Objectives Polycystic ovary syndrome (PCOS) is a common endocrine disorder associated with metabolic dysfunctions, oxidative stress (OXS), and liver abnormalities, including an increased risk of non-alcoholic steatotic liver. Chamomile (CHAM) (Matricaria chamomilla L.) is known for its antioxidant, anti-inflammatory, and hepatoprotective properties. This study investigates the hepatoprotective effects of CHAM extract in a PCOS-induced rat model.
Methods PCOS was induced in female Wistar rats, which were then treated with CHAM extract or metformin (METF) for 12 weeks. Serum levels of liver function markers (ALT, AST, LDH), OXS markers (MDA, GPx, CAT), and sex hormones (testosterone, estrogen) were analyzed. Histopathological and immunohistochemical assessments were performed to evaluate liver architecture and apoptosis markers (Bax and Bcl-2).
Results The induction of PCOS significantly increased serum testosterone and estrogen (p≤0.05), while CHAM administration significantly reduced them (p≤0.001 and p≤0.01, respectively). PCOS induction led to significant liver damage, as evidenced by increased levels of ALT (p<0.001), AST (p<0.01), and LDH (p<0.001), elevated MDA (p<0.001), and reduced activity of both GPx (p<0.01) and CAT (p<0.001). Histological examination revealed central vein dilation, hepatocyte apoptosis, and inflammatory infiltration. CHAM treatment reduced OXS (decreased MDA (p<0.001) and increased the activity of GPx (p<0.05) and CAT (p<0.01)), improved liver function markers, and restored hepatic architecture. Furthermore, CHAM decreased hepatic Bax expression while enhancing Bcl-2 expression, indicating an anti-apoptotic effect.
Conclusion CHAM extract exerts significant hepatoprotective effects in a PCOS model by mitigating OXS and reducing apoptosis. These findings support its potential as an adjunct therapy for managing PCOS-related liver dysfunction.