Recently, PPAR-$γ$ activation has emerged as a potential treatment for alcoholism. However, the adverse effects of synthetic PPAR-$γ$ activators, despite being effective drugs, prompted the need for novel PPAR-$γ$ agonists that retain efficacy and potency with a lower potential of side effects. Hence, naringin, a bioflavonoid isolated from citrus fruits and recently identified as a natural ligand of PPAR-$γ$, has begun to be evaluated for treatment of alcoholism. It is well known to possess several therapeutic benefits in addition to its anti-anxiety and antidepressant properties. In the present study, we assessed whether naringin treatment possesses anti-ethanol reward properties in C57BL/6 mice. We used the two-bottle choice drinking paradigm and ethanol-induced conditioned place preference (CPP) to examine the effect of naringin treatment on ethanol drinking. Results have shown that, compared with vehicle, naringin (10-100mg/kg) significantly and dose-dependently decreased voluntary ethanol intake and preference in a two-bottle choice drinking paradigm [3-15% (v/v) escalating over 2 weeks], with no significant effect observed on saccharin [0.02-0.08% (w/v)] or on quinine [15-60$μ$M (w/v)] intake. In addition, there was no significant difference in blood ethanol concentration (BEC) between groups following naringin administration of 3g of ethanol/kg body weight. Interestingly, when mice were treated with vehicle or naringin (30mg/kg) before injection of ethanol (1.5g/kg) during conditioning days, naringin inhibited the acquisition of ethanol-CPP. More importantly, these effects were significantly attenuated when mice were pre-injected with the peroxisome proliferator-activated receptor-$γ$ (PPAR-$γ$) antagonist, GW9662. Taken together, the present findings are the first to implicate naringin and PPAR-$γ$ receptors in the behavioral and reward-related effects of ethanol and raise the question of whether specific drugs that target PPAR-$γ$ receptors could potentially reduce excessive ethanol consumption and preference.