OBJECTIVETo investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro.

METHODSCultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80 µmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1% DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment.

RESULTSEmodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time- and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05).

CONCLUSIONEmodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.

Carcinoma, Squamous Cell ; pathology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; drug effects ; Cyclin E ; metabolism ; Cyclin-Dependent Kinase 2 ; metabolism ; Cyclin-Dependent Kinase Inhibitor p21 ; metabolism ; Emodin ; pharmacology ; Humans ; Mouth Neoplasms ; pathology ; Oncogene Proteins ; metabolism ; Signal Transduction

Objective:To investigate influences of ginsenoside Rg1 regulating miR-144-3p on neuroinflammation and blood-brain barrier damage in rats with experimental cerebral hemorrhage,and its regulation on formyl peptide receptor 2(FPR2)/p38 path-way.Methods:Ninety SD rats were randomly divided into control group,cerebral hemorrhage group,ginsenoside Rg1 low-dose group(10 mg/kg),ginsenoside Rg1 high-dose group(40 mg/kg),ginsenoside Rg1 high-dose+ago-miR-144-3p group(40 mg/kg ginseno-side Rg1+ago-miR-144-3p),with 18 mice in each group.Except for control group,experimental intracerebral hemorrhage rat model was constructed by injecting collagenase Ⅱ into right caudate nucleus,and then each group was given intraperitoneal administration and intracerebral injection as required.Neurological damage in rats was scored;rat brain water content was determined by dry-wet spe-cific gravity method;levels of TNF-α,IL-6 and IL-1β in rat brain tissues homogenate were determined by ELISA;ultrastructure around cerebral edema was observed by electron microscope;permeability of blood-brain barrier in rats was determined by Evans blue(EB)method;expressions of miR-144-3p/FPR2/p38 pathway were determined by qRT-PCR and Western blot.Results:Compared with control group,blood-brain barrier damage was aggravated in cerebral hemorrhage group,neurological function damage score,brain water content,miR-144-3p,TNF-α,IL-6,IL-1β,p38 mRNA,p-p38/p38 expressions in brain homogenate were increased(P<0.05),FPR2 mRNA and protein expressions were decreased(P<0.05);compared with cerebral hemorrhage group,blood-brain barrier damage was reduced in ginsenoside Rg1 low-dose group and ginsenoside Rg1 high-dose group,neurological function damage score,brain water content,miR-144-3p,TNF-α,IL-6,IL-1β,p38 mRNA,p-p38/p38 expressions in brain homogenate were decreased(P<0.05),FPR2 mRNA and protein expressions were increased(P<0.05);ago-miR-144-3p was able to reverse protective effects of gin-senoside Rg1 on blood-brain barrier and neuroinflammation in rats(P<0.05).Conclusion:Ginsenoside Rg1 may inhibit blood-brain barrier damage and neuroinflammation in rats by regulating miR-144-3p/FPR2/p38 axis.