Autor: |
Obafemi, Tajudeen Olabisi, Alfa, Joy Achenyo, Obafemi, Blessing Ariyo, Jaiyesimi, Kikelomo Folake, Olasehinde, Oluwaseun Ruth, Adewale, Olusola Bolaji, Akintayo, Christopher O., Adu, Isaac Adekola |
Předmět: |
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Zdroj: |
Comparative Clinical Pathology; Feb2024, Vol. 33 Issue 1, p115-125, 11p |
Abstrakt: |
Oxidative stress, endoplasmic reticulum stress, and inflammation are implicated in both pathogenesis and progression of type 2 diabetes. This study aimed to compare the effects of metformin and gliclazide on endoplasmic reticulum stress, oxidative stress, and inflammation in the liver and pancreas of type 2 diabetic rats. Twenty Wistar rats (180–200 g) were arbitrarily allocated to four groups containing five animals each. Group 1 was the normal control and was administered the vehicle (distilled water) while the study lasted. Groups 2 and 3 contained diabetic rats and were treated with metformin (100 mg/kg) and gliclazide (50 mg/kg), respectively, through oral gavage. Group 4 was the diabetic control and contained diabetic animals administered distilled water throughout the study. Experimental animals were made diabetic by a single intraperitoneal injection of 40 mg/kg streptozotocin subsequent to the administration of 10% fructose for 2 weeks. Treatment lasted for 28 days, after which experimental animals were sacrificed. The liver and pancreas were rapidly excised and stored at −20 °C until used. Polymerase chain reaction was used to evaluate the expression of activating transcription factor-6 (ATF6), C/EBP homologous protein (CHOP), nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) in the tissues. Results showed that both metformin and gliclazide substantially ameliorated stress as indicated by reduced expression of ATF6, CHOP, Nrf2 and NF-κB in the selected tissues. There was no clear-cut difference in the stress-ameliorating effects of metformin and gliclazide. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
Externí odkaz: |
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