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Hyaluronic acid prevents immunosuppressive drug-induced ovarian damage via up-regulating PGRMC1 expression.

Abstract
Chemotherapy treatment in women can frequently cause damage to the ovaries, which may lead to primary ovarian insufficiency (POI). In this study, we assessed the preventative effects of hyaluronic acid (HA) in immunosuppressive drug-induced POI-like rat models and investigated the possible mechanisms. We found that HA, which was reduced in primary and immunosuppressant-induced POI patients, could protect the immunosuppressant-induced damage to granulosa cells (GCs) in vitro. Then we found that HA blocked the tripterygium glycosides (TG) induced POI-like presentations in rats, including delayed or irregular estrous cycles, reduced 17 beta-estradiol(E2) concentration, decreased number of follicles, destruction of follicle structure, and damage of reproductive ability. Furthermore, we investigated the mechanisms of HA prevention effects on POI, which was associated with promotion of GC proliferation and PGRMC1 expression. In conclusion, HA prevents chemotherapy-induced ovarian damage by promoting PGRMC1 in GCs. This study may provide a new strategy for prevention and treatment of POI.
AuthorsGuangfeng Zhao, Guijun Yan, Jie Cheng, Xue Zhou, Ting Fang, Haixiang Sun, Yayi Hou, Yali Hu
JournalScientific reports (Sci Rep) Vol. 5 Pg. 7647 (Jan 06 2015) ISSN: 2045-2322 [Electronic] England
PMID25558795 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Glycosides
  • Immunosuppressive Agents
  • Membrane Proteins
  • Pgrmc1 protein, rat
  • RNA, Small Interfering
  • Receptors, Progesterone
  • Estradiol
  • Hyaluronic Acid
  • Aromatase
Topics
  • Adult
  • Animals
  • Aromatase (genetics, metabolism)
  • Cell Proliferation (drug effects)
  • Cell Survival (drug effects)
  • Cells, Cultured
  • Disease Models, Animal
  • Estradiol (metabolism)
  • Female
  • Glycosides (toxicity)
  • Granulosa Cells (cytology, drug effects, metabolism)
  • Humans
  • Hyaluronic Acid (blood, pharmacology, therapeutic use)
  • Immunosuppressive Agents (therapeutic use, toxicity)
  • Membrane Proteins (antagonists & inhibitors, genetics, metabolism)
  • Neoplasms (drug therapy)
  • Ovarian Follicle (drug effects, metabolism)
  • Primary Ovarian Insufficiency (chemically induced, prevention & control)
  • RNA Interference
  • RNA, Small Interfering (metabolism)
  • Rats
  • Receptors, Progesterone (antagonists & inhibitors, genetics, metabolism)
  • Reproduction (drug effects)
  • Tripterygium (chemistry, metabolism)
  • Up-Regulation (drug effects)
  • Young Adult

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