促性腺激素释放激素激动剂对辐射所致大鼠卵巢功能损伤的防护作用研究

Protective effect of gonadotropin-releasing hormone agonist on ovarian functional impairment caused by radiation in rats

    摘要
  • 摘要:
    目的探讨促性腺激素释放激素激动剂（GnRHa）对盆腔放疗辐射所致大鼠卵巢功能损伤的保护作用及可能机制。
    方法实验1：雌性Fischer 344大鼠5只，于动情间期皮下给予GnRHa 0.25 mg后，动态观察其血清卵泡刺激素（FSH）、雌二醇（E2）及抗苗勒管激素（AMH）水平变化情况。实验2：雌性大鼠40只，以随机数字表法分为对照组、GnRHa组、放疗组（R组）及GnRHa+R组并给予相应处理，盆腔照射后20 d，采用单因素方差分析及独立样本t检验比较各组间的体重、卵巢湿重、血清FSH、E2、AMH水平及卵泡数量的差异。对比各组大鼠卵巢凋亡指数和微血管密度。
    结果实验1：皮下给予GnRHa后，大鼠卵巢功能受到抑制，FSH、E2水平持续下降，15 d左右达到谷值，再过20 d后恢复至给药前水平。实验2：盆腔放疗后，GnRHa+R组、R组与对照组相比均出现不同程度的卵巢功能损伤，但GnRHa+R组与R组相比受损程度较轻，表现为E2水平偏高（t=12.79，P < 0.01），FSH水平偏低（t=4.65，P < 0.01），AMH水平偏高（t=5.65，P < 0.01）；卵泡计数显示，GnRHa+R组的原始及初级卵泡数显著高于R组（t=7.70，P < 0.01）；Tunnel和CD31染色结果显示R组卵巢内细胞凋亡指数和微血管密度显著高于GnRHa+R组（t=8.20和9.83，均P < 0.05）。
    结论放疗前应用GnRHa能够有效减轻放疗辐射对大鼠卵巢功能的损伤，这可能与GnRHa将卵泡发育抑制在原始、初级卵泡阶段以及减少卵巢组织血供及氧合进而降低卵巢放射敏感性有关。

     

    Abstract:
    Objective To investigate the protective effect of gonadotropin-releasing hormone agonist (GnRHa) on ovarian function in rats during pelvic irradiation and its possible mechanism.
    Methods 1. Five female Fischer-344 rats were subcutaneously injected with 0.25 mg of GnRHa. Changes in serum follicle -stimulating hormone(FSH), estradiol(E2), and anti -mullerian hormone(AMH) levels were observed continually. 2. Forty female rats were randomly divided into four groups(Control, GnRHa, R, and GnRHa+ R) and given their corresponding treatments. At 20 days after pelvic irradiation, the weight; ovarian wet weight; serum FSH, E2, and AMH levels; and follicular numbers of the four groups were compared using one-way ANOVA and independent-sample t-test. The apoptotic index and microvessel density(MVD) in the ovarian tissue of each group were also compared.
    Results 1. Treatment with GnRHa inhibited ovarian function. Under this treatment, serum FSH and E2 declined, reached the minimum values in approximately 15 days, and then normalized in approximately 20 days. 2. After pelvic radiotherapy, the GnRHa+R and R groups showed different degrees of ovarian function damage compared with the control group, but the damage to the GnRHa +R group was less severe compared with that to the other groups. The GnRHa +R group showed higher E2(t=12.79, P < 0.01), lower FSH(t=4.65, P < 0.01), and relatively higher AMH (t=5.65, P < 0.01) compared with the R group. Follicular classification revealed significantly more primordial and primary follicles in the GnRHa+R group than in the R group(t=7.70, P < 0.01). Tunnel and CD31 staining showed that the apoptotic index and MVD were significantly higher in the R group than in the GnRHa+R group(t=8.20 and 9.83, both P < 0.05).
    Conclusions Administration of GnRHa before radiotherapy can significantly decrease radiation damage to ovarian function in rats. GnRHa exerts its protective effect against ovarian functional impairment by inhibiting follicular development in primordial and primary follicles. It decreases the blood supply and oxygen of ovarian tissue, thereby reducing the radiation sensitivity of the ovary.

     

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