Kazak, FilizYarim, Gul FatmaAnadol, ElvanSalt, Ayris2024-09-182024-09-1820240372-54801331-8055https://doi.org/10.24099/vet.arhiv.2025https://hdl.handle.net/20.500.12483/9358In metabolic syndrome, activated inflammatory signaling pathways trigger the release of proinflammatory cytokines. Nowadays, the use of natural bioactive compounds is trending as an alternative method for the treatment and management of metabolic syndrome. This study aimed to assess the potential effects of hesperidin in the metabolic syndrome model by analyzing the proinflammatory and anti-inflammatory cytokines in serum and liver. Rats were divided into 4 groups: Control (Rats were fed a standard chow diet and water ad libitum), hesperidin [Rats were fed hesperidin supplemented standard chow diet (1%, 10 g/kg feed) and water ad libitum] metabolic syndrome (Rats were fed standard chow diet with 10% fructose-added-drinking-water), and metabolic syndrome + hesperidin (Rats were fed a hesperidin-added standard chow diet (1%, 10 g/kg) with 10% fructose-added-drinking-water). Rats were sacrificed under ketamine/xylazine anesthesia, blood was obtained and liver tissues were removed. Tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, interleukin-10, and transforming growth factor-beta in the serum and liver were measured by enzyme-linked immunosorbent assay. In the metabolic syndrome group, higher tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-6, but lower serum and liver interleukin-10 and transforming growth factor-beta were found in the serum and liver compared to the control group. In addition, in the metabolic syndrome + factor-beta were found in the serum and liver compared to the metabolic syndrome groups. Consequently, hesperidin response in the metabolic syndrome rat model.eninfo:eu-repo/semantics/openAccesscytokinehesperidininsulin resistance syndromeliverratArticle941677610.24099/vet.arhiv.20252-s2.0-85190978498Q4WOS:001167998500001N/A