Protective effect of proanthocyanidin against oxidative ovarian damage induced by 3-nitropropionic acid in mice

Zhang, J Q; Xing, Baosong; Zhu, Chengcheng; Shen, Ming; Yu, Fengxiang; Liu, H L

doi:10.4238/2015.march.30.6

Cited by 13 publications

(10 citation statements)

References 34 publications

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“…Furthermore, significant increase in the fluorescence intensity of granulosa cells treated with 3-NPA also indicated that 3-NPA increased ROS products. This result is consistent with a previous study in which Zhang et al [ 26 ] reported that 3-NPA increased ROS generation in mouse ovaries. These findings imply that 3-NPA promotes ROS generation and induces oxidative stress in tissues and cells in both mammals and birds.…”

Section: Discussionsupporting

confidence: 94%

“…The tumor suppressor p53 plays important roles in regulating intracellular redox [ 28 , 29 ]. 3-NPA can increase the mouse ovarian ROS levels and up-regulate the apoptosis-related gene Caspase 3 in mouse granulosa cells [ 26 ]. Our results showed that in goose granulosa cells, treatment with 3-NPA at 5.0 mmol/l down-regulated the mRNA expression of Pcna and p53 , while it up-regulated Caspase 3 mRNA expression.…”

Section: Discussionmentioning

confidence: 99%

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Effect of 3-nitropropionic acid inducing oxidative stress and apoptosis of granulosa cells in geese

Kang

Wang

et al. 2018

Bioscience Reports

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The mechanism of action by which oxidative stress induces granulosa cell apoptosis, which plays a vital role in initiating follicular atresia, is not well understood. In the present study, the effect of 3-nitropropionic acid (3-NPA) on oxidative stress and apoptosis in granulosa cells in geese was investigated. Our results showed that treatment with 3-NPA at 5.0 mmol/l for 24 h increased intracellular reactive oxygen species (ROS) production by 25.4% and decreased granulosa cell viability by 45.5% (P<0.05). Catalase and glutathione peroxidase gene expression levels in granulosa cells treated with 3-NPA were 1.32- and 0.49-fold compared with those of the control cells, respectively (P <0.05). A significant decrease in the expression level of B-cell lymphoma 2 (Bcl-2) protein and remarkable increases in the levels of Bax, p53 and cleaved-Caspase 3 proteins and the ratio of Bax/Bcl-2 expression in granulosa cells treated with 3-NPA were observed (P<0.05). Furthermore, a 38.43% increase in the percentage of early apoptotic cells was also observed in granulosa cells treated with 3-NPA (P<0.05). Moreover, the expression levels of NF-κB, Nrf2, Fhc, Hspa2 and Ho-1 in granulosa cells treated with 3-NPA were elevated 4.36-, 1.63-, 3.62-, 27.54- and 10.48-fold compared with those of the control cells (P<0.05), respectively. In conclusion, the present study demonstrates that treatment with 3-NPA induces ROS production and apoptosis and inhibits the viability of granulosa cells in geese. Furthermore, 3-NPA triggers increases in the expression of cleaved-Caspase 3 protein and the ratio of Bax/Bcl-2 expression, and induces the early apoptosis of granulosa cells.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Effect of 3-nitropropionic acid inducing oxidative stress and apoptosis of granulosa cells in geese

Kang

Wang

et al. 2018

Bioscience Reports

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“…These mice were given a standard granulated food and drinking water and were divided into five groups as follows: Group 1: Mice given Oil/water (1:1, v : v ) at 5 mL/kg BW; Group 2: Mice given GSPE at 100 mg/kg b.w. GSPE was at a dose of 100 mg/kg body weight because this was reported to be the most effective dose [ 39 , 40 ]; Group 3: Mice given AFB1 in oil/water (1:1, v : v ) at 100 μg/kg b.w. ; Group 4: Mice given 1 h prior to AFB1 administration a dose of GSPE of 50 mg/kg b.w., then the dose of AFB1 100 μg/kg b.w.…”

Section: Methodsmentioning

confidence: 99%

Intervention of Grape Seed Proanthocyanidin Extract on the Subchronic Immune Injury in Mice Induced by Aflatoxin B1

