Evidence map›Paper›PMID 24683245›Full record

ArticleCurrent therapeutic research, clinical and experimental2009

Effects of atorvastatin on smoking-induced alveolar injury in rat lungs.

Tekin Yildiz, M Serhan Tasdemir, Selcuk Tunik, Gungor Ates, Selahaddin Tekes, Iskender Kaplanoglu, Fusun Topcu, Murat Akkus

Open access · goldAbstract read
In one paragraph

Article in Current therapeutic research, clinical and experimental, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 82% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

8 authors at 1 institution in 1 country.

Tekin YildizDepartment of Chest Diseases, Dicle University, Diyarbakir, Turkey.
M Serhan TasdemirDepartment of Histology, Dicle University, Diyarbakir, Turkey.
Selcuk TunikDepartment of Histology, Dicle University, Diyarbakir, Turkey.
Gungor AtesDepartment of Chest Diseases, Dicle University, Diyarbakir, Turkey.
Selahaddin TekesDepartment of Medical Biology and Genetics, Dicle University, Diyarbakir, Turkey.
Iskender KaplanogluDepartment of Histology, Dicle University, Diyarbakir, Turkey.
Fusun TopcuDepartment of Chest Diseases, Dicle University, Diyarbakir, Turkey.
Murat AkkusDepartment of Histology, Dicle University, Diyarbakir, Turkey.
Dicle University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmoking is one of the most serious health care issues worldwide, as one third to one half of all people who smoke eventually use tobacco habitually. Chronic smoke exposure causes airway and lung parenchymal inflammation and the destruction of alveolar cell walls. Statins may have anti-inflammatory effects that would play a role in preventing the cellular damage associated with smoking.

objectiveThe aim of this study was to investigate whether atorvastatin protects against smoking-induced inflammation in alveolar epithelial type I (ATI) and type II (ATII) cells in the lungs of rats.

methodsAdult male albino Wistar rats (200-250 g) were randomly divided into 3 groups and exposed to cigarette smoke 8 hours per day for 15 days. During that 15-day period, the 2 treatment groups received atorvastatin 0.5 or 1.0 mg/kg/d in 2 mL of methyl cellulose solution and the control group received 2 mL of methyl cellulose solution alone, all via nasogastric catheter. After the 15 days, the lungs were excised and the tissues were examined by transmission electron microscopy.

resultsThirty rats were divided into 3 groups of 10 rats each. All rats survived the 15 days. In the atorvastatin 0.5-mg group, no changes were found in the ATI cells or in the blood-air barrier. In the atorvastatin 1.0-mg group, we observed hyperplasia in the common basal membranes. Hypertrophy, mitochondrial crystolysis (MC), and intracytoplasmic edema (ICE) were detected in the ATI cells in the 1.0-mg group, while chromatin condensation, atrophic appearance, cell shrinkage, and cyto-plasmic vacuolization were observed in the ATII cells. The rough endoplasmic reticulum (rER) tubules of the ATII cells appeared spiral-shaped. In the control group, minimal ICE was detected in the ATI cells. However, microvillus deformation, pseu-dopod formation, edema, mitochondrial swelling, and MC were observed in the ATII cells. We also observed MC, several pinocytic vesicles, and normal rER tubules in the endothelial cells of the control group.

conclusionsThe administration of atorvastatin 0.5 mg/kg/d was associated with some attenuation of lung injury caused by smoke inhalation in these rat lungs. However, atorvastatin 1.0 mg/kg/d was associated with lung damage. Future studies are needed to evaluate the dose-response relationship of atorvastatin to smoking-induced alveolar damage.

Indexed as

atorvastatinlungratultrastructural changes

Identifiers

PMID24683245
PMCPMC3967291
OpenAlexW2067604599

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.