El Bakly Wesam, Medhat Marwa, Shafei Mohamed, Tash Reham, Elrefai Mohamed, Shoukry Yousef, Omar Nesreen Nabil
Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
Department of Pharmacology, National Center for Social & Criminological Research, Egypt.
Heliyon. 2020 Sep 21;6(9):e05006. doi: 10.1016/j.heliyon.2020.e05006. eCollection 2020 Sep.
Platelet rich plasma contains a collection of growth factors, and an optimal formulation, named O-rPRP, contains the highest possible concentration of growth factors.
Challenging the healing power of O-rPRP in a high-galactose diet-induced premature ovarian insufficiency (POI) experimental rat model.
Rats were divided into four groups of ten rats each and treated for four week as follows; 1) the control group, fed with normal diet and received intraperitoneal (i.p.) injection of PBS once/week; 2) the POI group, fed with galactose diet (50%) and received PBS (i.p.) once/week; 3) the POI/O-rPRP group, fed a 50% galactose diet and received O-rPRP (i.p.) once/week; 4) the O-rPRP group (negative control), fed with a normal diet and received O-rPRP (i.p.) once/week. The levels of galactose, follicle stimulating hormone, 17 β-estradiol, anti-mullerian hormone and inhibin B were measured in serum samples. Western blotting and quantitative real-time PCR assays were employed to investigate the levels of miR-223, β1 integrin, p70S6k and MCL-1 in ovarian tissues.
After O-rPRP treatment, β1 integrin expression was enhanced, and miR-223 expression was decreased. Unlike the untreated galactose group, in the group treated with O-rPRP, p70S6k and MCL-1 expression levels were increased, indicating that the mTOR growth signaling pathway was active and that apoptosis was inactive. After the introduction of O-rPRP, the number of follicles and the follicular maturation improved, which was consistent with the improvement of inhibin B levels and subsequent inhibition of FSH.
O-rPRP inhibited galactose-induced excessive atresia and provided an overall protective effect on the ovarian follicles.
富血小板血浆含有多种生长因子，一种名为O-rPRP的优化配方含有尽可能高浓度的生长因子。
在高糖饮食诱导的卵巢早衰（POI）实验大鼠模型中挑战O-rPRP的愈合能力。
将大鼠分为四组，每组十只，进行如下四周治疗；1）对照组，喂食正常饮食，每周腹腔注射一次PBS；2）POI组，喂食半乳糖饮食（50%），每周腹腔注射一次PBS；3）POI/O-rPRP组，喂食50%半乳糖饮食，每周腹腔注射一次O-rPRP；4）O-rPRP组（阴性对照），喂食正常饮食，每周腹腔注射一次O-rPRP。检测血清样本中半乳糖、促卵泡激素、17β-雌二醇、抗苗勒管激素和抑制素B的水平。采用蛋白质免疫印迹法和定量实时PCR法检测卵巢组织中miR-223、β1整合素、p70S6k和MCL-1的水平。
O-rPRP治疗后，β1整合素表达增强，miR-223表达降低。与未治疗的半乳糖组不同，在O-rPRP治疗组中，p70S6k和MCL-1表达水平升高，表明mTOR生长信号通路活跃，细胞凋亡不活跃。引入O-rPRP后，卵泡数量和卵泡成熟度得到改善，这与抑制素B水平的改善及随后FSH的抑制一致。
O-rPRP抑制了半乳糖诱导的过度闭锁，对卵巢卵泡提供了全面的保护作用。
