Kallikrein-kinin system (KKS) is involved in vascular reactivity and inflammatory response to cytotoxic drugs. Since cisplatin is a widely used chemotherapy and its cytotoxic mechanism can trigger inflammation and oxidative damage, in this work we evaluated the role of KKS in an animal model of cisplatin-induced ovarian toxicity. Biomarkers of ovarian stem cells, activity of KKS, inflammation and oxidative damage were measured in ovarian tissue of C57BL/6 female mice treated with vehicle or cisplatin (2.5 mg/kg). Cisplatin group presented greater number of atretic follicles, and lower numbers of antral and total viable follicles. Ki67, DDX4 and OCT-4 markers were similar between groups. Cisplatin triggered plasma and ovarian tissue kallikrein generation; and increased expression of bradykinin receptors B1 and B2. Neutrophil and macrophage infiltration markers increased. Superoxide anion generation also increased, while reduced glutathione levels decreased. These results suggest that KKS is activated and contributes to ovarian injury during cisplatin treatment.

激肽释放酶激肽系统（KKS）参与血管反应和对细胞毒性药物的炎症反应。由于顺铂是一种广泛使用的化学疗法，其细胞毒性机制可引发炎症和氧化损伤，因此在这项工作中，我们评估了KKS在顺铂诱导的卵巢毒性动物模型中的作用。在接受媒介物或顺铂（2.5 mg / kg）治疗的C57BL / 6雌性小鼠的卵巢组织中测量了卵巢干细胞的生物标记，KKS活性，炎症和氧化损伤。顺铂组表现出更多的闭锁卵泡，而较少的胃窦和总生存卵泡。组之间的Ki67，DDX4和OCT-4标记相似。顺铂触发血浆和卵巢组织激肽释放酶的产生；和缓激肽受体B1和B2的表达增加。中性粒细胞和巨噬细胞浸润标志物增加。超氧化物阴离子的产生也增加，而减少的谷胱甘肽水平下降。这些结果表明，在顺铂治疗期间，KKS被激活并导致卵巢损伤。