<p>Asherman syndrome (AS) is a gynecological abnormality that causes complications such as infertility, menstrual abnormalities, and recurrent miscarriages in women. In this study, we aimed to investigate the effects of caffeic acid phenethyl ester (CAPE) administration on intrauterine adhesions, uterine morphology, fibrosis, and inflammation in a rat trichloroacetic acid (TCA)-induced AS model. Thirty-two Wistar albino adult female rats were used in this study, and all rats were divided into four groups (<i>n</i> = 8): control, AS, AS + CAPE, and CAPE. AS model was created by intrauterine TCA administration. Uterus tissues were examined by hematoxylin eosin (H&amp;E) and Masson’s trichrome staining methods. Nuclear factor-kappa beta (NF-κB) and tumor necrosis factor-alpha (TNF-α) immunoreactivity in the uterine endometrium, serum TNF-α, interleukin-6 (IL-6), and interleukin-6 (IL-10) levels were determined. We found that the uterine gland count, the endometrial fibrosis, and the endometrial thickness were significantly different between AS group and control groups. In addition, uterine NF-κB and TNF-α immunoreactivity and serum IL-6 and TNF-α levels were significantly increased in the AS group compared to the control group, while IL-10 level was diminished in AS group. CAPE treatment not only supported the preservation of uterine morphology and regeneration but also significantly reduced NF-κB, TNF-α, and IL-6 expressions and increased IL-10 levels. CAPE promotes uterine morphology and regeneration by regulating the NF-κB signaling and the production of proinflammatory cytokines, which play key roles in AS’s pathogenesis.</p>