Evidence map›Paper›PMID 31715069›Full record

ArticleFEBS open bio2020

Panax notoginseng saponins ameliorate cisplatin-induced mitochondrial injury via the HIF-1α/mitochondria/ROS pathway.

Qingqing Li, Xueyan Liang, Yufang Yang, Xian Zeng, Xiaobin Zhong, Chun Huang

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Exercise performance reduction and preventive measures in highland sports.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. [Therapeutic effect ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Regulated cell death in cisplatin-induced AKI: relevance ofAmerican journal of physiology. Renal physiology · 2021
    Article
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

Qingqing LiDepartment of Pharmacy, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Xueyan LiangDepartment of Pharmacy, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Yufang YangDepartment of Pharmacy, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.ORCID 0000-0001-6978-2838
Xian ZengDepartment of Pharmacy, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Xiaobin ZhongRegenerative Medicine Research Center of Guangxi Medical University, Nanning, China.
Chun HuangDepartment of Pharmacy, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is a major antineoplastic drug that is used to treat solid tumors, but its use is restricted by its nephrotoxicity. Such cisplatin-induced nephrotoxicity (CIN) is believed to occur primarily through mitochondrial damage and reactive oxygen species (ROS) generation. Our previous studies have indicated that Panax notoginseng saponins (PNSs) mitigate CIN by enhancing hypoxia-inducible factor 1α (HIF-1α)-induced mitochondrial autophagy. In this study, the role of the HIF-1α/mitochondria/ROS pathway in PNSs protection against CIN was investigated using a rat model. A CIN model was generated by giving rats intraperitoneal injections with cisplatin (a single dose) and then treating them with or without 2-methoxyestradiol (HIF-1α inhibitor) and PNSs. We then measured ROS levels, superoxide dismutase, glutathione, catalase malondialdehyde and nitric oxide (to evaluate oxidative stress) and ATP, mitochondrial membrane potential and mitochondrial permeability transition pore opening (to evaluate mitochondrial function) in kidneys at different time points. We observed that PNSs remarkably reduced the levels of ROS, malondialdehyde and nitric oxide, as well as the opening of mitochondrial permeability transition pore, which is increased by cisplatin and further increased by HIF-1α inhibition. In addition, PNSs increased the levels of superoxide dismutase, catalase and glutathione, as well as ATP and mitochondrial membrane potential in renal tissues; these are all reduced by cisplatin and further reduced by HIF-1α inhibition. In conclusion, we demonstrate here that PNSs protects against mitochondrial damage induced by cisplatin through HIF-1α/mitochondria/ROS.

Indexed as

Administration, OralAnimalsAntineoplastic AgentsCisplatinHypoxia-Inducible Factor 1, alpha SubunitMaleMitochondriaPanax notoginsengRatsRats, Sprague-DawleyReactive Oxygen SpeciesSaponinsAntineoplastic AgentsCisplatinHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitReactive Oxygen SpeciesSaponinscisplatinHIF-1αmitochondriaPanax notoginseng saponinsROS

Identifiers

PMID31715069
PMCPMC6943232
OpenAlexW2988033985

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.