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Gum Arabic modifies tissue heat shock proteins associated with decrease in oxidative stress and 11β-Hydroxysteroid dehydrogenase type I in mice

International Journal of Complementary & Alternative Medicine
Abdelkareem A Ahmed,1,2,3,4 Mohammed Elmujtba Adam Essa,4Hussein Ahmed,5 Adriano Mollica,4,6 Azzurra Stefanucci,4,6Gokhan Zengin4,7

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  1. Heat shock proteins (HSPs) are known to plays crucial roles in cellular cytoprotectant and are essential protein for the cells to boost toleration for pathogenic and environmental adaptation conditions. Gum Arabic (GA, Acacia senegal) works as a dietary fiber that improves antioxidant capacity. Yet, the effects of the GA on HSPs and its association with 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) have not been reported. In the present study, 20 female CD-1 mice of 90days old were randomly divided into two groups (n=10 of each group). Control group and GA group provided GA in the form of drink (10% w/v) for 15weeks. The treatment of GA significantly (P<0.05) reduced food intake and body weight body associated with decreased blood glucose and corticosterone levels. Similarly, the treatment of GA significantly (P<0.01) increased hepatic, muscle and cardiac HSP72 and HSP90 contents associated with increased activities of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) compared control group. In addition, the treatment of GA significantly(P<0.05) decreased tissue MDA correlated with decreases in plasma total cholesterol, LDL-c concentrations whereas, increased HDL-c concentrations compared to the control group. However, the treatment of GA did not affect cardiac and muscle HSP 25 protein contents. The treatment of GA significantly (P<0.05) suppressed hepatic and cardiac 11β-HSD1 mRNA expression compared to control. On the other hand, the treatment of GA significantly (P<0.05) increased hepatic11β-HSD2 mRNA expression compared to control. In conclusion, GA may offer potential for improving the antioxidant defense against tissue damage.


gum arabic, liver, mice, 11?-hydroxysteroid dehydrogenases, heat shock protein