Evidence map›Paper›PMID 31853613›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2020

Protection from doxorubicin-induced nephrotoxicity by clindamycin: novel antioxidant, anti-inflammatory and anti-apoptotic roles.

Kamilia M Ibrahim, Eman M Mantawy, Mona M Elanany, Hend S Abdelgawad, Nuha M Khalifa, Rada H Hussien, Nermeen N El-Agroudy, Ebtehal El-Demerdash

Erratum issuedAbstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 40 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 2 countries.

Kamilia M IbrahimDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Badr University, Cairo, Egypt.
Eman M MantawyDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Mona M ElananyDepartment of Biochemistry, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Hend S AbdelgawadDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Nuha M KhalifaDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Rada H HussienDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Nermeen N El-AgroudyDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Ebtehal El-DemerdashDepartment of Pharmacology & Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt. ebtehal_dm@yahoo.com.ORCID 0000-0002-0537-4445
Ain Shams University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was performed to examine whether clindamycin could protect against doxorubicin (DOX)-induced acute nephrotoxicity, and if so, what molecular mechanisms responsible for this protective effect. Male albino rats were pretreated with clindamycin once per day for 5 consecutive days at a dose of 300 mg/kg, i.p, then received a single dose of DOX (15 mg/kg; i.p) on the 5th day. DOX-induced marked renal injury as indicated by the presence of inflammatory cell infiltration, congestion, and edema accompanied by elevation in serum levels of creatinine and urea. These effects were alleviated by clindamycin pretreatment. DOX caused glutathione depletion and reduction in level of the antioxidant enzyme, catalase. Pretreatment with clindamycin markedly prohibited DOX-induced oxidative damage in renal tissue. Moreover, DOX provoked inflammatory responses in renal tissues as confirmed by increased expressions of NF-κB and COX-2 which were significantly reduced by clindamycin pretreatment. Besides, DOX-triggered apoptotic cascades in renal tissues as evidenced by elevated expression of pro-apoptotic proteins; Bax and cytochrome c, enhancing activity of caspase-3 enzyme whereas reducing the expression of anti-apoptotic Bcl-2 protein. Clindamycin pretreatment counteracts these apoptotic effects of DOX. Summarily, our results provide an evidence for the first time that clindamycin has a potential protective action against DOX-induced acute nephrotoxicity through inhibiting oxidative stress, inflammatory cascades, and apoptotic tissue injury.

Indexed as

AnimalsAntibiotics, AntineoplasticAnti-Inflammatory AgentsAntioxidantsApoptosisClindamycinDoxorubicinKidneyKidney DiseasesMaleRats, Sprague-DawleyAntibiotics, AntineoplasticAnti-Inflammatory AgentsAntioxidantsClindamycinDoxorubicinApoptosisClindamycinDoxorubicinInflammationNephrotoxicityOxidative stress

Identifiers

PMID31853613
OpenAlexW2995655208

What OpenQuestion holds

Textmetadata
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.