| Autor: |
Alaaeldin R; Department of Biochemistry, Faculty of Pharmacy, Deraya University, Minia 61111, Egypt., Mohyeldin RH; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Deraya University, Minia 61111, Egypt., Bekhit AA; Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia 61519, Egypt., Gomaa W; Department of Pathology, Faculty of Medicine, Minia University, Minia 61519, Egypt., Zhao QL; Department of Radiology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan., Fathy M; Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia 61519, Egypt.; Department of Regenerative Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama 930-0194, Japan. |
| Jazyk: |
angličtina |
| Zdroj: |
Molecules (Basel, Switzerland) [Molecules] 2023 Jun 09; Vol. 28 (12). Date of Electronic Publication: 2023 Jun 09. |
| DOI: |
10.3390/molecules28124665 |
| Abstrakt: |
Idiopathic pulmonary fibrosis is a progressive, irreversible lung disease that leads to respiratory failure and death. Vincamine is an indole alkaloid obtained from the leaves of Vinca minor and acts as a vasodilator. The present study aims to investigate the protective activity of vincamine against EMT in bleomycin (BLM)-induced pulmonary fibrosis via assessing the apoptotic and TGF-β1/p38 MAPK/ERK1/2 signaling pathways. In bronchoalveolar lavage fluid, protein content, total cell count, and LDH activity were evaluated. N-cadherin, fibronectin, collagen, SOD, GPX, and MDA levels were determined in lung tissue using ELISA. Bax , p53 , bcl2 , TWIST , Snai1 , and Slug mRNA levels were examined using qRT-PCR. Western blotting was used to assess the expression of TGF-β1, p38 MAPK, ERK1/2, and cleaved caspase 3 proteins. H & E and Masson's trichrome staining were used to analyze histopathology. In BLM-induced pulmonary fibrosis, vincamine reduced LDH activity, total protein content, and total and differential cell count. SOD and GPX were also increased following vincamine treatment, while MDA levels were decreased. Additionally, vincamine suppressed the expression of p53 , Bax , TWIST , Snail , and Slug genes as well as the expression of factors such as TGF-β1, p/t p38 MAPK, p/t ERK1/2, and cleaved caspase 3 proteins, and, at the same time, vincamine increased bcl2 gene expression. Moreover, vincamine restored fibronectin, N-Catherine, and collagen protein elevation due to BLM-induced lung fibrosis. In addition, the histopathological examination of lung tissues revealed that vincamine attenuated the fibrotic and inflammatory conditions. In conclusion, vincamine suppressed bleomycin-induced EMT by attenuating TGF-β1/p38 MAPK/ERK1/2/TWIST/Snai1/Slug/fibronectin/N-cadherin pathway. Moreover, it exerted anti-apoptotic activity in bleomycin-induced pulmonary fibrosis. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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