Long

Zhang

et al. 2016

IJMS

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The aim was to investigate the prevention of grape seed proanthocyanidin extract (GSPE) on the subchronic immune injury induced by aflatoxin B1 (AFB1) and the possible ameliorating effect of GSPE in mice. The subchronic AFB1-induced immune injury mice model was set up with the continuous administration of 100 μg/kg body weight (BW) AFB1 for six weeks by intragastric administration. Then, intervention with different doses (50 and 100 mg/kg BW) of GSPE was conducted on mice to analyze the changes of body weight, immune organ index, antioxidant capability of spleen, serum immunoglobulin content, and the expression levels of inflammatory cytokines. The prevention of GSPE on the immune injury induced by AFB1 was studied. The GSPE could relieve the AFB1-induced reduction of body weight gain and the atrophy of the immune organ. The malondialdehyde (MDA) level of the spleen in the AFB1 model group significantly increased, but levels of catalase (CAT), glutathione (GSH), glutathione peroxidase (GSH-PX), and superoxide dismutase (SOD) significantly decreased. The GSPE could significantly inhibit the oxidative stress injury of the spleen induced by AFB1. AFB1 exposure could not significantly change the contents of IgA, IgG, or IgM. AFB1 significantly improved the expression of interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ). Additionally, GSPE could decrease the expression of these four proinflammatory factors to different degrees and inhibit the inflammatory reaction of mice. The results suggest that GSPE alleviates AFB1-induced oxidative stress and significantly improves the immune injury of mice induced by AFB1.

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“…Activation Direct AS101 [26], everolimus (RAD001) [27], INK128 [27], melatonin [29], ghrelin [29] Indirect AMH [31] Apoptosis Direct GnRH agonists [40,41], GnRH antagonist [42], LH [46], ATM/ATR inhibitor [21], CHEK2 inhibitor [19,24], and CK1 inhibitor [18], imatinib [48] Indirect S1P [51,61], ceramide-1-phosphate [52], zingerone [53], proanthocyanidin [54], gallic acid [55], mangafodipir [56], resveratrol [57], curcumin [58], capsaicin [58], erythropoietin [62], G-CSF [63], tamoxifen [64], dexrazoxane [65][66][67] AMH, anti-Müllerian hormone; GnRH, gonadotropin-releasing hormone; LH, luteinizing hormone; ATM, ataxia-telangiectasia mutated; ATR, ataxia telangiectasia and Rad3-related; CHEK2, checkpoint kinase 2; CK1, casein kinase 1; S1P, sphingosine-1-phosphate; G-CSF, granulocytecolony stimulating factor.…”

Section: Proposed Mechanism Of Loss Of Pfs Proposed Adjuvantsmentioning

confidence: 99%

“…In addition, it adversely affects the production of ovarian hormones and mature oocytes from healthy follicles. Of relevance to the preservation of fertility, reports suggest that the antioxidants such as S1P [51], ceramide-1-phosphate [52], zingerone [53], proanthocyanidin [54], gallic acid [55], mangafodipir [56], resveratrol [57], curcumin [58], and capsaicin [58] protect the ovary from ovotoxins including chemotherapeutic agents. Thus, oxidative stress-induced damage can be prevented by antioxidants through attenuating the free radical induced ovarian damages.…”

Section: Indirect Apoptosis By Reactive Oxygen Speciesmentioning

confidence: 99%

Consequences of chemotherapeutic agents on primordial follicles and future clinical applications

2019

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The ovarian reserve is necessary for female fertility and endocrine health. Commonly used cancer therapies diminish the ovarian reserve, thus, resulting in primary ovarian insufficiency, which clinically presents as infertility and endocrine dysfunction. Prepubertal children who have undergone cancer therapies often experience delayed puberty or cannot initiate puberty and require endocrine support to maintain a normal life. Thus, developing an effective intervention to prevent loss of the ovarian reserve is an unmet need for these cancer patients. The selection of adjuvant therapies to protect the ovarian reserve against cancer therapies underlies the mechanism of loss of primordial follicles (PFs). Several theories have been proposed to explain the loss of PFs. The "burn out" theory postulates that chemotherapeutic agents activate dormant PFs through an activation pathway. Another theory posits that chemotherapeutic agents destroy PFs through an "apoptotic pathway" due to high sensitivity to DNA damage. However, the mechanisms causing loss of the ovarian reserve remains largely speculative. Here, we review current literature in this area and consider the mechanisms of how gonadotoxic therapies deplete PFs in the ovarian reserve.

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Protective effect of proanthocyanidin against oxidative ovarian damage induced by 3-nitropropionic acid in mice

Cited by 13 publications

References 34 publications

Effect of 3-nitropropionic acid inducing oxidative stress and apoptosis of granulosa cells in geese

Effect of 3-nitropropionic acid inducing oxidative stress and apoptosis of granulosa cells in geese

Intervention of Grape Seed Proanthocyanidin Extract on the Subchronic Immune Injury in Mice Induced by Aflatoxin B1

Consequences of chemotherapeutic agents on primordial follicles and future clinical applications

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