependent

The xanthine derivative propentofylline (HWA 285) has been reported to show protective effects against neuronal damage induced by cerebral ischemia. In the present study, microfluorometry was used to investigate the effect of propentofylline on the hypoxia–hypoglycemia-induced intracellular calcium accumulation in gerbil hippocampal slices. When slices were superfused with hypoxic–hypoglycemic medium that did not contain propentofylline, an acute increase in calcium accumulation was detected 75–200 s (mean latency of 123 s) after the beginning of hypoxia–hypoglycemia. When slices were superfused with hypoxic–hypoglycemic mediums that contained 10 μ M, 100 μ M, and 1 m M propentofylline, the latency of the acute increase in calcium accumulation was prolonged in all subregions of the hippocampus in a dose-dependent manner: mean latencies in field CA1 were 146, 168, and 197 s after hypoxia–hypoglycemia, respectively. This retardation in calcium accumulation may be involved in the mechanisms by which propentofylline diminishes ischemic injury.

PROTECTIVE EFFECTS OF VITAMIN C AGAINST CISPLATIN-INDUCED NEPHROTOXICITY AND LIPID PEROXIDATION IN ADULT RATS: A DOSE-DEPENDENT STUDY

2000 ◽  
Vol 41 (4) ◽  
pp. 405-411 ◽  
Author(s):  
LUSÂNIA M. GREGGI ANTUNES ◽  
JOANA D'ARC C. DARIN ◽  
MARIA DE LOURDES P. BIANCHI
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin C ◽  
Protective Effects ◽  
Adult Rats ◽  
Dose Dependent

Antioxidative properties of Sambacus nigra extracts

2015 ◽  
Vol 69 (9) ◽  
Author(s):  
Dominika Topoľská ◽  
Katarína Valachová ◽  
Peter Rapta ◽  
Stanislav Šilhár ◽  
Elena Panghyová ◽  
...  
Keyword(s):  
Acute Inflammation ◽  
Radical Scavenging ◽  
Oxidative Degradation ◽  
Protective Effects ◽  
Radical Scavenging Capacity ◽  
Scavenging Capacity ◽  
Diammonium Salt ◽  
Dose Dependent ◽  
Oxidative System

AbstractPotential protective effects of elderberry (Sambucus nigra) extracts against oxidative degradation of hyaluronan (HA) were detected in vitro. To induce free-radical-mediated HA degradation, Weissberger’s biogenic oxidative system, which mimics the situation of acute inflammation, was applied. Time- and dose-dependent changes of dynamic viscosity of the HA solutions in the presence and absence of two elderberry extracts produced in 2006 and 2012 were recorded by rotational viscometry (RV). Radical scavenging capacity of both extracts was investigated by the spectrocolorimetric ABTS [2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt] assay and the “inverted” ABTS assay. Oxygen consumption of the system oxidizing HA either in the absence or presence of the elderberry extracts was determined. The results of RV revealed that an addition of the newer extract (2012) promoted the inhibition of HA degradation more markedly compared to the older extract (2006). The same effect of both extracts on ABTS

scholarly journals Hepatoprotective effects of Sapium sebiferum in paracetamol-induced liver injury

2015 ◽  
Vol 10 (2) ◽  
pp. 393 ◽  
Author(s):  
Liaqat Hussain ◽  
Muhammad Sajid Hamid Akash ◽  
Madeha Tahir ◽  
Kanwal Rehman
Keyword(s):  
Liver Injury ◽  
Serum Levels ◽  
Therapeutic Effects ◽  
Sapium Sebiferum ◽  
Dependent Manner ◽  
Protective Effects ◽  
Drug Induced ◽  
Standard Drug ◽  
Hepatoprotective Effects ◽  
Dose Dependent

<span><em>Sapium sebiferum</em> leaves were used to determine its hepatoprotective effects against paracetamol-induced hepatotoxicity in mice. A dose dependent study was conducted using two different doses (200 mg/kg and 400 mg/kg) of the extract of </span><em>S. sebiferum</em><span> against toxic effects of paracetamol (500 mg/kg) in experimental animal model. Silymarin (50 mg/kg) was used as standard drug to compare therapeutic effects of </span><em>S. sebiferum</em><span> with control and paracetamol-treated groups. Paracetamol significantly increased the serum levels of liver enzyme markers like alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total bilirubin, and direct bilirubin. The extract showed protective effects by normalizing the liver enzymes markers in a dose dependent manner. Histopathological results confirmed the hepatoprotective effects of leaves of </span><em>S. sebiferum</em><span>. We conclude that leaves of </span><em>S. sebiferum</em><span> have strong hepatoprotective effects against paracetamol-induced liver injury and can be used in liver injuries caused by drug-induced toxicity.</span>

scholarly journals Prostaglandin E2 Signaling Mediates Oenocytoid Immune Cell Function and Lysis, Limiting Bacteria and Plasmodium Oocyst Survival in Anopheles gambiae

2021 ◽  
Vol 12 ◽  
Author(s):  
Hyeogsun Kwon ◽  
David R. Hall ◽  
Ryan C. Smith
Keyword(s):  
Immune Responses ◽  
Prostaglandin E2 ◽  
Anopheles Gambiae ◽  
Cell Function ◽  
Immune Cell ◽  
Protective Effects ◽  
Immune Cell Function ◽  
Humoral Immune ◽  
High Concentrations ◽  
Prostaglandin E2 Receptor

Lipid-derived signaling molecules known as eicosanoids have integral roles in mediating immune and inflammatory processes across metazoans. This includes the function of prostaglandins and their cognate G protein-coupled receptors (GPCRs) to employ their immunological actions. In insects, prostaglandins have been implicated in the regulation of both cellular and humoral immune responses, yet in arthropods of medical importance, studies have been limited. Here, we describe a prostaglandin E2 receptor (AgPGE2R) in the mosquito Anopheles gambiae and demonstrate that its expression is most abundant in oenocytoid immune cell populations. Through the administration of prostaglandin E2 (PGE2) and AgPGE2R-silencing, we demonstrate that prostaglandin E2 signaling regulates a subset of prophenoloxidases (PPOs) and antimicrobial peptides (AMPs) that are strongly expressed in populations of oenocytoids. We demonstrate that PGE2 signaling via the AgPGE2R significantly limits both bacterial replication and Plasmodium oocyst survival. Additional experiments establish that PGE2 treatment increases phenoloxidase (PO) activity through the increased expression of PPO1 and PPO3, genes essential to anti-Plasmodium immune responses that promote oocyst killing. We also provide evidence that the mechanisms of PGE2 signaling are concentration-dependent, where high concentrations of PGE2 promote oenocytoid lysis, negating the protective effects of lower concentrations of PGE2 on anti-Plasmodium immunity. Taken together, our results provide new insights into the role of PGE2 signaling on immune cell function and its contributions to mosquito innate immunity that promote pathogen killing.

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