Tripterygium Glycosides Impairs the Proliferation of Granulosa Cells and Decreases the Reproductive Outcomes in Female Rats

Su, Jing; Cheng, Jie; Sun, Haixiang; Diao, Zongli; Zhen, Xin; Yang, Jun; Ding, Lijun; Hu, Yali

doi:10.1002/bdrb.21111

Cited by 12 publications

(12 citation statements)

References 26 publications

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“…As early as 1985, Ataya observed that long-acting GnRH-a TRI could protect against cyclophosphamide-induced ovarian damage in a rat model [15]. Subsequently, Yuan and Meirow confirmed the above conclusions in animal experiments [16], showing that GnRH-a could protect rat ovarian functions, save most of the primary follicles, and thus prevent quiescent follicles from damage caused by chemotherapeutic drugs [17,18]. Numerous clinical studies have confirmed that GnRH-a protects ovarian functions in patients from chemotherapy-induced damage [19,20].…”

Section: Discussionmentioning

confidence: 90%

Protective mechanisms of triptorelin against tripterygium glycoside-induced ovarian dysfunction

Zhao¹,

Lv²,

Li³

et al. 2018

biomedicalresearch

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The aim of this study was to investigate the protective effects of Triptorelin (TRI) on Tripterygium Glycoside-induced Ovarian Dysfunction (TG-OD). Thirty mice with normal estrous cycles were randomly divided into three groups (n=10): the control group (group A) was orally administered 0.35 ml of saline daily; the TH group (group B) was orally administered 0.35 ml of TG solution from the 8 th d for 10 w continuously; the TG+TRI group (group C) was subcutaneously injected with 0.1 mg/kg TRI daily, as well as orally administered 0.35 ml of TG solution from the 8 th d for 10 w continuously. All mice were sacrificed during the 11th week to detect blood anti-Mullerian hormone, follicle-stimulating hormone, luteinizing hormone, and estradiol; calculate the ovarian index; and observe the morphologies of ovarian tissues. Mice in group C were more flexible, and had increased weight, reduced folliclestimulating hormone and luteinizing hormone, and increased anti-Mullerian hormone and estradiol; additionally, ovarian follicles and mature follicles increased. TG caused gonad and ovarian dysfunction in female mice; TRI exhibited protective effects against TG-induced gonad and ovarian dysfunction in female mice.

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Section: Discussionmentioning

confidence: 90%

Protective mechanisms of triptorelin against tripterygium glycoside-induced ovarian dysfunction

Zhao¹,

Lv²,

Li³

et al. 2018

biomedicalresearch

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“…A POI-like rat model was induced using TG as previously reported 30 . Female SD rats aged 12 weeks and weighing 220–250 g were provided by the experimental animal center of Nanjing Medical University.…”

Section: Methodsmentioning

confidence: 99%

“…It was reported that CYC may act primarily on primordial follicles through induction of apoptotic changes in pre-granulosa cells which lead to follicle loss 28 29 . In our previous study, we found that TG inhibited the proliferation of rat GCs in vitro 30 . Then we constructed the TG induced POI rat model and found fewer layers of GCs in developing follicles in TG-treated ovaries as compared to normal ovaries and TG decreased reproductive outcomes in female rats 30 .…”

mentioning

confidence: 85%

“…In our previous study, we found that TG inhibited the proliferation of rat GCs in vitro 30 . Then we constructed the TG induced POI rat model and found fewer layers of GCs in developing follicles in TG-treated ovaries as compared to normal ovaries and TG decreased reproductive outcomes in female rats 30 . Thus, GC survival could be prolonged by inhibiting apoptosis to reverse TG- or CYC-induced POI.…”

mentioning

confidence: 85%

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

Zhao

Yan

Cheng

et al. 2015

Sci Rep

Self Cite

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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.

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“…As an essential cell for follicular growth, granulosa cell (GC) is becoming the focus of research in recent years. 10,13 GC is a somatic cell of the sex cord that is closely associated with the developing female gamete in the ovary of mammals. Its main functions include producing sex steroids and providing nutrition for oocyte.…”

Section: Introductionmentioning

confidence: 99%

Exposure to triptolide affects follicle development in NIH mice

Zeng

Sun

et al. 2016

Hum Exp Toxicol

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Triptolide (TPL) is a main active compound isolated from Tripterygium wilfordii Hook f. Despite its positive therapeutic effect, the female reproductive toxicity of TPL is still the bottleneck of clinical application. The study was designed to investigate the adverse effects on mice ovary and underlying mechanism of TPL. Adult female NIH mice were treated with two therapeutic doses of TPL (25 and 50 μg/kg/d) for 50 days, respectively. Mice estrous cycle was detected by vaginal cytology method. Half mice from each group were selected randomly to perform superovulation. Quality and quantity of ovulated eggs were evaluated. Other mice from each group were executed for morphological study. Ovarian histological sections were stained by H&E staining for ovarian pathologic detection and follicular counts. Apoptotic granulosa cell (GC) was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Endoplasmic reticulum (ER) stress-related proteins and antiapoptotic X-linked inhibitor of apoptosis protein (XIAP) were detected by immunohistochemical method. Two doses of TPL resulted in estrous cycle disorder and follicles in development reservoir impairment. Quality and quantity of mice ovulated eggs significantly decreased after TPL treatment. Ovarian pathologic examination revealed TPL-induced TUNEL-positive GCs increase and ER stress–related proteins (78-kDa glucose-regulated protein, p-protein kinase-like endoplasmic reticulum kinase, p-eukaryotic initiation factor 2α, and CCAAT/enhancer binding protein homologous protein) expression upregulation. Meanwhile, the expression of antiapoptosis protein XIAP in mice ovary was obviously inhibited by TPL. Our results may demonstrate that therapeutic doses of TPL can injure ovary function, but there is no difference between high-dose and low-dose groups. GCs apoptosis by ER stress pathway and antiapoptotic function impairment may partly mediate TPL-induced ovary toxicity.

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Tripterygium Glycosides Impairs the Proliferation of Granulosa Cells and Decreases the Reproductive Outcomes in Female Rats

Cited by 12 publications

References 26 publications

Protective mechanisms of triptorelin against tripterygium glycoside-induced ovarian dysfunction

Protective mechanisms of triptorelin against tripterygium glycoside-induced ovarian dysfunction

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

Exposure to triptolide affects follicle development in NIH mice

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