Sumatriptan mitigates bleomycin-induced lung fibrosis in male rats : Involvement of inflammation, oxidative stress and α-SMA
Copyright © 2024 Elsevier Ltd. All rights reserved..
INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung condition that produces symptoms including coughing which may cause by excessive accumulation of scar tissue inflammatory and oxidative stress exacerbation. Sumatriptan, utilized for migraine treatment as a selective 5-HT1B/1D receptor agonist, has demonstrated significant anti-inflammatory and antioxidant properties in multiple preclinical investigations. Operating primarily on serotonin receptors, sumatriptan leverages the diverse physiological functions of serotonin, playing a pivotal role in regulating both inflammation and oxidative stress which is particularly relevant in the context of IPF.
MATERIALS & METHODS: Thirty-five male Wistar rats were divided to five group, including: Sham (without IPF induction), control (BLM 5 mg/kg, intraperitoneally), and three fibrosis group with sumatriptan (0.5, 1, and 3 mg/kg, i.p. for 2 weeks) administration. IPF was induced by injection of BLM (single dose, 5 mg/kg intratracheally). Lung tissues were separated for measurement of myeloperoxidase (MPO) as an oxidative stress hallmark, and tumor necrosis factor-α (TNF-α), interleukin-1β (IL-β), and transforming growth factor-β (TGF-β) as inflammatory markers as well as alpha smooth muscle actin (α-SMA). Also, for histological investigations, tissue damages were assessed by Hematoxylin-eosin (H&E) and Masson's trichrome staining method.
RESULTS: BLM-induced fibrosis could increase α-SMA, MPO, TNF-α, IL-1β, and TGF-β, while treatment with sumatriptan has reversed the α-SMA, MPO, and IL-1β levels. Moreover, the results of H&E and Masson's trichrome staining indicated that sumatriptan (1 and 3 mg/kg) reduced tissue damages, alveolar wall thickness, collagen accumulation, and pulmonary fibrosis induced by BLM.
CONCLUSION: According to the data achieved from this study, Sumatriptan appears to have therapeutic benefits in IPF, possibly via reducing α-SMA as well as inflammation and the toxicity caused by oxidative stress.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:88 |
|---|---|
| Enthalten in: |
Tissue & cell - 88(2024) vom: 12. März, Seite 102349 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Bahramifar, Ayda [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Bleomycin |
|---|
| Anmerkungen: |
Date Revised 16.03.2024 published: Print-Electronic Citation Status Publisher |
|---|
| doi: |
10.1016/j.tice.2024.102349 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM369821076 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM369821076 | ||
| 003 | DE-627 | ||
| 005 | 20240317233427.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240317s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.tice.2024.102349 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1333.xml |
| 035 | |a (DE-627)NLM369821076 | ||
| 035 | |a (NLM)38492426 | ||
| 035 | |a (PII)S0040-8166(24)00050-8 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Bahramifar, Ayda |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Sumatriptan mitigates bleomycin-induced lung fibrosis in male rats |b Involvement of inflammation, oxidative stress and α-SMA |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Revised 16.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status Publisher | ||
| 520 | |a Copyright © 2024 Elsevier Ltd. All rights reserved. | ||
| 520 | |a INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a fibrotic lung condition that produces symptoms including coughing which may cause by excessive accumulation of scar tissue inflammatory and oxidative stress exacerbation. Sumatriptan, utilized for migraine treatment as a selective 5-HT1B/1D receptor agonist, has demonstrated significant anti-inflammatory and antioxidant properties in multiple preclinical investigations. Operating primarily on serotonin receptors, sumatriptan leverages the diverse physiological functions of serotonin, playing a pivotal role in regulating both inflammation and oxidative stress which is particularly relevant in the context of IPF | ||
| 520 | |a MATERIALS & METHODS: Thirty-five male Wistar rats were divided to five group, including: Sham (without IPF induction), control (BLM 5 mg/kg, intraperitoneally), and three fibrosis group with sumatriptan (0.5, 1, and 3 mg/kg, i.p. for 2 weeks) administration. IPF was induced by injection of BLM (single dose, 5 mg/kg intratracheally). Lung tissues were separated for measurement of myeloperoxidase (MPO) as an oxidative stress hallmark, and tumor necrosis factor-α (TNF-α), interleukin-1β (IL-β), and transforming growth factor-β (TGF-β) as inflammatory markers as well as alpha smooth muscle actin (α-SMA). Also, for histological investigations, tissue damages were assessed by Hematoxylin-eosin (H&E) and Masson's trichrome staining method | ||
| 520 | |a RESULTS: BLM-induced fibrosis could increase α-SMA, MPO, TNF-α, IL-1β, and TGF-β, while treatment with sumatriptan has reversed the α-SMA, MPO, and IL-1β levels. Moreover, the results of H&E and Masson's trichrome staining indicated that sumatriptan (1 and 3 mg/kg) reduced tissue damages, alveolar wall thickness, collagen accumulation, and pulmonary fibrosis induced by BLM | ||
| 520 | |a CONCLUSION: According to the data achieved from this study, Sumatriptan appears to have therapeutic benefits in IPF, possibly via reducing α-SMA as well as inflammation and the toxicity caused by oxidative stress | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Bleomycin | |
| 650 | 4 | |a Inflammation | |
| 650 | 4 | |a Oxidative stress | |
| 650 | 4 | |a Pulmonary fibrosis | |
| 650 | 4 | |a Sumatriptan | |
| 700 | 1 | |a Jafari, Razieh Mohammad |e verfasserin |4 aut | |
| 700 | 1 | |a Sheibani, Mohammad |e verfasserin |4 aut | |
| 700 | 1 | |a Manavi, Mohammad Amin |e verfasserin |4 aut | |
| 700 | 1 | |a Rashidian, Amir |e verfasserin |4 aut | |
| 700 | 1 | |a Tavangar, Seyed Mohammad |e verfasserin |4 aut | |
| 700 | 1 | |a Akbariani, Mostafa |e verfasserin |4 aut | |
| 700 | 1 | |a Mohammadi Hamaneh, Amirabbas |e verfasserin |4 aut | |
| 700 | 1 | |a Goudarzi, Ramin |e verfasserin |4 aut | |
| 700 | 1 | |a Shadboorestan, Amir |e verfasserin |4 aut | |
| 700 | 1 | |a Dehpour, Ahmad Reza |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Tissue & cell |d 1969 |g 88(2024) vom: 12. März, Seite 102349 |w (DE-627)NLM000215767 |x 1532-3072 |7 nnns |
| 773 | 1 | 8 | |g volume:88 |g year:2024 |g day:12 |g month:03 |g pages:102349 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.tice.2024.102349 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 88 |j 2024 |b 12 |c 03 |h 102349 | ||