饱和氢盐水对化疗致卵巢损伤的保护作用

目的:研究饱和氢盐水对环磷酰胺(CTX)所致大鼠卵巢损伤的影响。方法:将54只雌性SD大鼠随机分为3组:A组为正常对照组,B组为CTX组,C组为CTX+饱和氢盐水组。腹腔注射CTX复制化疗所致卵巢损伤模型,首日负荷量为50 mg/kg,后以每日8 mg/kg的维持量持续14 d。饱和氢盐水处理为首次给予CTX开始每日早晚8点2次腹腔注射饱和氢盐水10 ml/kg,持续14 d。于停药后第1日(即15 d)、第16日(即30 d)和第31日(即45 d)分批处死大鼠,留取卵巢固定,HE染色观察卵巢病理;外周血离心取血清,检测卵泡刺激素(FSH)、雌二醇(E2)、超氧化物岐化酶(SOD)、过氧化氢酶(CAT)、丙二醛(MDA)的变化情况。结果:血清FSH和E2的检测结果显示:B组动物血清FSH表达高于A组,E2低于A组,差异有统计学意义(P<0.05);而C组动物血清FSH显著低于B组、E2高于B组(P<0.05)。病理切片显示:B组动物卵巢内卵泡丢失、闭锁,卵巢间质严重损害,可见血管壁增厚,呈玻璃样变,局部可见纤维化;C组可见卵巢皮质、髓质结构清晰,各级卵泡丰富。血清SOD、CAT和MDA的检测结果显示:与A组相比,B组动物血清SOD、CAT水平降低,MDA升高(P<0.05);而与B组相比,C组动物血清SOD和CAT含量增加,MDA降低(P<0.05)。结论:饱和氢盐水可有效防止化疗药物诱发的卵巢损伤,可能与调节体内氧化与抗氧化平衡有关。

Protective Effects of Hydrogen Rich Saline against Chemotherapy-induced Ovarian Damage in Rats

Objective: To investigate the protective effects of hydrogen rich saline against cyclophosphamide(CTX)-induced ovarian damage in rats.Methods: Fifty-four female rats were randomized into 3 groups.Rats in normal group(group A) received nothing.Rats in control group(group B) and treatment group(group C) were intraperitoneally injected with CTX(50 mg/kg for the first day and 8 mg/kg per day for the next 14 d).The group C animals were intraperitoneally injected of hydrogen rich saline(10 ml/kg each time,bid at 8∶00 am and 8∶00 pm).After the last injection,the animals were executed in batches on the day 15,day 30 and day 45.The pathology of ovaries was observed by hematoxylin-eosin staining.The levels of follicle-stimulating hormone(FSH),estradiol(E2),superoxide dismutase(SOD),catalase(CAT) and malondialdehyde(MDA) in serum were detected.Results: Compared with group B,the serum levels of FSH and MDA reduced significantly in group C(P<0.05),while the levels of E2,CAT and SOD increased significantly(P<0.05).The pathological sections showed that massive primordial follicles loss,evident stromal ovarian damages,blood vessels hyalinization and focal fibrosis occurred in group B,which improved significantly in group C.Conclusion: Hydrogen rich saline may have protective effects against chemotherapy-induced ovarian damage via regulating oxidant-antioxidant system.