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Circulating Levels of Pro-inflammatory Cytokines in Patients with Nonalcoholic Fatty Liver Disease and Non-Alcoholic Steatohepatitis | ||
Iranian Journal of Immunology | ||
مقاله 7، دوره 16، شماره 4، اسفند 2019، صفحه 327-333 اصل مقاله (210.37 K) | ||
نوع مقاله: Short Paper | ||
شناسه دیجیتال (DOI): 10.22034/iji.2019.80284 | ||
نویسندگان | ||
Abolghasem Hadinia1؛ Amir Hossein Doustimotlagh* 2، 3؛ Hamed Reza Goodarzi1؛ Arash Arya4؛ Mojtaba Jafarinia1 | ||
1Department of Genetic, Marvdasht branch, Islamic Azad University, Marvdasht, Iran | ||
2Cellular and Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran | ||
3Department of Clinical Biochemistry, Faculty of Medicine, Yasuj University of Medical Sciences, Yasuj, Iran | ||
4Internal Medicine, Yasuj University of Medical Sciences, Yasuj, Iran | ||
چکیده | ||
Background: Pro-inflammatory cytokines are associated with systemic inflammatory responses. Objective: To investigate the levels of pro-inflammatory cytokines (IL-1b, IL-6, and TNF-a) in patients with non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis (NASH) compared to healthy individuals. Methods: This case-control study was conducted on 30 patients with NAFL, 30 patients with NASH, and 30 healthy volunteers. The plasma level of IL-1b, IL-6, and TNF-a were determined by ELISA, and biochemical parameters were measured using colorimetric methods. Results: IL-1b and IL-6 levels were significantly higher in patients with NASH compared with NAFL and control group. However, TNF-a levels had no significant variations in NAFL and NASH patients compared to the control group (p=0.903 and p=0.960, respectively). Conclusion: Results showed that the levels of ALT activity and pro-inflammatory cytokines were higher in patients with NASH compared to control and NAFL subjects; Therefore, steatosis and inflammation develop as a result of excessive pro-inflammatory factors in NASH. | ||
کلیدواژهها | ||
Interleukin-1β؛ Interleukin-6؛ Non-Alcoholic Fatty Liver؛ Non-Alcoholic Steatohepatitis؛ Tumor Necrosis Factor-α | ||
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