کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8545427 | 1561564 | 2017 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Asiatic acid abridges pre-neoplastic lesions, inflammation, cell proliferation and induces apoptosis in a rat model of colon carcinogenesis
ترجمه فارسی عنوان
اسید آسیاییک باعث کاهش ضایعات پیش از نئوپلاستیک، التهاب، تکثیر سلولی و ایجاد آپوپتوز در یک مدل موشهای سرطانزا کولون می شود
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کلمات کلیدی
GSTDT-diaphoraseazoxymethaneCDNBDTDPCNAUDPGTMAMDMHAOMTEMEDUDP-glucuronyl transferaseACFDCPIPAgNORsSDSAB-PASDABDMRTAlcian blue-periodic acid Schiff1-chloro-2,4-dinitrobenzene - 1-کلرو-2،4-دینیتروبنزن1,2-dimethylhydrazine - 1،2-دی متیل هیدرازین2,6-dichlorophenol indophenol - 2،6-dichlorophenol indophenol3,3′-diaminobenzidine - 3،3'-diaminobenzidineBSA - BSADMSO - DMSOH&E - H & EDuncan's Multiple Range Test - آزمایش چندتایی دانکنbovine serum albumin - آلبومین سرم گاوProliferating Cell Nuclear Antigen - آنتیژن هسته ای تکثیر سلولیAsiatic acid - اسید آسیاییANOVA - تحلیل واریانس Analysis of varianceone-way analysis of variance - تحلیل واریانس یک راههCell proliferation - تکثیر سلولیDimethyl sulfoxide - دیمتیل سولفواکسیدsodium dodecyl sulphate - سدیم دودسیل سولفاتColorectal cancer - سرطان روده بزرگColon cancer - سرطان کولونaberrant crypt foci - فوریه کریپت ناپایدارmethylazoxymethanol - متیلازوکمتانولArgyrophilic nucleolar organizer regions - مناطق برگزیده ارگروفیلیس هسته ایhaematoxylin and eosin - هماتوکسیلین و ائوزینChemoprevention - پیشگیری شیمیاییCRC - کد افزونگی دورهای glutathione S-transferase - گلوتاتیون S-ترانسفراز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی
The utmost aim of this present study was to investigate the anti-inflammatory, antiproliferative and proapoptotic potential of Asiatic acid (AA) on 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in experimental rats. Rats were divided into six groups and received modified pellet diet for 32 weeks. Group 1 served as control rats. Group 2 received AA (4Â mg/kg b.w. p.o.). Group 3-6 rats received 15 DMH (20Â mg/kg b.w., s.c.) injections once a week starting from the 4th week. Besides DMH, rats received AA (4Â mg/kg b.w. p.o.) in group 4 starting 2 weeks before carcinogen treatment till the end of the last DMH; group 5 starting 2 days after last DMH till the end of the experiment; and group 6 throughout the experiment. Pre-neoplastic lesions, xenobiotic metabolizing enzymes, inflammation, cell proliferation and apoptotic markers were analysed in our study. Our results ascertained AA supplementation to DMH-exposed rats significantly decreased the incidence of aberrant crypt foci (ACF) and phase I xenobiotic enzymes; and increased the phase II xenobiotic enzymes and mucin content as compared to DMH-alone-exposed rats. Moreover the increased expressions of mast cells, argyrophilic nucleolar organizer regions (AgNORs), proliferating cell nuclear antigen (PCNA) and cyclin D1 observed in the DMH-alone-exposed rats were reverted and were comparable with those of the control rats, when treated with AA. Concordantly AA also induced apoptosis by downregulating the expression of Bcl-2 and upregulating Bax, cytochrome c, caspase-3 and -9 in the DMH-alone-exposed rats. Thus AA was able to inhibit DMH-induced colon carcinogenesis by detoxifying the carcinogen, decreasing the preneoplastic lesions by virtue of its anti-inflammatory, antiproliferative and proapoptotic effects. Therefore our findings suggest that AA could be used as an effective chemopreventive agent against DMH induced colon carcinogenesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 278, 25 December 2017, Pages 197-211
Journal: Chemico-Biological Interactions - Volume 278, 25 December 2017, Pages 197-211
نویسندگان
Aktarul Islam Siddique, Vijay Mani, Senbagarani Renganathan, Rajagopal Ayyanar, Ananthi Nagappan, Nalini Namasivayam,