# Comparative evaluation of ACRS and PRP on inflammation and lesion activity in a rat model of peritoneal endometriosis

## TL;DR

This study compares two treatments, ACRS and PRP, for reducing inflammation and lesion activity in a rat model of endometriosis.

## Contribution

The novel contribution is a direct comparison of ACRS and PRP effects on inflammation, angiogenesis, and fibrosis in a rat endometriosis model.

## Key findings

- Both ACRS and PRP reduced histopathological scores compared to untreated endometriosis.
- ACRS showed stronger anti-inflammatory effects but increased angiogenesis and fibrosis markers.
- PRP had less pronounced effects on inflammation but did not elevate angiogenesis.

## Abstract

This study aimed to comparatively evaluate the therapeutic effects of Autologous Cytokine-Rich Serum (ACRS) and Platelet-Rich Plasma (PRP) in a rat model of endometriosis, focusing on inflammation, angiogenesis, and myofibroblast activity.

A total of 36 adult female Wistar Albino rats were randomly assigned to six groups: healthy control, ACRS-only, PRP-only, endometriosis (EM), EM + ACRS, and EM + PRP. Endometriosis, modeled as lesion formation on the peritoneal wall, was surgically induced in the relevant groups. ACRS and PRP were prepared from autologous blood and administered intraovarianly and intraperitoneally. Lesions were excised for histopathological and immunohistochemical analysis of TNF-α, IL-6 (inflammation), VEGFA (angiogenesis), and α-SMA (fibrosis).

Histopathological scores decreased in both EM + ACRS and EM + PRP groups compared to the EM group. ACRS showed stronger anti-inflammatory effects, with lower TNF-α and IL-6 expression. However, ACRS-treated tissues also exhibited elevated VEGFA and α-SMA expression, suggesting increased angiogenesis and stromal activity.

Both ACRS and PRP showed therapeutic effects. ACRS more effectively suppressed inflammation but may promote lesion stabilization through enhanced angiogenesis and fibrotic remodeling. These findings highlight the complex biological activity of ACRS, which requires further investigation before clinical translation.