人参皂苷 Rg1 通过下调 p16INK4a 和上调 SIRT1 表达来减轻 D-半乳糖诱导的 POF 小鼠的卵巢早衰。
Ginsenoside Rg1 Attenuates Premature Ovarian Failure of D-gal Induced POF Mice Through Downregulating p16INK4a and Upregulating SIRT1 Expression.
机构信息
Department of Histology and Embryology, Dali University, Dali 671000, China.
Department of Child and Adolescent Healthcare, The Children\'s Hospital of Sochoow University, Suzhou, Jiangsu, 215021, China.
出版信息
Endocr Metab Immune Disord Drug Targets. 2022;22(3):318-327. doi: 10.2174/1871523020666210830164152.
BACKGROUND
Premature ovarian failure (POF) refers to pathological amenorrhea before 40 years.
OBJECTIVE
To explore the regulatory effect of Rg1 on POF and clarify associated mechanisms.
MATERIALS AND METHODS
POF mice were induced by injecting with D-galactose (D-gal, 200 mg/kg/- day). Mice were divided into phosphate buffered saline (PBS), D-gal (POF mice), D-gal/Rg1 group (POF mice administrating D-gal/Rg1). Weight growth rate and ovarian weight coefficient were measured. Serum estradiol (E2), follicle stimulating hormone (FSH), luteinizing hormone (LH), superoxide dismutase (SOD), catalase (CAT) levels were examined using ELISA. The status of follicle and corpus luteum was determined using hematoxylin-eosin (HE) staining. P16INK4a and silent- mating type information regulation-2 homolog-1 (SIRT1) were determined using western blotting and RT-PCR.
RESULTS
Weight growth rate and ovarian weight coefficient of mice in D-gal group were significantly decreased than PBS group (p<0.05). Serum E2, LH, SOD, CAT levels were significantly decreased, FSH levels were remarkably increased in D-gal group than PBS group (p<0.05). Rg1 (D-- gal/Rg1 group) significantly increased weight growth rate and ovarian weight coefficient, enhanced E2, LH, SOD, CAT levels and decreased FSH levels than D-gal group (p<0.05). HE staining demonstrated normal follicle morphology/structure of mice in PBS group and decreased the number of follicles, obvious vacuolation of corpus luteum and increased atretic follicles of mice in D-gal group. Compared with D-gal group, the number of follicles was increased, luteal follicles were decreased in mice in D-gal/Rg1 group (p<0.05). Rg1 significantly (D-gal/Rg1) downregulated p16INK4a and upregulated SIRT1 expression in ovarian tissues of mice compared to the D-gal group (p<0.05).
CONCLUSION
Rg1 could delay premature ovarian failure in D-gal induced POF mouse model through downregulating p16INK4a and upregulating SIRT1 expression.
背景
卵巢早衰（POF）是指 40 岁之前出现的病理性闭经。
目的
探讨 RG1 对 POF 的调控作用，并阐明相关机制。
材料和方法
采用 D-半乳糖（D-gal，200mg/kg/-天）注射诱导 POF 小鼠模型。将小鼠分为磷酸盐缓冲液（PBS）组、D-gal（POF 小鼠）组、D-gal/Rg1 组（POF 小鼠给予 D-gal/Rg1）。测量体重增长率和卵巢重量系数。采用酶联免疫吸附试验（ELISA）检测血清雌二醇（E2）、卵泡刺激素（FSH）、黄体生成素（LH）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）水平。采用苏木精-伊红（HE）染色法观察卵泡和黄体的状态。采用 Western blot 和 RT-PCR 检测 P16INK4a 和沉默交配型信息调节 2 同源物-1（SIRT1）。
结果
D-gal 组小鼠的体重增长率和卵巢重量系数明显低于 PBS 组（p<0.05）。D-gal 组血清 E2、LH、SOD、CAT 水平明显降低，FSH 水平显著升高（p<0.05）。与 D-gal 组相比，D-gal/Rg1 组体重增长率和卵巢重量系数明显增加，E2、LH、SOD、CAT 水平升高，FSH 水平降低（p<0.05）。HE 染色显示 PBS 组小鼠卵泡形态/结构正常，D-gal 组小鼠卵泡数量减少，黄体空泡明显，闭锁卵泡增多。与 D-gal 组相比，D-gal/Rg1 组小鼠卵泡数量增加，黄体卵泡减少（p<0.05）。与 D-gal 组相比，D-gal/Rg1 组小鼠卵巢组织中 p16INK4a 表达下调，SIRT1 表达上调（p<0.05）。
结论
Rg1 可通过下调 p16INK4a 和上调 SIRT1 表达，延缓 D-gal 诱导的 POF 小鼠模型的卵巢早衰。
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