کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5535151 | 1402217 | 2017 | 21 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dose dependent treatment with isotretinoin induces more changes in the ileum than in the duodenum and jejunum in Wistar rats
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
علوم کشاورزی و بیولوژیک (عمومی)
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چکیده انگلیسی
Acne is the most common skin disorder and can directly affect the patients' self-esteem. Systemic treatment has been indicated for nodular, cystic or persistent acne rather than another type of treatment, such as a topic one. Isotretinoin is an analogue of vitamin A and by suppressing the sebaceous glands the disease can be controlled. This study was designed to mimic the treatment performed in young patients using the dosage of 1Â mg/kg, and a higher one of 10Â mg/kg, for 60Â days in young male Wistar rats. 24 Wistar rats were divided into four groups: control(water), D0(soybean oil, control group), D1(1Â mg/kg of Isotretinoin solution), D10(10Â mg/kg of Isotretinoin solution). Using the morphometry tool and histochemical techniques we evaluated the villus, intestinal crypts, and goblet cells to find signs of possible alterations of the duodenum, jejunum and ileum segments of the small intestine. We found no signs of changes in the jejunum mucosa after 60 days of treatment with 1Â mg/kg and 10Â mg/kg. The duodenum is also less affected, whereas significant modifications were found in the ileum. The goblet cell frequency was altered, indicating a proliferative potential for the substance. Although some patients have described intestinal symptoms, no important alterations were found with this protocol, reaffirming the security involved in the treatment with this substance.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Tissue and Cell - Volume 49, Issue 2, Part B, April 2017, Pages 203-208
Journal: Tissue and Cell - Volume 49, Issue 2, Part B, April 2017, Pages 203-208
نویسندگان
B.F. Thomazini, M.A.H. Dolder,