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Anticancer Effect of Rosiglitazone, a PPAR-γ Agonist against Diethylnitrosamine-Induced Lung Carcinogenesis
Yanqiao Wu1, Nagaraja Sreeharsha2, Sanjay Sharma3
1Intensive Care Unit, People's Hospital of Ningjin County, Ningjin County, Shandong province 253400, China.
Abstract:
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.
Insights
Rosiglitazone, a PPAR-γ ligand, effectively inhibited lung cancer growth in rats induced by diethylnitrosamine (DENA). This compound reversed oxidative stress and modulated key protein expressions, offering a potential therapeutic strategy for lung cancer.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Peroxisome proliferator-activated receptor γ (PPAR-γ) influences cancer cell behavior.
- Synthetic PPAR-γ ligands, like rosiglitazone, show promise in inhibiting cancer cell growth.
Purpose of the Study:
- To evaluate rosiglitazone's effect on diethylnitrosamine (DENA)-induced lung carcinogenesis in Wistar rats.
- To elucidate the molecular mechanisms underlying rosiglitazone's anti-cancer activity in this model.
Main Methods:
- Wistar rats were divided into control, DENA-induced, and DENA-induced plus varying doses of rosiglitazone groups.
- Analysis included lipid peroxidation, antioxidant enzymes, histology, and gene/protein expression of caspase-3, Bcl-2, and Bax in lung tissues.
Main Results:
- Rosiglitazone treatment counteracted DENA-induced oxidative stress and inflammatory changes.
- It normalized the expression of genes and proteins involved in apoptosis, restoring a healthier cellular balance.
- Specifically, rosiglitazone reduced pro-apoptotic markers (caspase-3, Bax) and increased anti-apoptotic marker (Bcl-2) expression.
Conclusions:
- Rosiglitazone demonstrates significant anti-lung cancer properties in a DENA-induced rat model.
- The therapeutic effects are mediated through the modulation of oxidative stress and apoptosis-related protein expression.
- This suggests rosiglitazone as a potential therapeutic agent for lung cancer treatment.
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