Anticancer mechanism of troxerutin via targeting Nrf2 and NF-κB signalling pathways in hepatocarcinoma cell line

Thomas, Nisha Susan; George, Kiran; Selvam, Athavan Alias Anand

doi:10.1016/j.tiv.2018.10.018

Cited by 29 publications

(18 citation statements)

References 46 publications

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“…Our results show that TRX can modulate several signaling pathways that have important roles in the regulation of various BPs. Consistent with the bioinformatic data obtained in the present study, some previous studies regarding the mechanisms underlying TRX-regulated pharmacological effects have confirmed several TRX targets and TRX-related signalling pathways [38–40]. We found that both SRC and Akt were predicted to be possible direct protein targets of TRX according to the PharmMapper and idTarget servers, and the insulin signaling pathway (KEGG ID: 4910) was also enriched in the pathway analysis performed using STRING.…”

Section: Discussionsupporting

confidence: 91%

Combining an in silico approach with an animal experiment to investigate the protective effect of troxerutin for treating acute lung injury

Liu

et al. 2019

BMC Complement Altern Med

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Background Troxerutin (TRX), a naturally occurring flavonoid in various fruits, has been reported to exhibit numerous pharmacological and biological activities in vitro and in vivo. However, the molecular mechanisms underlying TRX as a treatment for disease are poorly understood. Methods Using pharmacophore mapping and inverse docking, a set of potential TRX target proteins that have been associated with multiple forms of diseases was obtained. Bioinformatic analyses were performed using the Enrichr and STRING servers to analyse the related biological processes and protein-protein networks. Furthermore, we investigated the potential protective effect of TRX against lipopolysaccharide-induced acute lung injury (ALI) using a mouse model. Morphological changes in the lungs were assessed using haematoxylin and eosin staining. Inflammatory cytokines, tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-10 were investigated using ELISA. Activation of MAPK and NF-κB was detected using western blotting. Results Our network pharmacology analysis revealed the existence of multiple TRX-related chemical-target interactions and the related biological processes. We found that pretreatment with TRX protected against histological changes and obviously regulated the inflammatory cell counts and inflammatory cytokine levels in bronchoalveolar lavage fluid. Based on bioinformatic and western blot analyses, TRX may exert a protective effect against ALI by inhibiting MAPK and NF-κB signalling. Conclusions TRX can ameliorate pulmonary injury by inhibiting the MAPK and NF-κB signalling pathways and has a potential protective effect against ALI. This study may be helpful for understanding the mechanisms underlying TRX action and for discovering new drugs from plants for the treatment of ALI. Electronic supplementary material The online version of this article (10.1186/s12906-019-2515-7) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 91%

Combining an in silico approach with an animal experiment to investigate the protective effect of troxerutin for treating acute lung injury

Liu

et al. 2019

BMC Complement Altern Med

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“…The redox imbalance, caused by over-accumulation of ROS, is responsible for the transfer of Nrf2 from cytoplasm to nucleus, where it controls the expression of its downstream proteins, such as SOD-1/-2 and HO-1 [36]. This process is involved in cancer cell apoptosis [67], which has been also reported in our separate experiments [68]. Taxifolin curbs the carcinogenesis of 1,2-dimethyl hydrazine induced colon cells, leading to their apoptosis by activating the Nrf2 signaling pathway [69].…”

Section: Discussionmentioning

confidence: 99%

The anti-carcinogenesis properties of erianin in the modulation of oxidative stress-mediated apoptosis and immune response in liver cancer

Zhang

Wang

et al. 2019

Aging

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In this study, erianin was found to reduce the viability of cancer cells, inhibit their proliferation and migration, induce G2/M phase arrest, enhance cancer cell apoptosis, promote an increase in levels of intracellular reactive oxygen species and a decrease in mitochondrial membrane potential, and regulate the expression levels of anti- and pro-apoptosis-related proteins in HepG2 and SMMC-7721 cells. Erianin inhibited tumor growth in HepG2- and SMMC-7721-xenograft tumor nude mouse models, reduced the expression levels of anti-apoptosis proteins and enhanced the expression levels of pro-apoptosis proteins in tumor tissues. Erianin inhibited tumor growth in immunosuppressed BALB/c mice bearing heterotopic tumors. Among 111 types of cytokines detected in proteome profiling of tumor tissues, erianin substantially influenced levels of 38 types of cytokines in HepG2-xenografted tumors and of 15 types of cytokines in SMMC-7721-xenografted tumors, most of which are related to immune functions. Erianin strongly affected the serum levels of cytokines, and regulated the activation of nuclear factor-kappa B (NF-κB), and the expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream proteins in spleen. The anti-liver cancer properties of erianin were found to be related mostly to its modulation of oxidative stress-mediated mitochondrial apoptosis and immune response.

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“…Nrf-2 is a pleiotropic protein and a key antioxidant sensor. The activation of this protein is crucial for cellar hemostasis [24–27]. Under physiological conditions, Nrf-2 is bound to its natural inhibitor Keap-1 in the cytoplasm.…”

Section: Discussionmentioning

confidence: 99%

Milk Fat Globule-Epidermal Growth Factor-Factor 8 Reverses Lipopolysaccharide-Induced Microglial Oxidative Stress

Li¹,

Cai

et al. 2019

Oxidative Medicine and Cellular Longevity

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Oxidative stress plays an important role in various neurological disorders. Milk fat globule-epidermal growth factor-factor 8 (MFG-E8) is a regulatory protein for microglia. However, its involvement in microglial oxidative stress has not been established. In this study, we observed microglial oxidative stress in response to lipopolysaccharide (LPS) both in vitro and in vivo. LPS induced significant elevation of TNF-α, IL-6, MDA, and ROS and reduction of GSH and SOD in the mouse brains and primary microglia, which were reversed by MFG-E8 pretreatment. MFG-E8 induced the expression of Nrf-2 and HO-1 that was reduced by LPS incubation. Moreover, LPS-increased Keap-1 expression was reversed by MFG-E8. But the above tendencies were not seen when MFG-E8 was applied alone. The current study established the involvement of MFG-E8 in antioxidant effects during neuroinflammation. It may achieve the effects through the regulation of Keap-1/Nrf-2/HO-1 pathways.

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Anticancer mechanism of troxerutin via targeting Nrf2 and NF-κB signalling pathways in hepatocarcinoma cell line

Cited by 29 publications

References 46 publications

Combining an in silico approach with an animal experiment to investigate the protective effect of troxerutin for treating acute lung injury

Combining an in silico approach with an animal experiment to investigate the protective effect of troxerutin for treating acute lung injury

The anti-carcinogenesis properties of erianin in the modulation of oxidative stress-mediated apoptosis and immune response in liver cancer

Milk Fat Globule-Epidermal Growth Factor-Factor 8 Reverses Lipopolysaccharide-Induced Microglial Oxidative Stress

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