Cannabidiol mitigates secondary genital injury after thoracic trauma by regulating systemic inflammation and hormone receptor signaling.

Abstract

Blunt thoracic trauma-induced pulmonary contusion is a major cause of acute lung injury and triggers a systemic inflammatory response characterized by cytokine release, oxidative stress, and apoptosis. These systemic effects may disrupt vascular homeostasis and contribute to secondary injury in distant organs, particularly within the female reproductive system, which is dependent on vascular and hormonal balance. This study evaluated the effects of cannabidiol (CBD), a non-psychotropic phytocannabinoid with anti-inflammatory, antioxidant, and anti-apoptotic properties, on secondary reproductive organ injury following blunt thoracic trauma. Forty adult female Wistar albino rats were assigned to Sham, Trauma, Trauma + CBD, and CBD groups. Pulmonary contusion was induced using a standardized weight-drop model (200 g from 1 m), and CBD (5 mg/kg, i.p.) was administered 30 min before trauma. Forty-eight hours later, lung, ovary, uterus, and fallopian tube tissues were collected for histopathological and immunohistochemical analyses. Trauma induced pulmonary injury accompanied by degenerative changes in reproductive tissues, including reduced estrogen receptor (ER) expression and increased hypoxia-inducible factor-1α (HIF-1α) and oxytocin receptor (OTR) expressions. CBD treatment attenuated pulmonary and reproductive tissue injury, preserved ER immunoreactivity, and reduced HIF-1α and OTR expression. These findings indicate that CBD mitigates secondary reproductive organ injury after thoracic trauma by modulating systemic inflammatory responses and regulating receptor expression, suggesting its potential role as a cytoprotective agent in trauma-related multi-organ injury.