The objective of this work was to analyze the involvement of AhR in bone metabolism using a rat model of experimental osteoporosis and to analyze the mechanisms behind its activity. Rats were assigned randomly to the subsequent groups; Control, received no treatment; ovariectomized (OVX) rats; Sham; Sham+RES received resveratrol; OVX+RES and OVX+CH received AhR’s antagonist, CH223191 (CH); and finally OVX+CHR group received both AhR antagonist along with resveratrol. Resveratrol and AhR antagonist treatment started 7 days after surgery and continued to 45 days. The serum of osteocalcin (OC) and Ca+2 was measured by ELISA and spectrophotometer, respectively. X-ray was used to estimate bone density of rats. In molecular levels, Ahr, Esr1 and Esr2 gene expression were quantified in the Control, OVX, OVX+RES, OVX+CH and OVX+CHR groups. Supplementation of RES and CH223191 significant increased (P<0.05) in serum Ca+2 and bone density in treated groups compared OVX groups while serum OC decreased. The Ahr gene expression was significantly higher in OVX+RES than in OVX+CHR, OVX and Control groups. Esr1 gene was actively expressed than Esr2 gene in the bone metabolism in this study. In conclusion, the administration of phosphoric acid with/without combination with ovariectomy procedure had enhanced the mediation of osteoporosis while administration of resveratrol led to resumption of nearly normal bone metabolism via the overexpression of AhR signaling and reduction of osteocalcin production in estrogen-independent manner.
