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Abstract Title:

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

Abstract Source:

Environ Sci Pollut Res Int. 2021 Jun 11. Epub 2021 Jun 11. PMID: 34117542

Abstract Author(s):

Ibtesam S Alanazi, Mohamed Emam, Mabrouk Elsabagh, Saad Alkahtani, Mohamed M Abdel-Daim

Article Affiliation:

Ibtesam S Alanazi

Abstract:

This study was aimed at elucidating the protective effects of 18β-glycyrrhetinic acid (18βGA) 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 18βGA orallyafter 2 weeks from STZ injection (18βGA group), 20 mg/kg Acr after 1month from STZ injection (Acr group), STZ plus Acr (STZ-Acr group), STZ plus 18βGA (STZ-18βGA group), Acr plus 18βGA (Acr-18βGA group), or STZ plus Acr plus 18βGA (STZ-Acr-18βGA group). Administration of 18βGA 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-1β, 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 18βGA normalized STZ and Acr-induced elevations in oxidative defense variables in the liverand 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 18βGA to inhibit reactive oxygen species generation and restore the antioxidant defenses in diabetic rats with Acr-induced liver and kidney cytotoxicity.

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