Chemoprotective effect of baicalin against cyclophosphamide induced ovarian toxicity in mice via inhibition of TGF-β

Abstract

Ovarian toxicity is most common gynecologically related malignancy, arising for most cases owing to the advanced stage of diagnosis. The aim of the current study was to explore the anticancer potential of baicalin against cyclophosphamide (CP) induced ovarian toxicity in mice and explore the possible mechanism. ovarian cancer cells (Hey, SKOv3ip and HO891PM) were treated with different doses of baicalin and examined via flow cytometry and cell proliferation assay. Subcutaneous administration of CP (200 mg/kg) was used to induce the ovary toxicity and mice were received the oral administration of baicalin. Oxidative, pro-inflammatory, inflammatory, apoptosis parameters, progesterone, estrogen hormones and histopathological were also estimated at end of the study. Baicalin increased the apoptosis and caused the cell cycle arrest at the G2/M stage in ovarian cancer cells. Baicalin significantly (P < 0.001) reduced the level of TGF-β in the HO8910PM, SKOv3ip and Hey cell lines. Baicalin significantly (P < 0.001) increased the body weight and reduced the tumor volume in mice. Baicalin significantly (P < 0.001) increased the level of estrogen and progesterone. Baicalin significantly (P < 0.001) reduced the level of malonaldehyde (MDA) and increased the level of superoxide dismutase (SOD) and catalase (CAT). Baicalin significantly (P < 0.001) decreased the level of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and inflammatory parameter such as nuclear kappa B factor (NF-κB), respectively. Baicalin significantly (P < 0.001) reduced the level of the caspase-3. Baicalin, act as the potential agent against the ovarian toxicity by alteration of TGF-β and inflammatory pathways.