Oral contraceptive (Ethinylestradiol and Levonorgestrel) modulates the expression of proinflammatory and antioxidant genes in rat tissues

Abstract

Ethinylestradiol/levonorgestrel (E/L), a commonly used hormonal oral contraceptive among women of childbearing age, has been linked to cardiovascular diseases (CVDs). Oxidative stress and inflammation collectively contribute to the initiation and progression of CVDs. This study investigated the impact of E/L on the expression of oxidative stress- and inflammation-associated genes (PON2, TNF-α, and IL-1α). Thirty-two female albino rats were randomly assigned to four groups (n=8 each): Group A (control) received DMSO and distilled water, while Groups B, C, and D were administered graded E/L dosages of 0.015, 0.03, and 0.060 mg/kg body weight, respectively. At the end of the experiment, tissues including the brain, liver, and kidney were harvested for total RNA extraction and purification. Gene expression was assessed by RT-PCR using specific primers. Notably, PON2 was significantly upregulated in the brain but downregulated in the liver and kidney of all E/L-treated animals. Conversely, TNF-α and IL-1α were significantly upregulated in all organs except the liver. Collectively, this study provides preliminary evidence that E/L administration modulates the expression of key genes involved in oxidative stress and inflammation in a tissue-specific manner. These findings underscore the need for further research to elucidate the functional consequences of these changes and their relevance to cardiovascular health.