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Aim To study the effect of resveratrol on proliferation of liver cancer SMMC-7721 cells and the relevant mechanism.Methods SMMC-7721 cells were treated with different concentrations of resveratrol.Cell proliferation was tested by cell proliferation assay and colony-forming experiment.The effect of resveratrol on cell cycle of SMMC-7721 cells was detected by flow cytometry.The activation of mTOR/p-mTOR proteins was detected by Western blot.Results Compared with control group, resveratrol inhibited SMMC-7721 cell proliferation in a dose-dependent manner(P<0.01);cell cycle detection showed that SMMC-7721 cells were arrested at G0/G1 phase by resveratrol;Westren blot assay showed that resveratrol down-regulated p-mTOR expression.Conslusion Resveratrol inhibits human SMMC-7721 cell proliferation and arrests the cell cycle at G0/G1 phase, while the inhibition mechanism may be related to activation of mTOR signaling pathway by resveratrol.
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Objective To identify the significance of expression and phosphorylation of protein kinase R(PKR) and nuclear factor NF-κB p65 in cervical lesions, and the effect of high-risk human papilloma virus(hsHPV) on expression and phosphorylation of R(PKR) and NF-κB p65. Methods A total of 67 patients with cervical cancer, 149 patients with cervi-cal intraepithelial neoplasia (CINⅠ-Ⅲ) and 15 normal control were included in this study. The expression levels of PKR, phosphorylated PKR (p-PKR), NF-κB p65 and phosphorylated NF-κB p65 (p-NF-κB p65) were detected by immunohisto-chemical SP method in three groups. Results The positive expression rates of PKR and p-PKR in cytoplasm were signifi-cantly lower in hsHPV positive group than those in hsHPV negative group (27.2% and 11.0% vs 41.1% and 21.1%,χ2 =4.858 and 4.371,P<0.05). The positive expression rates of NF-κB p65 and p-NF-κB p65 in cytoplasm and nucleus were significantly higher in hsHPV positive group than those in hsHPV negative group (46.3%, 25.7%, 22.8% and 12.5% vs 32.6%, 14.7%, 11.6%and 4.2%,χ2=4.345,4.048,4.729 and 4.650 respectively,P<0.05). The positive expression rates of PKR in kytoplasm and karyon were significantly lower in NF-κB p65 (+) group than those in NF-κB p65 (-) group (25.5%vs 38.0%and 20.4%vs 36.3%,χ2=3.898 and 4.396 respectively, P<0.05). The positive expression rate of PKR in kyto-plasm was significantly lower in p-NF-κB p65 (+) group than those in p-NF-κB p65 (-) group (19.0%vs 36.0%,χ2=4.462, P<0.05). Conclusion hsHPV may inhibit the expression and phosphorylation of PKR but promote the expression and phosphorylation of NF-κB p65. The expression and phosphorylation of NF-κB p65 may inhibit the expression of PKR. Regu-lating effects of three may be associated with the generation and progression of cervical cancer.