Evidence map›Paper›PMID 28826042›Full record

ArticleRedox biology2018

Carnosine attenuates cyclophosphamide-induced bone marrow suppression by reducing oxidative DNA damage.

Jie Deng, Yi-Fei Zhong, Yan-Ping Wu, Zhuo Luo, Yuan-Ming Sun, Guo-En Wang, Hiroshi Kurihara, Yi-Fang Li, Rong-Rong He

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.6field-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

42 citing papers in PubMed, 89 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Jie DengAnti-stress and Health Research Center, College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632, PR China; Institute of Traditional Chinese Medicine & Natural Products, Jinan University, Guangzhou, Guangdong 510632, PR China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, Guangdong 510632, PR China.
Yi-Fei ZhongAnti-stress and Health Research Center, College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632, PR China; Institute of Traditional Chinese Medicine & Natural Products, Jinan University, Guangzhou, Guangdong 510632, PR China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, Guangdong 510632, PR China.
Yan-Ping WuAnti-stress and Health Research Center, College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632, PR China; Institute of Traditional Chinese Medicine & Natural Products, Jinan University, Guangzhou, Guangdong 510632, PR China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, Guangdong 510632, PR China.
Zhuo LuoAnti-stress and Health Research Center, College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632, PR China; Institute of Traditional Chinese Medicine & Natural Products, Jinan University, Guangzhou, Guangdong 510632, PR China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, Guangdong 510632, PR China.
Yuan-Ming SunGuangdong Provincial Key Lab of Food Safety and Quality, South China Agricultural University, Guangzhou, Guangdong 510642, PR China.
Guo-En WangAnti-stress and Health Research Center, College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632, PR China; Institute of Traditional Chinese Medicine & Natural Products, Jinan University, Guangzhou, Guangdong 510632, PR China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, Guangdong 510632, PR China.
Hiroshi KuriharaAnti-stress and Health Research Center, College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632, PR China; Institute of Traditional Chinese Medicine & Natural Products, Jinan University, Guangzhou, Guangdong 510632, PR China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, Guangdong 510632, PR China.
Yi-Fang LiAnti-stress and Health Research Center, College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632, PR China; Institute of Traditional Chinese Medicine & Natural Products, Jinan University, Guangzhou, Guangdong 510632, PR China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, Guangdong 510632, PR China.
Rong-Rong HeAnti-stress and Health Research Center, College of Pharmacy, Jinan University, Guangzhou, Guangdong 510632, PR China; Institute of Traditional Chinese Medicine & Natural Products, Jinan University, Guangzhou, Guangdong 510632, PR China; Guangdong Province Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, Jinan University, Guangzhou, Guangdong 510632, PR China.
Jinan University · CNSouth China Agricultural University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative DNA damage in bone marrow cells is the main side effect of chemotherapy drugs including cyclophosphamide (CTX). However, not all antioxidants are effective in inhibiting oxidative DNA damage. In this study, we report the beneficial effect of carnosine (β-alanyl-l-histidine), a special antioxidant with acrolein-sequestering ability, on CTX-induced bone marrow cell suppression. Our results show that carnosine treatment (100 and 200mg/kg, i.p.) significantly inhibited the generation of reactive oxygen species (ROS) and 8-hydroxy-2'-deoxyguanosine (8-oxo-dG), and decreased chromosomal abnormalities in the bone marrow cells of mice treated with CTX (20mg/kg, i.v., 24h). Furthermore, carnosine evidently mitigated CTX-induced G2/M arrest in murine bone marrow cells, accompanied by reduced ratios of p-Chk1/Chk1 and p-p53/p53 as well as decreased p21 expression. In addition, cell apoptosis caused by CTX was also suppressed by carnosine treatment, as assessed by decreased TUNEL-positive cell counts, down-regulated expressions of Bax and Cyt c, and reduced ratios of cleaved Caspase-3/Caspase-3. These results together suggest that carnosine can protect murine bone marrow cells from CTX-induced DNA damage via its antioxidant activity.

Indexed as

8-Hydroxy-2'-DeoxyguanosineAnimalsAntioxidantsBone Marrow CellsCarnosineCaspase 3Cell Cycle CheckpointsCells, CulturedCheckpoint Kinase 1Chromosome AberrationsCyclin-Dependent Kinase Inhibitor p21CyclophosphamideDeoxyguanosineDNA DamageMaleMice8-Hydroxy-2'-DeoxyguanosineAntioxidantsCarnosineCaspase 3Checkpoint Kinase 1Cyclin-Dependent Kinase Inhibitor p21CyclophosphamideDeoxyguanosineReactive Oxygen SpeciesTumor Suppressor Protein p53ApoptosisCarnosineCell cycle arrestCyclophosphamideOxidative DNA damageSister chromatid exchange

Identifiers

PMID28826042
PMCPMC5565745
OpenAlexW2742930384

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.