کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5845893 | 1561172 | 2016 | 35 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Improved bioavailability of targeted Curcumin delivery efficiently regressed cardiac hypertrophy by modulating apoptotic load within cardiac microenvironment
ترجمه فارسی عنوان
بهبود زیستی در دسترس بودن تحویل کورکومین به طور موثر باعث کاهش هیپرتروفی قلبی با تعدیل بار آپوپتوتیک در محیط میکروایوسی قلب
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کلمات کلیدی
NHSβMHCbeta myosin heavy chainANGIIPARPBcl2ANFN-hydroxysuccinimidep-p53di-tert-butyl dicarbonatePCNArpl32COX IVEDCCMCBoc2O1-ethyl-3-(3-dimethylaminopropyl) carbodiimide - 1-اتیل-3- (3-dimethylaminopropyl) carbodiimideProliferating Cell Nuclear Antigen - آنتیژن هسته ای تکثیر سلولیCardiomyocyte apoptosis - آپوپتوز Cardiomyocytecon - باBax - باکسTerminal deoxynucleotidyl transferase dUTP nick end labeling - ترمینال deoxynucleotidyl transferase dUTP نام نهایی پایان نامهTUNEL - تونلControl cells - سلولهای کنترلatrial natriuretic factor - فاکتور natriuretic دهلیزیB-cell lymphoma 2 - لنفوم سلول B 2Cardiac hypertrophy - هیپرتروفی قلبیbody weight - وزن بدنHeart weight - وزن قلبBcl-2-associated X protein - پروتئین X مرتبط با Bcl-2poly ADP ribose polymerase - پلی ADA ریبوز پلی مرازCarboxymethyl chitosan - کربوکسی متیل کیتوزانPositive control - کنترل مثبتnegative control - کنترل منفیCurcumin - کورکومین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی
Cardiomyocyte apoptosis acts as a prime modulator of cardiac hypertrophy leading to heart failure, a major cause of human mortality worldwide. Recent therapeutic interventions have focussed on translational applications of diverse pharmaceutical regimes among which, Curcumin (from Curcuma longa) is known to have an anti-hypertrophic potential but with limited pharmacological efficacies due to low aqueous solubility and poor bioavailability. In this study, Curcumin encapsulated by carboxymethyl chitosan (CMC) nanoparticle conjugated to a myocyte specific homing peptide was successfully delivered in bioactive form to pathological myocardium for effective regression of cardiac hypertrophy in a rat (Rattus norvegicus) model. Targeted nanotization showed higher cardiac bioavailability of Curcumin at a low dose of 5 mg/kg body weight compared to free Curcumin at 35 mg/kg body weight. Moreover, Curcumin/CMC-peptide treatment during hypertrophy significantly improved cardiac function by downregulating expression of hypertrophy marker genes (ANF, β-MHC), apoptotic mediators (Bax, Cytochrome-c) and activity of apoptotic markers (Caspase 3 and PARP); whereas free Curcumin in much higher dose showed minimal improvement during compromised cardiac function. Targeted Curcumin treatment significantly lowered p53 expression and activation in diseased myocardium via inhibited interaction of p53 with p300-HAT. Thus attenuated acetylation of p53 facilitated p53 ubiquitination and reduced the apoptotic load in hypertrophied cardiomyocytes; thereby limiting cardiomyocytes' need to enter the regeneration cycle during hypertrophy. This study elucidates for the first time an efficient targeted delivery regimen for Curcumin and also attributes towards probable mechanistic insight into its therapeutic potential as a cardio-protective agent for regression of cardiac hypertrophy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 290, 1 January 2016, Pages 54-65
Journal: Toxicology and Applied Pharmacology - Volume 290, 1 January 2016, Pages 54-65
نویسندگان
Aramita Ray, Santanu Rana, Durba Banerjee, Arkadeep Mitra, Ritwik Datta, Shaon Naskar, Sagartirtha Sarkar,