The impact of ellagic acid on some apoptotic gene expressions: a new perspective for the regulation of pancreatic Nrf-2/NF-κB and Akt/VEGF signaling in CCl₄-induced pancreas damage in rats

Abstract

Objective

The aim of this study was to evaluate the potential effect of ellagic acid (EA) in the treatment of pancreatic injury. EA has been found to have strong anti-inflammatory, antioxidative, and anticancer properties. The effects of EA on pancreati˜c star cell (PSC) activation and cell functions have been evaluated and it has been shown that it inhibits the activation of basic cell functions and PSCs and^. it has antidiabetic activity through its effect on β-pancreas cells.

Materials and methods

In this work, 36 Wistar albino rats (n = 36, 8 weeks old) were used. Rats were divided to 4 groups and 9 rats were each group. Groups: Group 1: control group; Group 2: EA group; Group 3: carbon tetrachloride (CCl₄) group; Group 4: EA + CCl₄ group. Animals were decapitated after 8 weeks and their pancreas tissue samples were taken and researched. In pancreas tissue, NF-κB, TNF-α, Nrf-2, VEGF, Bcl-2, caspase-3, and Akt proteins expression ratios were analyzed by western blotting method, CAT activity and GSH levels were determined by spectrophotometer and ROS production was detected by MDA.

Results

In our results, the Nrf-2 and caspase-3 protein expressions, catalase activities and GSH levels increased, TNF-α, NF-κB, Bcl-2, VEGF, and Akt protein expressions and MDA levels reduced in EA + CCl₄ group comparable to the CCl₄ group.

Conclusions

These findings reveal that EA decreases pancreas tissue injury in rats and that EA may also be used as a drug against pancreas tissue injury in the future.

Keywords:

• Protein kinase B
• B-cell lymphoma 2
• ellagic acid
• nuclear factor kappa B
• pancreas damage

Acknowledgments

Some parts results of this manuscript submitted as orally at the 8th International Molecular Biology and Biotechnology Congress (17–20 December 2019), Afyonkarahisar, Turkey.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by Firat University Research Projects Unit (FUBAP) [Grant No. FF.16.42].