Evidence map›Paper›PMID 29890735›Full record

ArticleToxins2018

Resveratrol Ameliorates Microcystin-LR-Induced Testis Germ Cell Apoptosis in Rats via SIRT1 Signaling Pathway Activation.

Haohao Liu, Shenshen Zhang, Chuanrui Liu, Jinxia Wu, Yueqin Wang, Le Yuan, Xingde Du, Rui Wang, Phelisters Wegesa Marwa, Donggang Zhuang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Toxins, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Fine Particulate Matter (Environmental health perspectives · 2025
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  5. Review
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  10. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Haohao LiuCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. Liuhlin2018@126.com.
Shenshen ZhangCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. zsslb2005@163.com.
Chuanrui LiuCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. lcr0624@126.com.
Jinxia WuCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. wjxsir@126.com.
Yueqin WangCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. wyq2018@stu.zzu.edu.cn.
Le YuanCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. yl19920215@126.com.
Xingde DuCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. dxd1993@163.com.
Rui WangCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. wr935314032@163.com.
Phelisters Wegesa MarwaCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. wegesalee@gmail.com.
Donggang ZhuangCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. zdg@zzu.edu.cn.
Xuemin ChengCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. cxm@zzu.edu.cn.
Huizhen ZhangCollege of Public Health, Zhengzhou University, Zhengzhou 450001, China. huizhenzhang@zzu.edu.cn.
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microcystin-leucine arginine (MC-LR), a cyclic heptapeptide produced by cyanobacteria, is a strong reproductive toxin. Studies performed in rat Sertoli cells and Chinese hamster ovary cells have demonstrated typical apoptosis after MC-LR exposure. However, little is known on how to protect against the reproductive toxicity induced by MC-LR. The present study aimed to explore the possible molecular mechanism underlying the anti-apoptosis and protective effects of resveratrol (RES) on the co-culture of Sertoli⁻germ cells and rat testes. The results demonstrated that MC-LR treatment inhibited the proliferation of Sertoli⁻germ cells and induced apoptosis. Furthermore, sirtuin 1 (SIRT1) and Bcl-2 were inhibited, while p53 and Ku70 acetylation, Bax expression, and cleaved caspase-3 were upregulated by MC-LR. However, RES pretreatment ameliorated MC-LR-induced apoptosis and SIRT1 inhibition, and downregulated the MC-LR-induced increase in p53 and Ku70 acetylation, Bax expression, and caspase-3 activation. In addition, RES reversed the MC-LR-mediated reduction in Ku70 binding to Bax. The present study indicated that the administration of RES could ameliorate MC-LR-induced Sertoli⁻germ cell apoptosis and protect against reproductive toxicity in rats by stimulating the SIRT1/p53 pathway, suppressing p53 and Ku70 acetylation and enhancing the binding of Ku70 to Bax.

Indexed as

AnimalsApoptosisCoculture TechniquesGerm CellsMaleMarine ToxinsMicrocystinsProtective AgentsRats, Sprague-DawleyResveratrolSertoli CellsSignal TransductionSirtuin 1cyanoginosin LRMarine ToxinsMicrocystinsProtective AgentsResveratrolSirt1 protein, ratSirtuin 1apoptosismicrocystin-LR (MC-LR)reproductive toxicityresveratrolsirtuin 1 (SIRT1)

Identifiers

PMID29890735
PMCPMC6024601
OpenAlexW2805831171

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.