Boric acid is associated with the suppression of apoptosis and endoplasmic reticulum stress in rat model of paracetamol -induced hepatotoxicity

Abstract

Paracetamol (also known as acetaminophen or APAP) is an analgesic and antipyretic drug that is widely used all over the world. Boron is an element proven by many studies that it has indispensable effects on human health. In light of the information expressed about boron, we investigated whether there are any effects of boron on paracetamol-induced liver damage. We analyzed the 8-hydroxyguanosine (8-OHG), ALT, AST, glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and nitric oxide (NO) levels in serum or erythrocyte and liver tissue. At the same time, TNF-α, IL-1β, IL-18 levels were examined in liver tissues to determine the effect of boron on inflammation caused by paracetamol in serum and liver tissue. In this study to determine the effect of ER stress-mediated apoptosis, signal transducers that lead the cell to ER stress-mediated apoptosis, IRE1, ATF6 and PERK, caspase 1, 3, 8, 9 and 12, which play a role in the apoptotic process, antiapoptotic factors bcl2, bcl-xL mRNA gene expressions were determined and the effect level of boron on ER stress-mediated apoptosis was determined by immunohistochemical methods. This study demonstrate that boric acid protects against paracetamol-induced liver damage in association with the augmentation of biomarkers of oxidative and nitrosative stress, inflammation and the ER stress / apoptosis axis in rats.

Keywords

• Paracetamol
• boron
• rat
• oxidative stress
• apoptosis
• inflammation