## 4 Discussion
Moreover, AhR signaling may promote the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), whose pathway acts in an antagonist way to the PPAR\(\gamma\) pathway [48]. Our study showed that the expression of \(AlR\) and \(NF\)-\(kB\) mRNA increased after the treatment of the BJ cells with rosigiltazone, but at the same time, the level of \(NF\)-\(kB\) expression decreased in the group exposed to Les-4370. In the CACO-2 cell line, an increase in the level of \(AlR\) mRNA expression was observed after the treatment of the cells with Les-4368, Les-4370, and rosigiltazone, while the level of \(NF\)-\(kB\) expression in the CACO-2 cells decreased after the treatment with Les-4370 and rosigiltazone. Similar results were obtained by [PERSON] et al. who described a decrease in AhR protein expression after BJ cell treatment with (Z)-5-[5-(4-chlorophenylphenyl)-3-phenyl-4,5-dihydroxyrazol-1-ylmethylene]-3-(3-acetoxyphenyl)-2-thioxo-thiazol-4-ones (Les-4369) and (5\({}^{\prime}\)Z)-3\({}^{\prime}\)-(4-chlorophenylphenyl)-5\({}^{\prime}\)[(4-isopropylphenyl)methyl-lene]spiro[indoline-3,2\({}^{\prime}\)-thiazol]-2,4\({}^{\prime}\)-dione (Les-3467). While Les-4369 and Les-3467 increase in AhR protein expression in the A549 cell line [49], studies conducted by [PERSON] et al. showed that Les-2769 and Les-3266 increased the expression of \(NF\)-\(kB\) mRNA in healthy BJ cells and SCC-15 tumor cells [10]. [PERSON] et al. proved that after 14 days of differentiation of rosigiltazone-induced 3T3-L1 cells, there was an increase in the level of \(NF\)-\(kB\) compared to controls [50]. Moreover, [PERSON] et al. showed that similar to our experiments cimilamthiazolidinone hybrid molecules 3-[5-[(Z,2Z)-2- chloro-3-(4-nitrophenyl)]-2-propenylidene]-4-oxo-2-thioxothiazolidin-3-yl]propanoic acid (Les-45) and 5-[2-chloro-3-(4-nitrophenyl)]-2 propenylidene]-2-(3-hydroxyphenyla-mino)thiazol-4(5H)-one (Les-247) decrease in NF-\(\kappa\)B protein expression in BJ cells [51]. Our study showed a statistically significant increase in the level of _NF-\(\kappa\)B_ mRNA expression as a result of the treatment of the BJ cells with rosiglitzazone. Les-4368 caused an increase in the _NF-\(\kappa\)B_ expression in the CACO-2 cells, and rosiglitzazone and Les-4370 decreased the _NF-\(\kappa\)B_ expression. [PERSON] et al. showed that an increase in _NF-\(\kappa\)B_ activation by microparticles (MPs) in A549 was inhibited by PPARy agonists, including rosiglitzazone [52]. Moreover, by interacting with NF-\(\kappa\)B, PPARy may have a pro-apoptotic effect [53]. A study conducted by [PERSON] et al. showed that rosiglitzazone inhibited the NF-\(\kappa\)B signaling pathway in mouse mononuclear macrophage leukemia cells (RAW264.7) treated with lipopolysaccharide-LPS. The activity of the NF-\(\kappa\)B-driven luciferase reporter gene was significantly elevated after LPS induction [54]. Our study has shown that for the treatment of normal BJ and CACO-2 cancer cells, Les-4368, Les-4370, and rosiglitzazone resulted in a decrease in _PPAR\(\gamma\)_ mRNA expression. [PERSON] et al. showed a decrease in the expression of _PPAR\(\gamma\)_ mRNA in SCC-15 and CACO-2 cell lines after exposure to 1 \(\upmu\)M Les-236 [12]. Interestingly, [PERSON] et al. reported that 10 \(\upmu\)M Les-2194, Les-3377, or Les-3640 decreased _PPAR\(\gamma\)_ mRNA expression in the SCC-15 cell line [17]. We showed in the present study that, after 24 h, the PPAR\(\gamma\) protein levels were decreased by the treatment of both BJ and CACO-2 cells with the antagonist (GW9662), the agonist (rosiglitzazone), and Les-4370. In the co-treatment of the BJ and CACO-2 cells with Les-4370 and GW9662, a decrease in the PPAR\(\gamma\) protein levels was observed. The same decrease was observed in Les-4368 and GW9662 co-treatment. Only Les-4368 increased the PPAR protein expression in both tested cell lines. [PERSON] et al.