Evidence map›Paper›PMID 32848363›Full record

ArticleDrug design, development and therapy2020

Hirudin Protects Against Kidney Damage in Streptozotocin-Induced Diabetic Nephropathy Rats by Inhibiting Inflammation via P38 MAPK/NF-κB Pathway.

Jiarui Han, Xinxin Pang, Yage Zhang, Zining Peng, Xiujie Shi, Yufeng Xing

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Research Progress of Pyroptosis in Diabetic Kidney Disease.International journal of molecular sciences · 2024
    Review
  20. Hirudin in the Treatment of Chronic Kidney Disease.Molecules (Basel, Switzerland) · 2024
    Review
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.

Jiarui HanDepartment of Nephropathy, Henan Provincial Hospital of Traditional Chinese Medicine, Zhengzhou, Henan Province, People's Republic of China.
Xinxin PangDepartment of Nephropathy, Henan Provincial Hospital of Traditional Chinese Medicine, Zhengzhou, Henan Province, People's Republic of China.ORCID 0000-0001-7941-4860
Yage ZhangDepartment of Nephropathy, Henan Provincial Hospital of Traditional Chinese Medicine, Zhengzhou, Henan Province, People's Republic of China.
Zining PengDepartment of Nephropathy, Henan Provincial Hospital of Traditional Chinese Medicine, Zhengzhou, Henan Province, People's Republic of China.
Xiujie ShiDepartment of Nephropathy, Henan Provincial Hospital of Traditional Chinese Medicine, Zhengzhou, Henan Province, People's Republic of China.
Yufeng XingDepartment of Nephropathy, Henan Provincial Hospital of Traditional Chinese Medicine, Zhengzhou, Henan Province, People's Republic of China.
Henan University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInflammation-induced podocyte apoptosis plays an important role in kidney injury during diabetic nephropathy (DN). Hirudin (HIR), a natural compound extracted from leeches, can inhibit inflammation. However, whether HIR can protect the kidneys against inflammation during DN is unknown. In the present study, we aimed to study the effects of HIR on kidney damage in a DN rat model and explore its anti-inflammatory properties.

methodsA streptozotocin-induced DN rat model was generated, and HIR was administered subcutaneously. Immortal podocytes and primary peritoneal macrophages were used for vitro studies. Hematoxylin and eosin staining was used to evaluate renal pathological changes; quantitative polymerase chain reaction and immunoblotting were used to detect gene expression; and TUNEL staining was used to detect apoptotic cells.

resultsOur results showed that HIR protected against renal injury, as indicated by kidney weight/body weight, serum creatinine, renal pathological changes, blood urea nitrogen, and detection of urine proteins. Notably, HIR treatment reduced macrophage infiltration, pro-inflammatory cytokine expression, and podocyte apoptosis in the kidney tissues of DN rats. In vitro, high glucose (HG) induced the activation of M1 macrophages, which was accompanied by increased podocyte apoptosis. HIR could decrease HG-induced podocyte apoptosis and suppress pro-inflammatory cytokine expression in podocytes in vitro. This was achieved via inhibition of p38 MAPK/NF-κB activation in renal tissues and podocytes.

conclusionHIR could inhibit inflammation via the p38 MAPK/NF-κB pathway, prevent podocyte apoptosis, and protect against kidney damage in a DN rat model.

Indexed as

AnimalsApoptosisDiabetic NephropathiesDisease Models, AnimalHirudinsInflammationInjections, SubcutaneousKidneyLeechesMacrophagesMaleNF-kappa Bp38 Mitogen-Activated Protein KinasesPodocytesProtective AgentsRatsHirudinsNF-kappa Bp38 Mitogen-Activated Protein KinasesProtective AgentsStreptozocinapoptosisdiabetic nephropathyhirudininflammationkidney damage

Identifiers

PMID32848363
PMCPMC7425656
OpenAlexW3047040868

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.