Vitamin E protects against the modulation of TNF-α-AMPK axis and inhibits pancreas injury in a rat model of L-arginine-induced acute necrotising pancreatitis

Abstract

Background

Acute pancreatitis (AP) associated with the modulation of TNF-α-AMPK axis in the presence and absence of vitamin E has not been investigated before.

Material and methods

Rats were either injected with L-arginine (2.5 gm/kg) before being sacrificed after 48 h or were pre-treated with vitamin E (60 mg/kg) and continued receiving vitamin E until the end of the experiment.

Results

AP was developed as demonstrated by infiltration of inflammatory cells and profound pancreas tissue damage, which were substantially protected by vitamin E. In addition, L-arginine injections significantly (p < .0001) increased the expression of TNF-α mRNA and protein, and decreased phospho-AMPK and IL-10 mRNA and protein that was significantly (p < .0001) protected by vitamin E. Furthermore, vitamin E inhibited L-arginine-induced blood levels of LDH, amylase, and myeloperoxidase.

Conclusions

L-arginine-induced acute pancreatitis modulates TNF-α-AMPK axis, IL-10 and other AP biomarkers, which is protected by vitamin E; thus, may offer therapeutic potential in humans.

Keywords:

• Acute pancreatitis
• L-arginine
• vitamin E
• AMPK
• TNF-α
• rat model

Acknowledgements

The authors would like to thank Dr. Mariam Al-Ani from Dental Care Partnership, Sutton Coldfield, Birmingham, UK for proofreading the manuscript.

Disclosure statement

The authors declare that there are no conflicts of interest.

Data availability statement

The data that support the findings of this study are available on request from the corresponding author, [MH]. The data are not publicly available because the data generated by this grant project is not only limited to the information provided by this manuscript. However, as we stated above, we are willing to share with others upon request.

Additional information

Funding

The authors extend their appreciation to the Deanship of Scientific Research at King Khalid University for funding this work through Research Group Project under grant number [R.G.P.1/219/41].