Gönüllü, Uğur

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Profile URL
https://hdl.handle.net/20.500.14411/8455
Name Variants
U., Gonullu
G., Ugur
Gönüllü, Uğur
G.,Uğur
Uğur, Gönüllü
U.,Gonullu
Gönüllü,U.
Ugur, Gonullu
G.,Ugur
U.,Gönüllü
Gonullu, Ugur
Gonullu,U.
Job Title
Profesör Doktor
Email Address
ugur.gonullu@atilim.edu.tr
Main Affiliation
Internal Medical Sciences
Status
Former Staff
Website
ORCID ID
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID

Sustainable Development Goals

NO POVERTY1
NO POVERTY
0
Research Products
ZERO HUNGER2
ZERO HUNGER
0
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GOOD HEALTH AND WELL-BEING3
GOOD HEALTH AND WELL-BEING
7
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QUALITY EDUCATION4
QUALITY EDUCATION
0
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GENDER EQUALITY5
GENDER EQUALITY
0
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CLEAN WATER AND SANITATION6
CLEAN WATER AND SANITATION
0
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AFFORDABLE AND CLEAN ENERGY7
AFFORDABLE AND CLEAN ENERGY
0
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DECENT WORK AND ECONOMIC GROWTH8
DECENT WORK AND ECONOMIC GROWTH
0
Research Products
INDUSTRY, INNOVATION AND INFRASTRUCTURE9
INDUSTRY, INNOVATION AND INFRASTRUCTURE
0
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REDUCED INEQUALITIES10
REDUCED INEQUALITIES
0
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SUSTAINABLE CITIES AND COMMUNITIES11
SUSTAINABLE CITIES AND COMMUNITIES
0
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RESPONSIBLE CONSUMPTION AND PRODUCTION12
RESPONSIBLE CONSUMPTION AND PRODUCTION
0
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CLIMATE ACTION13
CLIMATE ACTION
0
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LIFE BELOW WATER14
LIFE BELOW WATER
0
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LIFE ON LAND15
LIFE ON LAND
0
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PEACE, JUSTICE AND STRONG INSTITUTIONS16
PEACE, JUSTICE AND STRONG INSTITUTIONS
0
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PARTNERSHIPS FOR THE GOALS17
PARTNERSHIPS FOR THE GOALS
0
Research Products
This researcher does not have a Scopus ID.
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Scholarly Output

8

Articles

5

Views / Downloads

2/0

Supervised MSc Theses

0

Supervised PhD Theses

0

WoS Citation Count

26

Scopus Citation Count

29

Patents

0

Projects

0

WoS Citations per Publication

3.25

Scopus Citations per Publication

3.63

Open Access Source

5

Supervised Theses

0

JournalCount
Indian Pediatrics3
International Journal of General Medicine2
Biological Trace Element Research1
International Journal of Environmental Research and Public Health1
Turkish Journal of Biology1
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Has files: falseSubject: cannabinoid

Scholarly Output Search Results

Now showing 1 - 1 of 1
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    Article
    Citation - WoS: 1
    Citation - Scopus: 2
    Cannabinoid Receptor Ligands Modulate Fibrosis and Inflammation in Idiopathic Pulmonary Fibrosis: a Preliminary Study
    (Tubitak Scientific & Technological Research Council Turkey, 2024) Kose, Sevil; Onen, Selin; Gizer, Merve; Boduroglu, Esin; Gonullu, Ugur; Korkusuz, Petek
    Background/aim: No specific pharmacological treatment regimen for idiopathic pulmonary fibrosis (IPF) exists. Therefore, new antiinflammatory therapeutic strategies are needed. Cannabinoids (CBs), known for their inflammation-modulating and antifibrotic effects, may be potential medication candidates for treating IPF. We aim to evaluate the inflammation-modulating and antifibrotic effects of CB receptor (CBR) agonists and antagonists in lipopolysaccharide-stimulated normal human lung fibroblast, epithelial cells, IPF fibroblast cells, and monocytes. Materials and methods: We detected CBRs in normal human lung fibroblasts (LL24) and IPF fibroblast cells (LL29), epithelial cells (A549) and monocytes (THP-1) by flow cytometry. We determined TGF-(31, IL-8, and TNF-alpha inflammatory cytokines in the LL24, LL29, A549, and THP-1 cell culture supernatants on days 1 and 5 by ELISA. We evaluated the cell viability in LL24, LL29, and A549 cells on days 1, 3, and 5 spectrophotometrically and detected collagen Type I (ColI) production in the LL24 and LL29 cell culture supernatants on days 1, 3, and 5 by ELISA. Results: LL24, LL29, A549, and THP-1 cells exhibited CB1 (CB1R) and CB2 (CB2R) receptors. CB1R and CB2R agonists WIN55,2122 and JWH015 inhibited fibroblastic and epithelial cell proliferation on day 5. TGF-(31 and TNF-alpha release increased, while IL-8 release decreased in LL24, LL29, A549, and THP-1 cells in response to the administration of WIN55,212-2 and JWH015 at a 10-2 mM concentration. CB1R and CB2R antagonists AM251 and AM630 did not block agonistic responses, suggesting a nonclassical CBRmediated pathway. CB2R agonist JWH015 decreased ColI expression in IPF lung fibroblasts LL29 on day 3. Conclusion: These results suggest that CB signaling regulates the progression of pulmonary inflammation and fibrosis via CBR activation. This may offer a potential pharmacological tool for developing antifibrosis therapies.