Evidence map›Paper›PMID 21879311›Full record

ArticleMolecular and cellular biochemistry2012

Nitric oxide synthase inhibition abrogates hydrogen sulfide-induced cardioprotection in mice.

Bhavesh Sojitra, Yogesh Bulani, Uday Kumar Putcha, Abhinav Kanwal, Prachi Gupta, Madhusudana Kuncha, Sanjay Kumar Banerjee

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In one paragraph

Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.7field-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

23 citing papers in PubMed, 46 citations in OpenAlex.

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  15. Review
  16. Hydrogen Sulfide and Cellular Redox Homeostasis.Oxidative medicine and cellular longevity · 2016
    Review
  17. Review
  18. Chemical foundations of hydrogen sulfide biology.Nitric oxide : biology and chemistry · 2013
    Review
  19. Review
  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

7 authors at 2 institutions in 1 country.

Bhavesh SojitraDivision of Pharmacology and Chemical Biology, Indian Institute of Chemical Technology, Hyderabad, India.
Yogesh Bulani
Uday Kumar Putcha
Abhinav Kanwal
Prachi Gupta
Madhusudana Kuncha
Sanjay Kumar Banerjee
Indian Institute of Chemical Technology · INNational Institute of Nutrition · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cardioprotective property of hydrogen sulfide (H(2)S) is recently reported. However, cellular signaling cascades mediated by H(2)S are largely unclear. This study was undertaken to explore the molecular mechanism of H(2)S-induced cardioprotection in mouse heart by utilizing in vivo model of cardiac injury. We report here that intraperitoneal administration of sodium hydrogen sulfide (NaHS, 50 μmol kg(-1 )day(-1) for 2 days), a H(2)S donor, significantly (P ≤ 0.05) increased nitric oxide levels in serum as well as myocardium without any sign of myocardial injury. Typical characteristics of myocardial injury induced by isoproterenol (ISO) administration was significantly (P ≤ 0.05) abrogated by NaHS administration as evidenced from reduction in elevated thiobarbituric acid reactive substances (TBARS) and normalization of glutathione (GSH), glutathione peroxidase, superoxide dismutase (SOD), and catalase activity. Further, decrease in TNF-α expression and improvement in myocardial architecture was also observed. However, co-administration of N-nitro-L-arginine methyl ester, a nitric oxide synthase (NOS) inhibitor, and Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor along with NaHS and ISO abrogated the beneficial effect of H(2)S differentially. Inhibition of NOS significantly (P ≤ 0.05) increased serum creatine kinase, lactate dehydrogenase, serum glutamic oxaloacetic transaminase activity and myocardial TBARS, along with significant (P ≤ 0.05) reduction of myocardial GSH, SOD, and catalase. This was followed by increase in TNF-α expression and histopathological changes. Our results revealed that H(2)S provides myocardial protection through interaction with NOS and COX-2 pathway and inhibition of NOS completely abrogates the hydrogen sulfide-induced cardioprotection in mice.

Indexed as

AnimalsBiomarkersCardiotonic AgentsCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsGene ExpressionHeartHeart InjuriesHydrogen SulfideIsoproterenolMaleMiceMyocardiumNG-Nitroarginine Methyl EsterNitric OxideBiomarkersCardiotonic AgentsCelecoxibCyclooxygenase 2Cyclooxygenase 2 InhibitorsHydrogen SulfideIsoproterenolNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthasePyrazolesSulfonamidesThiobarbituric Acid Reactive SubstancesTumor Necrosis Factor-alpha

Identifiers

PMID21879311
OpenAlexW1989541200

What OpenQuestion holds

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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.