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1.
J Adv Res ; 6(4): 563-9, 2015 Jul.
Article in English | MEDLINE | ID: mdl-26199746

ABSTRACT

A solid polymer electrolyte system based on poly(vinyl alcohol) (PVA) and poly(3,4-Etylenedioxythiophene):poly(styrenesulfonate) ( PEDOT: PSS) complexed with magnesium bromide (MgBr2) salt was prepared using solution cast technique. The ionic conductivity is observed to increase with increasing MgBr2 concentration. The maximum conductivity was found to be 9.89 × 10(-6) S/cm for optimum polymer composite film (30 wt.% MgBr2) at room temperature. The increase in the conductivity is attributed to the increase in the number of ions as the salt concentration is increased. This has been proven by dielectric studies. The increase in conductivity is also attributable to the increase in the fraction of amorphous region in the electrolyte films as confirmed by their structural, thermal, electrical and optical properties.

2.
Arch Iran Med ; 15(11): 674-80, 2012 Nov.
Article in English | MEDLINE | ID: mdl-23102243

ABSTRACT

BACKGROUND: Paracetamol overdose causes severe hepatotoxicity that leads to liver failure in both humans and experimental animals. The present study investigates the protective effect of honey against paracetamol-induced hepatotoxicity in Wistar albino rats. We have used silymarin as a standard reference hepatoprotective drug. METHODS: Hepatoprotective activity was assessed by measuring biochemical parameters such as the liver function enzymes, serum alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST). Equally, comparative effects of honey on oxidative stress biomarkers such as malondialdyhyde (MDA), reduced glutathione (GSH) and glutathione peroxidase (GPx) were also evaluated in the rat liver homogenates.  We estimated the effect of honey on serum levels and hepatic content of interleukin-1beta (IL-1ß) because the initial event in paracetamol-induced hepatotoxicity has been shown to be a toxic-metabolic injury that leads to hepatocyte death, activation of the innate immune response and upregulation of inflammatory cytokines. RESULTS: Paracetamol caused marked liver damage as noted by significant increased activities of serum AST and ALT as well as the level of Il-1ß. Paracetamol also resulted in a significant decrease in liver GSH content and GPx activity which paralleled an increase in Il-1ß and MDA levels. Pretreatment with honey and silymarin prior to the administration of paracetamol significantly prevented the increase in the serum levels of hepatic enzyme markers, and reduced both oxidative stress and inflammatory cytokines. Histopathological evaluation of the livers also revealed that honey reduced the incidence of paracetamol-induced liver lesions. CONCLUSION: Honey can be used as an effective hepatoprotective agent against paracetamol-induced liver damage.


Subject(s)
Acetaminophen/toxicity , Analgesics, Non-Narcotic/toxicity , Antioxidants/therapeutic use , Chemical and Drug Induced Liver Injury/prevention & control , Honey , Alanine Transaminase/blood , Animals , Aspartate Aminotransferases/blood , Chemical and Drug Induced Liver Injury/blood , Chemical and Drug Induced Liver Injury/pathology , Glutathione/metabolism , Glutathione Peroxidase/metabolism , Interleukin-1beta/blood , Interleukin-1beta/metabolism , Liver/metabolism , Male , Malondialdehyde/metabolism , Oxidative Stress , Rats , Rats, Wistar , Silymarin/therapeutic use
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