The protective effects of 18ß-glycyrrhetinic acid against acrylamide-induced cellular damage in diabetic rats.

This study was aimed at elucidating the protective effects of 18ß-glycyrrhetinic acid (18ßGA) against acrylamide (Acr)-induced cellular damage in diabetic rats. Rats were randomly assigned into eight groups (n = 8) following 12 h of fasting: control group, a single dose of 50 mg/kg streptozotocin (STZ) intraperitoneally (diabetic group), 50 mg/kg 18ßGA orally after 2 weeks from STZ injection (18ßGA group), 20 mg/kg Acr after 1month from STZ injection (Acr group), STZ plus Acr (STZ-Acr group), STZ plus 18ßGA (STZ-18ßGA group), Acr plus 18ßGA (Acr-18ßGA group), or STZ plus Acr plus 18ßGA (STZ-Acr-18ßGA group). Administration of 18ßGA alone increased GSH, GSH-PX, SOD, and CAT in both liver and kidneys. While STZ injection was associated with diabetic and oxidative stress changes as indicated by the higher serum glucose, cholesterol, creatinine, IL-1ß, IL-6, TNF-α, and antioxidant enzyme activities, together with increased lipid peroxides and decreased antioxidant biomarkers in the liver and kidneys. Similarly, the co-administration of STZ and Acr was associated with similar, more augmented effects, compared to STZ alone. The administration of 18ßGA normalized STZ and Acr-induced elevations in oxidative defense variables in the liver and kidney tissues and blood biomarkers. Thus, our study demonstrated that the damaging effects of Acr were more exaggerated in diabetic rats. Furthermore, it showed the ability of 18ßGA to inhibit reactive oxygen species generation and restore the antioxidant defenses in diabetic rats with Acr-induced liver and kidney cytotoxicity.