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Anticancer Effect of Rosiglitazone, a PPAR-γ Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis
[Image: see text] Multiple effects on cancer cells are exerted by the peroxisome proliferator-activated receptor γ (PPAR-γ). Recent studies have shown that rosiglitazone, a synthetic PPAR-γ ligand, inhibits the growth of cells. This research was designed to assess the impact of rosiglitazone on diet...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Chemical Society
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081392/ https://www.ncbi.nlm.nih.gov/pubmed/32201822 http://dx.doi.org/10.1021/acsomega.9b04357 |
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author | Wu, Yanqiao Sreeharsha, Nagaraja Sharma, Sanjay Mishra, Anurag Singh, Avinash Kumar Gubbiyappa, Shiva Kumar |
author_facet | Wu, Yanqiao Sreeharsha, Nagaraja Sharma, Sanjay Mishra, Anurag Singh, Avinash Kumar Gubbiyappa, Shiva Kumar |
author_sort | Wu, Yanqiao |
collection | PubMed |
description | [Image: see text] Multiple effects on cancer cells are exerted by the peroxisome proliferator-activated receptor γ (PPAR-γ). Recent studies have shown that rosiglitazone, a synthetic PPAR-γ ligand, inhibits the growth of cells. This research was designed to assess the impact of rosiglitazone on diethylnitrosamine (DENA)-induced lung carcinogenesis in Wistar rats and to study the underlying molecular mechanism. A total of 40 adult male Wistar rats were separated into four groups as follows: group 1 is known as a control. Group 2 is known as the DENA group (150 mg/kg, i.p.). Group 3 and group 4 denote DENA-induced rats treated with 5 and 10 mg/kg rosiglitazone, respectively. Lipid peroxidation, various antioxidant enzymes, histological perceptions, and caspase-3, Bcl2, and Bax gene expression were measured in lung tissues. Rosiglitazone treatment reverted the DENA-induced changes in the expression of these genes, inflammatory cytokines, and oxidative stress. However, blotting analysis discovered reduced caspase-3 and BAX expressions and elevated Bcl-2 expression in DENA-induced rats. The expression of such proteins causing DENA lung cancer was restored by rosiglitazone therapy. |
format | Online Article Text |
id | pubmed-7081392 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | American Chemical Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-70813922020-03-20 Anticancer Effect of Rosiglitazone, a PPAR-γ Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis Wu, Yanqiao Sreeharsha, Nagaraja Sharma, Sanjay Mishra, Anurag Singh, Avinash Kumar Gubbiyappa, Shiva Kumar ACS Omega [Image: see text] Multiple effects on cancer cells are exerted by the peroxisome proliferator-activated receptor γ (PPAR-γ). Recent studies have shown that rosiglitazone, a synthetic PPAR-γ ligand, inhibits the growth of cells. This research was designed to assess the impact of rosiglitazone on diethylnitrosamine (DENA)-induced lung carcinogenesis in Wistar rats and to study the underlying molecular mechanism. A total of 40 adult male Wistar rats were separated into four groups as follows: group 1 is known as a control. Group 2 is known as the DENA group (150 mg/kg, i.p.). Group 3 and group 4 denote DENA-induced rats treated with 5 and 10 mg/kg rosiglitazone, respectively. Lipid peroxidation, various antioxidant enzymes, histological perceptions, and caspase-3, Bcl2, and Bax gene expression were measured in lung tissues. Rosiglitazone treatment reverted the DENA-induced changes in the expression of these genes, inflammatory cytokines, and oxidative stress. However, blotting analysis discovered reduced caspase-3 and BAX expressions and elevated Bcl-2 expression in DENA-induced rats. The expression of such proteins causing DENA lung cancer was restored by rosiglitazone therapy. American Chemical Society 2020-03-04 /pmc/articles/PMC7081392/ /pubmed/32201822 http://dx.doi.org/10.1021/acsomega.9b04357 Text en Copyright © 2020 American Chemical Society This is an open access article published under an ACS AuthorChoice License (http://pubs.acs.org/page/policy/authorchoice_termsofuse.html) , which permits copying and redistribution of the article or any adaptations for non-commercial purposes. |
spellingShingle | Wu, Yanqiao Sreeharsha, Nagaraja Sharma, Sanjay Mishra, Anurag Singh, Avinash Kumar Gubbiyappa, Shiva Kumar Anticancer Effect of Rosiglitazone, a PPAR-γ Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis |
title | Anticancer Effect of Rosiglitazone, a PPAR-γ
Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis |
title_full | Anticancer Effect of Rosiglitazone, a PPAR-γ
Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis |
title_fullStr | Anticancer Effect of Rosiglitazone, a PPAR-γ
Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis |
title_full_unstemmed | Anticancer Effect of Rosiglitazone, a PPAR-γ
Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis |
title_short | Anticancer Effect of Rosiglitazone, a PPAR-γ
Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis |
title_sort | anticancer effect of rosiglitazone, a ppar-γ
agonist against diethylnitrosamine-induced lung carcinogenesis |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081392/ https://www.ncbi.nlm.nih.gov/pubmed/32201822 http://dx.doi.org/10.1021/acsomega.9b04357 |
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