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In present study, we showed that the mRNA and protein levels of HO-1 and Hsp70 in solanesol-treated L02 cells were significantly increased. The induction of the HO-1 by solanesol is majorly achieved via enhancing the nuclear translocation and transactivity of Nrf2 through enhancement of Hsp90-Keap1 interaction, while solanesol-elevated Hsp70 is related with promoting the nuclear translocation of HSF1 through the involvement of chaperones interaction. Furthermore, the induction of HO-1 and Hsp70 by solanesol could protect against ethanol-induced liver injury, including significantly suppressing the elevation of the activities of LDH and AST, attenuating ethanol-induced increase of the MDA, ROS level and decrease of the GSH level. Moreover, solanesol also suppressed ethanol-induced apoptosis of L02 cells by inhibition of nuclear morphological damage, procaspase 3 and cleavage of caspase 3 and PARP, suggesting solanesol may be beneficial against ALD. Solanesol also promoted tBHQ-mediated protective effects. However, treatment cells with SnPP or PES markedly abrogated the protective effects of solanesol on ethanol-induced cell injury. These results strongly suggested that solanesol could protect ethanol-induced L02 cell damage, which might be attributed to the activation of HO-1 and Hsp70., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

The current study aimed to identify the effect and primary mechanism of Curcumol on the migration of nasopharyngeal carcinoma (NPC) cells in vitro and in vivo. Curcumol was dissolved in absolute ethyl alcohol and the experiment was performed in NPC 5‑8F cells in vitro and in vivo. The effect of different concentrations of Curcumol on cell migration was determined using wound healing and Transwell assays. A cell counting kit‑8 (CCK‑8) assay was also performed in order to determine cell viability. Flow cytometry was used to detect the effect of Curcumol on apoptosis. The expression of epithelial‑mesenchymal transition (EMT)‑associated proteins and genes was evaluated by western blotting, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and ELISA. In addition, the antitumor activity of Curcumol was investigated in female BALB/C nude mice with orthotopic tumor implants. The results indicated that cell apoptosis was increased and the viability of NPC 5‑8F cells was decreased following treatment with Curcumol at doses of 0.1, 0.2 and 0.4 μM/ml. The results of in vivo experiments indicated that tumor growth and weight were decreased following Curcumol administration. Furthermore, the results of western blotting and RT‑qPCR demonstrated that Curcumol altered the level of E‑cadherin and N‑cadherin in a dose‑dependent manner in vivo. Curcumol also regulated the secretion of protein markers in the serum that were associated with EMT and TGF‑β1 in the 5‑8F xenograft mouse model. Thus, the results indicated that Curcumol induced TGF‑β1‑mediated EMT arrest by regulating E‑cadherin and N‑cadherin, which may prevent further development of NPC. [ABSTRACT FROM AUTHOR]