Evaluation the Protective Effect of Zinc Supplementation on Depression and Mir 129-GPR39 Gene Expression in the Hippocampus of Diabetic Rat

Abstract

Background: MicroRNAs (miRs) has growing evidence in the pathogenesis of diabetic depression. The present study evaluated the oral administration of zinc (Zn) on depression behaviors induced by alterations in the mir-129 and G protein-coupled receptor 35 (GPR35) in the hippocampus of diabetic rats.

Method: Rats were divided into six groups of 10 each. Healthy and diabetic group, healthy and diabetic group received 200 mg of Zn, and healthy and diabetic group received 350 mg of Zn. Animals were made diabetic by an intraperitoneal (i.p.) injection of newly ready Streptozotocin (STZ; 50 mg/kg body weight). After four weeks of oral gavage, the forced swim test (FST) was investigated to assess depression. The expression of the mir-129 and GPR35 gene level in the hippocampus was measured using the real-time PCR method. Data were shown as mean ± SEM and analyzed for comparison using one-way ANOVA in SPSS20 software.

Result: The analysis of behavioral tests demonstrated the improvement of immobility over the course of the test in the diabetic rats, whereas swimming behavior increased in rats received 200 and 350 mg of Zn (P-value˂0.001). GPR35 and mir-129 gene expression dropped significantly in diabetic rats but Zinc supplementation did not restored their expression in them (P-value > 0.05). Expression of GPR35 gene in rats received 350 mg of Zn elevated significantly in compare to diabetic mice (P-value˂0.001).

Conclusion: Our findings revealed that Zn has ability to induce an antidepressant-like effect and ameliorate the rat mobility, suggesting a possible antidepressant action of Zn in diabetic rats.