Inhibitory effect of MIL glycoprotein on expression of pro-inflammatory mediators in carbon tetrachloride-induced mice liver damage

التفاصيل البيبلوغرافية
العنوان: Inhibitory effect of MIL glycoprotein on expression of pro-inflammatory mediators in carbon tetrachloride-induced mice liver damage
المؤلفون: Phil-Sun Oh, Kye-Taek Lim, Jin Lee
المصدر: Journal of Applied Toxicology. 30:754-760
بيانات النشر: Wiley, 2010.
سنة النشر: 2010
مصطلحات موضوعية: Male, Interleukin-1beta, Drug Evaluation, Preclinical, CCL4, Pharmacology, Biology, Toxicology, medicine.disease_cause, Thiobarbituric Acid Reactive Substances, Mice, chemistry.chemical_compound, Lactate dehydrogenase, TBARS, medicine, Animals, Carbon Tetrachloride, Glycoproteins, Plant Proteins, Liver injury, chemistry.chemical_classification, Mice, Inbred ICR, Carbon Tetrachloride Poisoning, Tumor Necrosis Factor-alpha, Interleukin, Alanine Transaminase, medicine.disease, Oxidative Stress, Liver, chemistry, Biochemistry, Cyclooxygenase 2, Tumor necrosis factor alpha, Morus, Chemical and Drug Induced Liver Injury, Inflammation Mediators, Glycoprotein, Oxidative stress
الوصف: The aim of the present study was to evaluate immunomodulatory and hepatoprotective effects of glycoprotein isolated from Morus indica Linne (MIL glycoprotein) on carbon tetrachloride (CCl4)-induced liver injury. In the present study, MIL glycoprotein (5 and 10 mg kg−1 body weight) was administered to ICR mice for 7 days prior to CCl4 treatment. We evaluated the activities of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and thiobarbituric acid-reactive substances (TBARS), and expression of inflammation-related mediators including cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-α, and interleukin (IL)-1β in CCl4-treated mice. Our results revealed that MIL glycoprotein reduced the activities of ALT, LDH and TBARS in serum from CCl4-treated mice. We also found that MIL glycoprotein reduced the activity of COX-2 and expression of TNF-α and IL-1β in liver from CCl4-treated mice. Moreover, administration of MIL glycoprotein suppressed on stress-activated protein kinase/c-jun N-terminal kinase phosphorylation and activator protein-1 transcriptional activation in livers from CCl4-treated mice. The results from these experiments indicate that MIL glycoprotein effectively protects against liver injury, mainly through downregulation of oxidative stress and the inflammatory response. In conclusion, we suggest that the MIL glycoprotein might be one component of health supplements for prevention of liver diseases. Copyright © 2010 John Wiley & Sons, Ltd.
تدمد: 0260-437X
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f4cdecf128e4024a665d77d8f90e15f7Test
https://doi.org/10.1002/jat.1557Test
حقوق: CLOSED
رقم الانضمام: edsair.doi.dedup.....f4cdecf128e4024a665d77d8f90e15f7
قاعدة البيانات: OpenAIRE