Green synthesis of silver nanoparticles using cranberry powder aqueous extract: characterization and antimicrobial properties

Asmaa A Ashour,1 Dina Raafat,2 Hanan M El-Gowelli,3 Amal H El-Kamel1 1Department of Pharmaceutics, 2Department of Pharmaceutical Microbiology, 3Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt Background: The growing threat of microbial resistance against traditional antibiotics has prompted the development of several antimicrobial nanoparticles (NPs), including silver NPs (AgNPs). In this article, a simple and eco-friendly method for the synthesis of AgNPs using the cranberry powder aqueous extract is reported.Materials and methods: Cranberry powder aqueous extracts (0.2%, 0.5%, and 0.8% w/v) were allowed to interact for 24 hours with a silver nitrate solution (10 mM) at 30°C at a ratio of 1:10. The formation of AgNPs was confirmed by ultraviolet-visible spectroscopy and their concentrations were determined using atomic absorption spectroscopy. The prepared NPs were evaluated by transmission electron microscopy, measurement of ζ-potential, and Fourier-transform infrared spectroscopy. The in vitro antimicrobial properties of AgNPs were then investigated against several microbial strains. Finally, in vivo appraisal of both wound-healing and antimicrobial properties of either plain AgNPs (prepared using 0.2% extract) or AgNP-Pluronic F-127 gel was conducted in a rat model after induction of a Staphylococcus aureus ATCC 6538P wound infection.Results: The formation of AgNPs was confirmed by ultraviolet-visible spectroscopy, where a surface-plasmon resonance absorption peak was observed between 432 and 438 nm. Both size and concentration of the formed AgNPs increased with increasing concentration of the extracts. The developed NPs were stable, almost spherical, and polydisperse, with a size range of 1.4–8.6 nm. The negative ζ-potential values, as well as Fourier-transform infrared spectroscopy analysis, indicated the presence of a capping agent adsorbed onto the surface of the particles. In vitro antimicrobial evaluation revealed a size-dependent activity of the AgNPs against the tested organisms. Finally, AgNPs prepared using 0.2% extract exhibited a substantial in vivo healing potential for full-thickness excision wounds in rats.Conclusion: AgNPs were successfully synthesized from a silver nitrate solution through a simple green route, using cranberry powder aqueous extract as a reducing as well as capping agent. Keywords: cranberry, silver nanoparticles, antimicrobial properties, wound healin

Publication trends in Naunyn-Schmiedeberg's Archives of Pharmacology: focus on pharmacology in Egypt

In a previous analysis of the country of origin of papers published in Naunyn-Schmiedeberg's Archives of Pharmacology, a major shift toward contributions from emerging market countries, was noticed in comparison of 2010 to 2001 publications. Repeating such analysis for 2012 publications in the journal confirmed this trend. An interesting new trend was the emerging presence of papers from a variety of Islamic countries including Egypt. Based on this trend, we shortly review the history and current structure of pharmacology in Egypt. It appears that the presence of Egyptian pharmacology in international journals including pharmacology journals has sharply been increasing over the last two decades. Challenges for a continuation of this encouraging trend are being discusse

The effect of phosphatidylcholine/ deoxycholate on nervous tissues: A histopathological study

Background Data: Phosphatidylcholine/deoxycholate is now widely used in injection lipolysis mainly for aesthetic purposes inducing lipolysis in subcutaneous fat for body contouring and also for shrinking small subcutaneous lipomas. In this work, the authors discuss the effects of phosphatidylcholine dissolved in deoxycholate on nervous tissues in rats to assess the hazards of injection lipolysis in treatment of spinal lipomas as an alternative to surgery. Purpose: to highlight the histopathological effects of phosphatidylcholine on neurological tissues of a rat model to determine whether it is safe to use it as a mesotherapeutic agent for treating spinal lipomas as an alternative for surgery. Study design: a prospective histopathological study on rat model. Material and Methods: 12 young female Wistar rats (2 month old) were divided equally into 2 groups. The treatment group was injected percutaneously by Lipostabil® (0.1 ml/rat/day containing 50 mg/ml phosphatidylcholine dissolved in deoxycholate) in the groin area infiltrating the femoral bundle and the control group was injected with 0.1 ml/rat/day normal saline. The injection was repeated for 4 successive days. Biopsies were harvested on the fourth day from the femoral bundle and studied by light microscopy. The pathology was scored semi-quantitatively for inflammation, necrosis, fibrosis, and nerve damage.Results: Repeated injection of phosphatidyl choline deoxycholate caused intense inflammation adjacent to the nerve leading to neural damage, deposition of collagen fibers amongst the inflammatory background as an early sign of fibrogenesis and tissue necrosis Conclusion: The current data highlights the risk of using such combinations near nerves not only spinal lipomas for its intense inflammatory and necrotic effects. (2013ESJ056

