Wu Yanqiao, Sreeharsha Nagaraja, Sharma Sanjay, Mishra Anurag, Singh Avinash Kumar, Gubbiyappa Shiva Kumar
Intensive Care Unit, People's Hospital of Ningjin County, Ningjin County, Shandong province 253400, China.
Department of Pharmaceutical Sciences, College of Clinical Pharmacy, King Faisal University, Al-Ahsa 31982, Saudi Arabia.
ACS Omega. 2020 Mar 4;5(10):5334-5339. doi: 10.1021/acsomega.9b04357. eCollection 2020 Mar 17.
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.
过氧化物酶体增殖物激活受体γ（PPAR-γ）对癌细胞具有多种作用。最近的研究表明，罗格列酮，一种合成的PPAR-γ配体，可抑制细胞生长。本研究旨在评估罗格列酮对二乙基亚硝胺（DENA）诱导的Wistar大鼠肺癌发生的影响，并研究其潜在的分子机制。总共40只成年雄性Wistar大鼠被分为以下四组：第1组为对照组。第2组为DENA组（150mg/kg，腹腔注射）。第3组和第4组分别表示用5mg/kg和10mg/kg罗格列酮治疗的DENA诱导大鼠。测定肺组织中的脂质过氧化、各种抗氧化酶、组织学观察以及半胱天冬酶-3、Bcl2和Bax基因表达。罗格列酮治疗逆转了DENA诱导的这些基因、炎性细胞因子和氧化应激表达的变化。然而，印迹分析发现DENA诱导的大鼠中半胱天冬酶-3和BAX表达降低，Bcl-2表达升高。罗格列酮治疗恢复了导致DENA肺癌的此类蛋白质的表达。
