Emodin reduces FFAs-induced fatty degeneration in HepG2 cells via the AMPK/SREBP-1 pathway / 中国医师杂志

Objective To investigate the effects of emodin on the triglyceride metabolism and oxidative stress in steatosis in HepG2 cells and possible underlying mechanisms.Methods The appropriate concentration of emodin on HepG2 cells were detected by methyl thiazolyl tetrazolium (MTT) assay.HepG2 cells were induced to fat overaccumulation by 1 mmol/L free fatty acids (FFA) (oleate∶ palmitate =2∶1).The model group exposed to 10 μmol/L,20 μmol/L,40 μmol/L emodin.The intracellular lipid accumulation was documented by Oil Red O staining and the content of triglyceride and total cholesterol was observed.Reactive oxygen species (ROS) was determined by flow cytometry.Western blotting was performed to analyze the protein levels of adenosine monophosphate-activated protein kinase (AMPK),phosphorylated AMPK,and sterol regulatory element-binding protein 1 (SREBP-1).Results Emodin reduced lipid accumulation and triglycerides (TG) content (P ＜ 0.05).At the same time,it significantly reduced ROS production (P ＜ 0.05).Moreover,the levels of AMPK and p-AMPK protein were significantly upregulated,and SREBP-1 protein was significantly downregulated with the treatment of emodin (P ＜ 0.01).Conclusions This study has demonstrated that emodin can reduce fatty degeneration induced by FFAs in hepatocytes,and this effect may be partially mediated by the AMPK/SREBP-1 pathway.

Effects of emodin on proliferation cycle and apoptosis of human bladder cancer cell line BIU87 / 中国医师杂志

ObjectiveTo study the suppressive role of emodin on the growth and its effect on the proliferation cycle and apoptosis of human bladder cancer cell line BIU87.MethodsThe effect of different concentration of emodin at different time point on cell proliferation of BIU87 were measured with methylthiazole (MTT) chromatometry, the cell proliferation cycle were detected with flow cytometry, expressions of bc1-2 and caspase-3 were detected by SP of immunohistochemistry.ResultsWithin a certain range, the higher concentration of emodin (10 ～ 80 μg/ml) and the longer action time are positive related the more significant inhibition of tumor cell growth and the higher apoptosis rate [(9.84 ± 1.13)％, (18.32 ±2.14)％ ,(29.73+1.42)％ ,(42.13 +2.36)％ ,respectively].Compared with control group [(2.01 ±0.92)％], the differences were statistically significant(F =531.85, P ＜0.01).Emodin could inhibit the proliferation of human bladder cancer cell BIU87 by blocking BIU87 cell in G0/G1 stage, thus cut down cell proportion in stage of S [(33.27 +1.26)％ ,(29.17 ±1.39)％, (16.94 ±0.86)％ ,(10.85 ± 1.47)％,respectively], compared with the control group [(35.45 ± 0.38) ％], the differences were statistically significant(F =524.64, P ＜0.01).After 48 h of emodin treatment, the bc1-2 expression(Grayscale values:122.65 + 2.12,131.37 ± 1.62,134.81 ± 1.36,145.55 ± 2.01, respectively) was decreased and the caspase-3 expression(Grayscale values : 135.26 + 1.41,130.22 ± 1.74,126.11 ± 1.77,118.36 + 1.53, respectively) was increased in a dose dependent manner.Compared with control group (Grayseale values:108.42 + 3.73,149.35 ± 1.82, respectively), the differences were statistically significant (F = 216.23,224.83, P ＜0.01).ConclusionsEmodin could significantly inhibit the growth and induce apoptosis of BIU87 cells in vitro, which may be through down regulation of bc1-2, and up regulation of caspase-3, and blocking BIU87 cell in G0/G1 stage.

Inhibitorv effect of emodin on heterotransplanted human bladder cancer in nude mice and its mechanism / 中国医师杂志

Objective To investigate the inhibitory effect of emodin on hetertransplanted human bladder cancer in nude mice and explore its mechanism.Methods Heterotransplanted models of human bladder cancer cell line BIU87 cells in nude mice were established.The mice were randomly divided into 4 groups during the experiment:blank control group,Z-VAD-FMK group,emodin group and emodin combined with Z-VAD-FMK group.The growth of tumors was observed and the growth curve was mapped.The nude mice were sacrificed 4 weeks later,the tumors were isolated and weighed.The pathological changes of tumor were observed after HE staining,the cells apoptosis were detected with flow cytometry,and the expression of AIF and Endo G were examined by reverse transcription PCR (RT-PCR) and Western blot.Results The tumor growth rate in emodin group was lower than that in the other three groups.The tumor quality in emodin group [(0.41 ± 0.05 ) g] and emodin combined with Z-VAD-FMK group [( 0.69 ±0.07)g]were lighter than that in the other two groups[(1.08 ±0.13,1.04 ±0.09)g,],and the differences were statistically significant( F =90.56,27.49,P ＜0.01 ).The quality difference in emodin group and emodin combined with Z-VAD-FMK group was statistically significant ( t =10.01,P ＜ 0.01 ).The apoptosis rate in emodin group [(42.71 ±2.69)％]was significantly higher than that in emodin combined with Z-VAD-FMK group[(34.38 ± 1.73)％] ( t =6.38,P ＜0.01 ).The expression of AIF and Endo G in emodin combined with Z-VAD-FMK group was significantly increased than other groups [( 1.65 ±0.12)vs(1.24±0.08),(0.51 ±0.07),(0.48 ±0.04);(2.12 ±0.16)vs(1.75 ±0.13),(0.57 ±0.06),(0.59±0.07);(2.42±0.13)vs(1.73 ±0.11),(0.78 ±0.07),(0.75 ±0.08);(3.13 ±0.25)vs(2.15± 0.18 ),(0.85 ± 0.09 ),(0.81 ± 0.14 )],and the differences were significant ( F =303.22,319.32,409.38,258.53,P ＜ 0.01 ).Conclusions Emodin could significantly inhibit the growth of hetertransplanted human bladder cancer in nude mice.The mechanism might be partly due to the expression increase of AIF and Endo G in bladder cancer cells,which might induce apoptosis through Caspase-independent pathway.

Study of aloe-emodin on the apoptosis in systemic scleroderma skin fibroblasts / 中国医师杂志

n Aloe-emodin induced the apoptotic of systemic scleroderma skin fibroblasts and could significantly inhibit the proliferation and collagen synthesis in cultured fibroblasts.