Hybrid polymeric matrices for oral modified release of Desvenlafaxine succinate tablets

Purpose: Desvenlafaxine succinate (DSV) is a water soluble anti-depressant drug, which is rapidly absorbed after oral administration exaggerating its side effects. The current work aimed to prepare controllable release DSV matrix to reduce DSV side effects related to its initial burst. Methods: Fifteen DSV matrix formulations were prepared using different polymers, polymer/drug ratios and matrix excipients and characterized using Differential Scanning Calorimetry (DSC), infrared (IR) spectroscopy, water uptake and in vitro DSV release. The release kinetics were calculated to determine the drug release mechanism. Ex-vivo DSV absorption via rat intestinal mucosal cells and the calculation of the apparent permeability coefficient (Papp) were performed using everted sac technique. Results: Maltodextrin was the best matrix excipient (F7 and F10) showing acceptable decrease in the initial burst compared to the innovator. The addition of negatively charged polymers sodium carboxy methyl cellulose (SCMC) or sodium alginate resulted in an interaction that was proved by DSC and IR findings. This interaction slowed DSV release. F10 showed an excellent absorption of more than 80% of DSV after 4 h and the highest similarity factor with the innovator (84.7). Conclusion: A controllable release pattern of DSV was achieved using Methocel, Maltodextrin and SCMC. The obtained results could be used as a platform to control the release of cationic water soluble drugs that suffer from side effects associated with their initial burst after oral administration

The renin-angiotensin system modulates endotoxic postconditioning of exacerbated renal vasoconstriction in preeclamptic offspring

Abstract We recently reported exacerbated endotoxic signs of neuroinflammation and autonomic defects in offspring of preeclamptic (PE) dams. Here, we investigated whether PE programming similarly modifies hemodynamic and renal vasoconstrictor responsiveness to endotoxemia in PE offspring and whether this interaction is modulated by gestational angiotensin 1–7 (Ang1-7). Preeclampsia was induced by gestational treatment with L-NAME. Adult offspring was challenged with lipopolysaccharides (LPS, 5 mg/kg) and systolic blood pressure (SBP) and renal vasoconstrictions were assessed 4 h later. Male, but not female, offspring of PE rats exhibited SBP elevations that were blunted by LPS. Renal vasoconstrictions induced by angiotensin II (Ang II), but not phenylephrine, were intensified in perfused kidneys of either sex. LPS blunted the heightened Ang II responses in male, but not female, kidneys. While renal expressions of AT1-receptors and angiotensin converting enzyme (ACE) were increased in PE offspring of both sexes, ACE2 was upregulated in female offspring only. These molecular effects were diminished by LPS in male offspring. Gestational Ang1-7 caused sex-unrelated attenuation of phenylephrine vasoconstrictions and preferentially downregulated Ang II responses and AT1-receptor and nuclear factor-kB (NFkB) expressions in females. Together, endotoxemia and Ang1-7 offset in sexually-related manners imbalances in renal vasoconstriction and AT1/ACE/ACE2 signaling in PE offspring

PI3K/Akt-independent NOS/HO activation accounts for the facilitatory effect of nicotine on acetylcholine renal vasodilations: modulation by ovarian hormones.

We investigated the effect of chronic nicotine on cholinergically-mediated renal vasodilations in female rats and its modulation by the nitric oxide synthase (NOS)/heme oxygenase (HO) pathways. Dose-vasodilatory response curves of acetylcholine (0.01-2.43 nmol) were established in isolated phenylephrine-preconstricted perfused kidneys obtained from rats treated with or without nicotine (0.5-4.0 mg/kg/day, 2 weeks). Acetylcholine vasodilations were potentiated by low nicotine doses (0.5 and 1 mg/kg/day) in contrast to no effect for higher doses (2 and 4 mg/kg/day). The facilitatory effect of nicotine was acetylcholine specific because it was not observed with other vasodilators such as 5'-N-ethylcarboxamidoadenosine (NECA, adenosine receptor agonist) or papaverine. Increases in NOS and HO-1 activities appear to mediate the nicotine-evoked enhancement of acetylcholine vasodilation because the latter was compromised after pharmacologic inhibition of NOS (L-NAME) or HO-1 (zinc protoporphyrin, ZnPP). The renal protein expression of phosphorylated Akt was not affected by nicotine. We also show that the presence of the two ovarian hormones is necessary for the nicotine augmentation of acetylcholine vasodilations to manifest because nicotine facilitation was lost in kidneys of ovariectomized (OVX) and restored after combined, but not individual, supplementation with medroxyprogesterone acetate (MPA) and estrogen (E2). Together, the data suggests that chronic nicotine potentiates acetylcholine renal vasodilation in female rats via, at least partly, Akt-independent HO-1 upregulation. The facilitatory effect of nicotine is dose dependent and requires the presence of the two ovarian hormones

