کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8545276 | 1561563 | 2018 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Unfolding the mechanism of cisplatin induced pathophysiology in spleen and its amelioration by carnosine
ترجمه فارسی عنوان
باز کردن مکانیزم پاتوفیزیولوژی ناشی از سیس پلاتین در طحال و بهبودی آن توسط کارنوسین
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کلمات کلیدی
IL-1βFpn1MCP-1IL-6JnkiNOSICAM-1IL-10DTTc-Jun N-terminal kinase - C-Jun N-terminal kinaseROS - ROSinflammation - التهاب( توروم) interleukin 1beta - اینترلوکین 1 بتاInterleukin 10 - اینترلوکین 10interleukin 6 - اینترلوکین 6Oxidative stress - تنش اکسیداتیوApoptosis - خزان یاختهایdihydroethidium - دی هیدروتیدیمdithiothreitol - دیتیوتریتولcisplatin - سیس پلاتینtumour necrosis factor - عامل نکروز تومورTNF-α - فاکتور نکروز توموری آلفاnuclear factor kappa B - فاکتور هسته ای کاپا Bintracellular adhesion molecule 1 - مولکول چسبندگی داخل سلولی 1DHE - وmonocyte chemoattractant protein - پروتئین شیمیایی monocyte chemoattractantCarnosine - کارنوزینReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی
cis-Diamminedichloroplatinum (cisplatin) is an effective chemotherapeutic and is widely used for the treatment of various types of solid tumors. Bio-distribution of cisplatin to other organs due to poor targeting towards only cancer cells constitutes the backbone of cisplatin-induced toxicity. The adverse effect of this drug on spleen is not well characterized so far. Therefore, we have set our goal to explore the mechanism of the cisplatin-induced pathophysiology of the spleen and would also like to evaluate whether carnosine, an endogenous neurotransmitter and antioxidant, can ameliorate this pathophysiological response. We found a dose and time-dependent increase of the pro-inflammatory cytokine, TNF-α, in the spleen tissue of the experimental mice exposed to 10 and 20 mg/kg body weight of cisplatin. The increase in inflammatory cytokine can be attributed to the activation of the transcription factor, NF-ĸB. This also aids in the transcription of other pro-inflammatory cytokines and cellular adhesion molecules. Exposure of animals to cisplatin at both the doses resulted in ROS and NO production leading to oxidative stress. The MAP Kinase pathway, especially JNK activation, was also triggered by cisplatin. Eventually, the persistence of inflammatory response and oxidative stress lead to apoptosis through extrinsic pathway. Carnosine has been found to restore the expression of inflammatory molecules and catalase to normal levels through inhibition of pro-inflammatory cytokines, oxidative stress, NF-ĸB and JNK. Carnosine also protected the splenic cells from apoptosis. Our study elucidated the detailed mechanism of cisplatin-induced spleen toxicity and use of carnosine as a protective agent against this cytotoxic response.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 279, 5 January 2018, Pages 159-170
Journal: Chemico-Biological Interactions - Volume 279, 5 January 2018, Pages 159-170
نویسندگان
Sharmistha Banerjee, Krishnendu Sinha, Sayantani Chowdhury, Parames C. Sil,