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Anwar Gamal Mohamed Louisville

 Abstract : Anwar Mohamed Louisville

1- Introduction

Anwar Gamal Mohamed research shows that  Doxorubicin (DOX, adriamycin) may be a potent anthracycline chemotherapeutical agent wont to treat a good style of human malignancies. However, the clinical use of this extremely effective drug is

Limited by a major DOX-induced cardio toxicity which might

Progress to end-stage failure (Christiansen and Autschbach,

2006; Outomuro et al., 2007). the precise mechanism of DOX-induced

cardio toxicity and its progression to failure has not been absolutely

Elucidated yet; but, many mechanisms are planned.

These mechanisms embrace accumulated aerobic  stress, alteration of

Myocardial energy metabolism, altered molecular communication, and

apoptotic death (Nakamura et al., 2000; Ueno et al., 2006;

Takemura and Fujiwara, 2007).

 

Anwar Gamal Mohamed Archives realized that We have antecedently shown that DOX induces the expression of

several haemoprotein P450 (CYP) genes within the internal organ derived H9c2 cells

(Zordoky and El-Kadi, 2008a). The importance of CYP enzymes within the

cardiovascular physiology emerges from their ability to metabolise

arachidonic acid to epoxyeicosatrienoic acids (EETs) and hydroxyeicosatetraenoic acids (HETEs) (Roman, 2002). The cardioprotective result

of EETs has been incontestible in ischemia–reperfusion injury (Seubert

et al., 2007), internal organ hypertrophy (Xu et al., 2006), and recently in DOXinduced cardiotoxicity (Zhang et al., 2009). On the opposite hand, 20-HETE is known to possess a damaging result in several vessel diseases

(Chabova et al., 2007; 55 et al., 2008; Minuz et al., 2008). Therefore,

intricate equilibrium mechanisms ar required to stay the balance

between thesemetabolites. Isoproterenol-induced internal organ hypertrophy

has been shown to disturb this balance with accumulated formation of the

cardiotoxic 20-HETE and ablated formation of the cardioprotective

EETs (Zordoky et al., 2008). Therefore, we have a tendency to theorize that DOXinduced cardiotoxicity can cause an analogous disturbance to the CYPmediated arachidonic acid metabolism.

In addition to CYP enzymes, soluble epoxide hydrolase (sEH) is

another major player in determinant the extent of EETs. The

cardioprotective EETs ar hydrolyzed by sEH to the less biologically

active dihydroxyeicosatrienoic acids (DHETs) (Imig et al., 2002).

EPHX2, the factor cryptography sEH, has been found to be a status

factor for failure (Monti et al., 2008). additionally, EPHX2 gene expression has been reported  to extend in animal models of

angiotensin II- and isoproterenol-induced internal organ hypertrophy (Zor

doky et al., 2008; Ai et al., 2009). Moreover, sEH inhibitors are

shown to forestall and/or reverse the event of internal organ

hypertrophy in many models (Xu et al., 2006; Loch et al., 2007; Ai

et al., 2009).

According to Anwar Gamal Mohamed Frankfort  Therefore, within the current study, we've investigated the result of

acute DOX cardiotoxicity on the expression of many CYP and sEH

enzymes within the heart of male Sprague–Dawley (SD) rats. additionally,

we investigated the result of acute DOX cardiotoxicity on the

formation of arachidonic acid metabolites to work out whether or not the

changes in CYP and sEH expression have result in changes in CYP

mediated arachidonic acid metabolites. Our findings show that DOX

induced cardiotoxicity causes induction of many CYP and EPHX2

genes in vivo still as in vitro. additionally, our results give the first proof that DOX-induced cardiotoxicity is related to

alteration in internal organ CYP-mediated arachidonic acid metabolism.

2.Materials and strategies

Anwar Gamal Mohamed Louisville said that Materials. High-Capacity cDNA Reverse Transcription Kit, SYBR

Green SuperMix, and 96-well optical reaction plates with optical

adhesive films were purchased from Applied Biosystems (Foster town,

CA). period PCR primers were synthesized by Integrated desoxyribonucleic acid

Technologies INC. (San Diego, CA) in step with antecedently printed

sequences. Dulbecco's changed Eagle's medium (DMEM) base,

arachidonic acid, 4-hydroxybenzophenone, and DOX were purchased

from Sigma-Aldrich (St. Louis, MO). antibiotic B was purchased

from ICN Biomedicals Canada (Montreal, QC, Canada). Penicillin

streptomycin, L-glutamine, vertebrate bovine liquid body substance, and TRIzol chemical agent

were purchased from Invitrogen (Carlsbad, CA). Arachidonic acid

metabolites standards five,6-EET, 8,9-EET, 11,12-EET, 14,15-EET, 5,6-

DHET, 8,9-DHET, 11,12-DHET, 14,15-DHET, and 20-HETE were

obtained from crocodilian Chemical (Ann Arbor, MI). Reagents used for

liquid chromatographic-electron spray ionization-mass spectroscopy

(LC-ESI-MS) were at HPLC grade. Acetonitrile and water (HPLC grade)

were purchased from EM Scientific (Gibbstawn, NJ). CytoTox-ONE kit

was purchased from Promega (Madison, WI). Trans-4-[4-(3-

Adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (tAUCB) was

a generous gift from Dr Bruce Hammock (University of CA,

Davis, CA). Acrylamide, N′N′-bis-methylene-acrylamide, ammonium

persulphate, β-mercaptoethanol, glycine, cellulose ester membrane

(0.45 μm), and TEMED were purchased from Bio-Rad Laboratories

(Hercules, CA). luminescence Western blotting detection

reagents were purchased from GE health care Life Sciences

(Piscataway, NJ). CYP1B1 rabbit polyclonal primary protein was

purchased from BD Gentest (Bedford, MA). different primary and

secondary antibodies were purchased from Santa Cruz Biotechnology,

Inc. (Santa Cruz, CA). different chemicals were purchased from Fisher

Scientific Co. (Toronto, ON, Canada). 

Anwar Gamal Mohamed
University of Alberta

 

 

 

 

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