Showing 2 results for Anti-Inflammatory
Fatemeh Nohtani, Morteza Behnam Rasouli, Sajad Sahab Negah, Masumeh Kheirabadi,
Volume 24, Issue 2 (6-2024)
Abstract
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.
Parisa Saberi-Hasanabadi,
Volume 24, Issue 5 (12-2024)
Abstract
Background: Despite advances in diabetes-related treatments, the effects of the disease have not yet been adequately reversed or prevented in patients. Therefore, there is an urgent need to develop more effective medication-assisted treatments in this field.
Methods: In this study, type 1 diabetes mice models was established using multiple low-dose alloxan, and the diabetic mice were treated with three doses of dimethyl fumarate (DMF) i.e low, medium, and high viz. 20, 40 and 80 mg/kg, respectively for a period of 21 days. Then, specific test were done to evaluate blood biochemical parameters, oxidative stress markers, inflammatory genes expression, and histopathological changes in the mice kidney and liver.
Results: The obtained results showed remarkably improved anti-diabetic, hepato-renal-protective, and oxidative stress indexes of DMF in alloxan-induced diabetic mice (P< 0.001). Treated mice with DMF demonstrated a noteworthy decrease in blood glucose levels when compared with diabetic group (P< 0.001). Diabetic liver and kidney tissues showed marked dilation of bile ducts, tubules, infiltration, and inflammation. On the contrary, the histological features of the treated mice with DMF improve as shown by normal size of glomerular capillaries along with decrease in less dilatation of ducts in comparison with diabetic mice. The real-time quantitative PCR results indicated that DMF injection decreased the alloxan-induced increase of significant elevations in mRNA levels of pro-inflammatory cytokines levels in both kidney and liver tissues. Meanwhile, mice treated with DMF showed an increase in Sirt1 and Nrf2 expression in comparison to diabetic group.
Conclusion: In conclusion, it can be concluded that DMF treatment provides hepato-renal protective effects on alloxan-induced diabetic mice model by attenuating ROS inflammatory pathways.
