Evidence map›Paper›PMID 34703213›Full record

ArticleDrug design, development and therapy2021

Unravelling the Protective Effects of Emodin Against Cyclophosphamide Induced Gonadotoxicity in Male Wistar Rats.

Yinhua Wang, Zhaoling Zou, Amit Jaisi, Opeyemi Joshua Olatunji

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Endocrine Disrupting Agents: Toxicological Aspects on Male Reproduction.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
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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

4 authors at 3 institutions in 2 countries.

Yinhua WangThe Second Peoples Hospital of Wuhu, Wuhu, 241001, Anhui, People's Republic of China.
Zhaoling ZouThe Second Peoples Hospital of Wuhu, Wuhu, 241001, Anhui, People's Republic of China.
Amit JaisiSchool of Pharmacy, Walailak University, Nakhon Si Thammarat, 80160, Thailand.ORCID 0000-0003-0261-7170
Opeyemi Joshua OlatunjiFaculty of Thai Traditional Medicine, Prince of Songkla University, Hat Yai, 90110, Thailand.ORCID 0000-0002-6800-4919
Wuhu Fourth People Hospital · CNPrince of Songkla University · THWalailak University · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOver the past few decades, cyclophosphamide (CP) has been extensively used as a broad-spectrum alkylating agent for the treatment of various cancers and solid tumors. However, the therapeutic actions on CP are not limited to only cancer cells, as it simultaneously exerts significant toxicities on healthy cells through the instigation of oxidative stress and oxidative damages. CP induced testicular toxicity is associated with impaired spermatogenesis, reduced sperm functionality, reproductive hormone and testicular weight. This study was aimed at unravelling the protective effects of emodin (EMD) on testicular toxicity following CP treatment.

methodsTwenty-four male Wistar rats were allotted into 4 groups as normal control group (NCG), CP control group (CPCG), EMD25+CP (25 mg/kg in 5% tween 80) and EMD50+CP groups (50 mg/kg in 5% tween 80). EMD was orally administered for 35 consecutive days, while four doses of CP (100 mg/kg/week) were administered intraperitoneally from the second to fifth week of treatment. Thereafter, the animals were sacrificed and histopathological examination of the testes as well as serum/testicular biochemical assays were conducted.

resultsThe results revealed that CP significantly impeded sperm function parameters including sperm count, viability and motility as well as decreased reproductive hormones (testosterone, LH and FSH) levels. In addition, CP enhanced testicular oxidative stress and proinflammatory markers (MDA, IL-6 and TNF-α), while simultaneously decreasing testicular antioxidant enzymes (GSH, GPx, SOD and CAT). Evidence of marked histopathological alterations was also observed in the H&E stained testicular tissues of CP treated rats. EMD significantly prevented these CP induced negative effects.

conclusionThis study provides a basis for the potential use of EMD in counteracting chemotherapy induced testicular toxicity. The results further suggest that EMD testicular protective effects in CP-treated rats may be mediated through its modulatory role on oxidative stress and inflammation.

Indexed as

AnimalsAntineoplastic Agents, AlkylatingAntioxidantsCyclophosphamideEmodinInflammationMaleOxidative StressRatsRats, WistarSpermatogenesisSpermatozoaTestisAntineoplastic Agents, AlkylatingAntioxidantsCyclophosphamideEmodincyclophosphamideemodininflammationoxidative stresstesticular toxicity

Identifiers

PMID34703213
PMCPMC8541740
OpenAlexW3205426565

What OpenQuestion holds

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LicenceCC BY-NC
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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.