Volume 24, Issue 2 (6-2024)
ijdld 2024, 24(2): 114-123 |
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Nohtani F, Behnam Rasouli M, Sahab Negah S, Kheirabadi M. Investigating the Expression of IL-6, IL-1β and TNF-Α Pro-Inflammatory Cytokines Genes in the Sciatic Nerve Tissue of Hyperglycemic Rats after the Administration of Metformin and Gallic Acid. ijdld 2024; 24 (2) :114-123
URL: http://ijdld.tums.ac.ir/article-1-6288-en.html
URL: http://ijdld.tums.ac.ir/article-1-6288-en.html
1- Biology Department, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
2- Biology Department, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran ,behnam@um.ac.ir
3- Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
2- Biology Department, Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran ,
3- Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Abstract: (484 Views)
Background: Under hyperglycemic conditions, inflammatory processes with damage to the peripheral nerves are involved in the occurrence of neuropathy. This study aimed to compare the anti-inflammatory effects of metformin (synthetic drug) with gallic acid (natural compound) in hyperglycemic conditions.
Methods: Hyperglycemia was induced in male rats by the intraperitoneal injection of Streptozotocin (STZ) at a dose of 60 mg/Kg. For this research, rats were divided into four groups. Two groups were healthy control and hyperglycemic control rats that did not receive any drugs. The other two groups were hyperglycemic rats, which respectively received Metformin at a dose of 300 mg/kg/day and gallic acid at a dose of 40 mg/kg/day. At the end of the 8-week period, the rats in all groups were anesthetized and a sample of their sciatic nerve was taken to measure the expression level of genes related to pro-inflammatory cytokines IL-6, IL-1β and TNF-α. Data analysis was done by SPSS software and comparison between average data was done by one-way ANOVA and Tukey's post hoc test.
Results: Induction of hyperglycemic conditions in rats increased the expression of genes related to pro-inflammatory cytokines IL-6 (p=0/000), IL-1β (p=0/008) and TNF-α (p=0/005). However, administration of metformin and gallic acid to hyperglycemic rats for 8 weeks reduced the expression of IL-6, IL-1β and TNF-α genes (p˂0.05).
Conclusion: Gallic acid, like metformin, with its anti-inflammatory properties, can be effective in improving complications caused by hyperglycemic conditions, especially neuroinflammation, and it is hoped that it will be clinically useful for diabetic patients in the future.
Methods: Hyperglycemia was induced in male rats by the intraperitoneal injection of Streptozotocin (STZ) at a dose of 60 mg/Kg. For this research, rats were divided into four groups. Two groups were healthy control and hyperglycemic control rats that did not receive any drugs. The other two groups were hyperglycemic rats, which respectively received Metformin at a dose of 300 mg/kg/day and gallic acid at a dose of 40 mg/kg/day. At the end of the 8-week period, the rats in all groups were anesthetized and a sample of their sciatic nerve was taken to measure the expression level of genes related to pro-inflammatory cytokines IL-6, IL-1β and TNF-α. Data analysis was done by SPSS software and comparison between average data was done by one-way ANOVA and Tukey's post hoc test.
Results: Induction of hyperglycemic conditions in rats increased the expression of genes related to pro-inflammatory cytokines IL-6 (p=0/000), IL-1β (p=0/008) and TNF-α (p=0/005). However, administration of metformin and gallic acid to hyperglycemic rats for 8 weeks reduced the expression of IL-6, IL-1β and TNF-α genes (p˂0.05).
Conclusion: Gallic acid, like metformin, with its anti-inflammatory properties, can be effective in improving complications caused by hyperglycemic conditions, especially neuroinflammation, and it is hoped that it will be clinically useful for diabetic patients in the future.
Type of Study: Research |
Subject:
Special
Received: 2023/08/29 | Accepted: 2024/01/30 | Published: 2024/06/30
Received: 2023/08/29 | Accepted: 2024/01/30 | Published: 2024/06/30
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