Cytokine Expression in HepG2 Cells and the Effects of Budesonide

Inflammation has been shown to play a crucial role in regulating both the development of cancer and the response to therapy. Several cytokines are associated with inflammation, chronic illness, and subsequent cancer. Anti-inflammatory molecules show promise as a preventative therapy for high-risk populations by targeting inflammation. Glucocorticoids are widely recognized for their potent anti-inflammatory properties, but their therapeutic utility is often associated by the development of substantial adverse effects with prolonged administration. Budesonide, a synthetic glucocorticoid, offers a more favorable therapeutic index. Characterized by reduced systemic bioavailability compared to other glucocorticoids, budesonide demonstrates reduced classic glucocorticoid-induced side effects. Budesonide has been successfully employed in the management of inflammatory conditions such as ulcerative colitis, autoimmune hepatitis, and asthma. This therapeutic profile positions budesonide as a promising candidate for further exploration in various disease states characterized by chronic inflammation. To utilize the anti-inflammatory potential of budesonide, we aimed to determine its suitability as a prophylactic or therapeutic strategy for liver cancer, specifically hepatocellular carcinoma, by investigating its inflammation-modulating effects. We treated liver cancer cells (HepG2) with Lipopolysaccharide (LPS) that induced inflammatory cytokines like tumor necrosis factor (TNF) α and examined the effect of budesonide to suppress the cytokine expression. Our study provides novel insights into the LPS-induced inflammatory pathway in HepG2 cells and assesses the therapeutic potential of budesonide.