Effect of nicotine (1 mg/kg/day, 2 weeks) on vasodilatory effects of acetylcholine (0.01–2.43 nmol) in phenylephrine (10 µM)-preconstricted isolated perfused kidneys obtained from sham, or ovariectomized (OVX) rats supplemented with estrogen (OVX/E2), medroxyprogesterone acetate (OVX/MPA), their combination (OVX/E2/MPA), or the vehicle. Values are means±S.E.M. of 6–8 observations.

<p>^*P<0.05 vs. corresponding control values.</p

Impairment of Nitric Oxide Synthase but Not Heme Oxygenase Accounts for Baroreflex Dysfunction Caused by Chronic Nicotine in Female Rats

<div><p>We recently reported that chronic nicotine impairs reflex chronotropic activity in female rats. Here, we sought evidence to implicate nitric oxide synthase (NOS) and/or heme oxygenase (HO) in the nicotine-baroreflex interaction. Baroreflex curves relating changes in heart rate to increases (phenylephrine) or decreases (sodium nitroprusside) in blood pressure were generated in conscious female rats treated with nicotine or saline in absence and presence of pharmacological modulators of NOS or HO activity. Compared with saline-treated rats, nicotine (2 mg/kg/day i.p., for 14 days) significantly reduced the slopes of baroreflex curves, a measure of baroreflex sensitivity (BRS). Findings that favor the involvement of NOS inhibition in the nicotine effect were (i) NOS inhibition (<i>N</i>_ω-Nitro-L-arginine methyl ester, L-NAME) reduced BRS in control rats but failed to do so in nicotine-treated rats, (ii) L-arginine, NO donor, reversed the BRS inhibitory effect of nicotine. Alternatively, HO inhibition (zinc protoporphyrin IX, ZnPP) had no effect on BRS in nicotine- or control rats and failed to reverse the beneficial effect of L-arginine on nicotine-BRS interaction. Similar to female rats, BRS was reduced by L-NAME, but not ZnPP, in male rats and the L-NAME effect was not accentuated after concomitant administration of nicotine. Baroreflex dysfunction caused by nicotine in female rats was blunted after supplementation with hemin (HO inducer) but not tricarbonyldichlororuthenium(II) dimer (CORM-2), a carbon monoxide (CO) releasing molecule, or bilirubin, the breakdown product of heme catabolism. The facilitatory effect of hemin was abolished upon simultaneous treatment with L-NAME or 1H-<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0098681#pone.0098681-Lande1" target="_blank">[1]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0098681#pone.0098681-Bullen1" target="_blank">[2]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0098681#pone.0098681-Mancia1" target="_blank">[4]</a> oxadiazolo[4,3-a] quinoxalin-1-one (inhibitor of soluble guanylate cyclase, sGC). The activities of HO and NOS in brainstem tissues were also significantly increased by hemin. Thus, the inhibition of NOS, but not HO, accounts for the baroreflex depressant of chronic nicotine. Further, hemin alleviates the nicotine effect through a mechanism that is NOS/sGC but not CO or bilirubin-dependent.</p></div

Effect of nicotine (0.5–4 mg/kg/day, 2 weeks) on areas under the curves (AUC, %vasodilation.nmol) of the cumulative renal vasodilatory effect of acetylcholine (0.01–2.43 nmol), NECA (1.6–50 nmol), and papaverine (1–2.43 nmol) in phenylephrine (10 µM)-preconstricted isolated perfused kidneys obtained from sham rats.

<p>Values are means±S.E.M. of 6–8 observations. ^*P<0.05 vs. saline values.</p

Effect of nicotine (0.5–4 mg/kg/day, 2 weeks) on cumulative vasodilatory effects of acetylcholine (0.01–2.43 nmol), NECA (1.6–50 nmol), and papaverine (1–2.43 nmol) in phenylephrine (10 µM)-preconstricted isolated perfused kidneys obtained from sham rats.

<p>Vasodilator responses are expressed as percentages of the phenylephrine-induced tone. Values are means±S.E.M. of 6–8 observations. ^*P<0.05 vs. saline values.</p