Endometriosis (END) is a chronic inflammatory disorder marked by the existence of endometrial-like tissue in the abnormal sites, resulting in immunological and inflammatory dysregulation. This study was to examine the impact of resveratrol and the AhR antagonist, CH223191, on the modulation of inflammatory and immunological responses in an experimental rat model of endometriosis. Adult female rats and adult male rats were employed in the current study. The female rats were randomly divided into the following: Naïve rats, donor rats for endometrial tissue transplantation, recipient endometriotic rats, and fertile male rats utilized for fertility tests. All endometriotic rats were equally divided into four groups, as follows: END group: Rats in this group served as positive controls and received no treatments; END+RES group: Endometriotic rats received a daily oral dose of resveratrol for four weeks; END+AhR‾ group: Endometriotic rats received intraperitoneal injections of CH223191 every three days for four weeks; END+DMSO group: Endometriotic rats were given dimethyl sulfoxide (DMSO), which was utilized in the preparation of resveratrol and AhR‾ treatments intraperitoneally every three days for four weeks, while Naïve rats served as the negative control group. At the endpoint of the experiments, three female rats from each group were mated with two pre-examined fertile male rats for fertility tests. Additionally, nine female rats from each group were euthanized to collect blood for biochemical assessments, peritoneal exudates (PE) for further analysis, spleens for Tgfβ gene expression, and uterine horns for histopathological examination. Statistical analysis of collected data revealed a significant (P<0.05) reduction in the litter size in all endometriotic rats, except END+RES, in comparison with the control group. Endometriosis in END and END+DMSO rats led to significant (P<0.05) upregulation of Tgfβ gene expression in splenocytes; these conditions significantly (P<0.05) increased TGF-β levels in the circulatory system and PE of these groups. Cancer antigen (CA-125) levels in circulation and PE significantly (P<0.05) increased in all endometriotic rats in comparison with the control, except those that were treated with RES did not show statistical change from controls. Upregulated biomarkers TGF-β and CA-125 resulted in deleterious changes in the uterine histological features. In conclusion, this study found that RES could have protective influences in endometriosis pathophysiology via its canonical pathway to suppress inflammatory responses.