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Background: Receptor-interacting protein kinase-1 (RIPK1) is an important protein in hepatocellular carcinoma (HCC) pathogenesis. Hesperidin (Hes) is a natural product found in citrus species and is believed to have an anti-cancer effect. Aims: This research was planned to elucidate the protective influence of Hes on the RIPK1 pathway in thioacetamide (TAA)-induced HCC. Materials and methods: HCC was induced in male Sprague Dawley rats using TAA and Hes was administered orally. Liver function tests, oxidative stress status, and antioxidant markers were evaluated. Histopathological examination of hepatic tissues was carried out by staining with hematoxylin and eosin stains. The protein level of RIPK1 was quantified by ELISA. Results: Hes exerted a hepatoprotective effect by significantly improving liver functions and oxidative stress status. This was supported by the integrity preservation of the liver tissues, which was indicated by histopathological examination. Moreover, Hes significantly increased the hepatic RIPK1 protein level. Conclusion: These results reveal that, Hes protected against HCC by decreasing oxidative stress and upregulation of RIPK1 protein level. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC) is one of the most common cancers, associated with a high rate of mortality. A disturbance between cell proliferation and cell death is one of the cancer hallmarks including HCC. Cell proliferation is mainly controlled by the cell cycle. The arrest of the cell cycle is one of the important targets of anticancer agents., Objectives: The present study tries to clarify the exact role of some natural products such as daidzein (DAZ) and alcoholic chicory leaf extract (CE), as possible regulators of cell cycle and apoptosis., Methods: HCC in rats was induced using diethylnitrosamine (DENA). Ninety rats were allocated and divided equally into nine groups, treated with CE, DAZ, a combination of both, and sorafenib with non-treated control groups., Results: Treatment with CE, DAZ, and their combination significantly downregulated hepatic tissue expression of cyclin D1/CDK4 axis as well as cyclin A/CDK2 axis. The suggested therapeutic protocol inhibited the proliferation and dampened Bcl-2 expression. Furthermore, the efficiency of combining CE and DAZ demonstrated a potency comparable to sorafenib in terms of cyclin D/CDK4 axis expression, as well as; this combination protocol was more potent in revealing a potentiated inhibitory effect on cyclin A and Ki-67 expression., Conclusion: Treatment with DAZ or CE alone, or in combination, could possess an inhibitory effect on hepatocarcinogenesis via cell cycle arrest, inhibition of proliferation through suppression of Ki-67 expression, and apoptosis induction, mediated by downregulation of Bcl-2., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)