Ginsenoside Rg3 suppresses vasculogenic mimicry by impairing DVL3-maintained stemness via PAAD cell-derived exosomal miR-204 in pancreatic adenocarcinoma.

BACKGROUND: Vasculogenic mimicry (VM) is an angiogenesis-independent process that potentially contributes to the poor clinical outcome of anti-angiogenesis therapy in multiple malignant cancers, including pancreatic adenocarcinoma (PAAD). Several studies have shown that ginsenoside Rg3, a bioactive component of ginseng, holds considerable potential for cancer treatment. Our previous work has proved that Rg3 can inhibit VM formation in PAAD. However, its underlying mechanism remains unclear. PURPOSE: To explore the underlying mechanism by which Rg3 affects VM formation in PAAD. METHODS: We first investigated the effects of Rg3 on the cellular phenotypes of two PAAD cell lines (SW-1990 and PCI-35), and the expression of EMT- and stemness-related proteins. SW-1990 cells were adopted to construct xenograft models, and the anti-tumor effects of Rg3 in vivo were validated. Subsequently, we isolated the exosomes from the two PAAD cell lines with Rg3 treatment or not, and explored whether Rg3 regulated VM via PAAD cell-derived exosomes. MiRNA sequencing, clinical analysis, and rescue experiments were performed to investigate whether and which miRNA was involved. Subsequently, the target gene of miRNA was predicted using the miRDB website (https://mirdb.org/), and rescue experiments were further conducted to validate those in vitro and in vivo. RESULTS: Rg3 indeed exhibited excellent anti-tumor effects both in vitro and in vivo, with inhibitory effects on EMT and stemness of PAAD cells. More interestingly, Rg3-treated PAAD cell-derived exosomes suppressed the tube-forming ability of HUVEC and PAAD cells, with a decrease in stemness-related protein expression, indicating that Rg3 inhibited both angiogenesis and VM processes. Subsequently, we found that Rg3 induced the up-regulation of miR-204 in PAAD cell-derived exosomes, and miR-204 alone inhibited tube and sphere formation abilities of PAAD cells like exosomes. Specifically, miR-204 down-regulated DVL3 expression, which was involved in regulating cancer cell stemness, and ultimately affected VM. The in vivo experiments further indicated that Rg3-treated SW-1990 cell-derived exosome-inhibited tumor growth, VM formation, and stemness-related protein expression can be abrogated by DVL3 overexpression. CONCLUSION: Ginsenoside Rg3 increased the PAAD cell-derived exosomal miR-204 levels, which subsequently inhibited its target genes DVL3 expression in the receptor PAAD cells, and the down-regulated DVL3 broke stemness maintenance, ultimately suppressing VM formation of PAAD. Our findings revealed a novel mechanism by which Rg3 exerted its anti-tumor activity in PAAD via inhibiting VM, and provided a promising strategy to make up for the deficiency of anti-angiogenesis therapy in cancer.

Effectiveness of acupuncture for breast cancer related lymphedema: protocol for a single-blind, sham-controlled, randomized, multicenter trial.

BACKGROUND: Although various treatments for breast cancer related lymphedema exist, there is still a need for a more effective and convenient approach. Pilot studies and our clinical observations suggested that acupuncture may be a potential option. This study aims to verify the effectiveness of acupuncture on BCRL and evaluate its safety using a rigorously designed trial. METHODS/DESIGN: Women who are clinically diagnosed as unilateral BCRL, with a 10% to 40% increase in volume compared to the unaffected arm, will be recruited. Following baseline assessment, participants will be randomized to either the real acupuncture group or sham-acupuncture group at a ratio of 1:1, and given a standard real acupuncture or sham-acupuncture treatment accordingly on both arms followed by the same usual care of decongestive therapy. Volume measurements of both arms will be performed for every participant after each treatment. Data collected at baseline and the last session will be used to calculate the primary outcome and secondary outcomes. Other data will be exploited for interim analyses and trial monitoring. The primary outcome is the absolute reduced limb volume ratio. Secondary outcomes are incidence of adverse events and change in quality of life. A t test or non-parameter test will be used to compare the difference between two groups, and assess the overall effectiveness of acupuncture using the SPSS software (version 12). DISCUSSION: This study will help expand our knowledge about the effectiveness of acupuncture on BCRL, and how acupuncture might be used in the management of this condition. Acupuncture may be a promising complement or alternative to conventional lymphedema treatment methods, if its effectiveness is confirmed. TRIAL REGISTRATION: ClinicalTrials.gov NCT02803736 (Registered on October 31, 2016).

Emodin enhances the demethylation by 5-Aza-CdR of pancreatic cancer cell tumor-suppressor genes P16, RASSF1A and ppENK.

5-Aza-2'-deoxycytidine (5-Aza-CdR) is currently acknowledged as a demethylation drug, and causes a certain degree of demethylation in a variety of cancer cells, including pancreatic cancer cells. Emodin, a traditional Chinese medicine (TCM), is an effective monomer extracted from rhubarb and has been reported to exhibit antitumor activity in different manners in pancreatic cancer. In the present study, we examined whether emodin caused demethylation and increased the demethylation of three tumor-suppressor genes P16, RASSF1A and ppENK with a high degree of methylation in pancreatic cancer when combined with 5-Aza-CdR. Our research showed that emodin inhibited the growth of pancreatic cancer Panc-1 cells in a dose- and time-dependent manner. Dot-blot results showed that emodin combined with 5-Aza-CdR significantly suppressed the expression of genome 5mC in PANC-1 cells. In order to verify the effect of methylation, methylation-specific PCR (MSP) and bisulfite genomic sequencing PCR (BSP) combined with TA were selected for the cloning and sequencing. Results of MSP and BSP confirmed that emodin caused faint demethylation, and 5-Aza-CdR had a certain degree of demethylation. When emodin was combined with 5-Aza-CdR, the demethylation was more significant. At the same time, fluorescent quantitative PCR and western blot analysis results confirmed that when emodin was combined with 5-Aza-CdR, the expression levels of P16, RASSF1A and ppENK were increased more significantly compared to either treatment alone. In contrast, the expression levels of DNA methyltransferase 1 (DNMT1) and DNMT3a were more significantly reduced with the combination treatment than the control or either agent alone, further proving that emodin in combination with 5-Aza-CdR enhanced the demethylation effect of 5-Aza-CdR by reducing the expression of methyltransferases. In conclusion, the present study confirmed that emodin in combination with 5-Aza-CdR enhanced the demethylation by 5-Aza-CdR of tumor-suppressor genes p16, RASSF1A and ppENK by reducing the expression of methyltransferases DNMT1 and DNMT3a.

Emodin inhibits angiogenesis in pancreatic cancer by regulating the transforming growth factor-ß/drosophila mothers against decapentaplegic pathway and angiogenesis-associated microRNAs.

Emodin is a traditional Chinese medicine, which has been demonstrated to inhibit the growth of pancreatic cancer cells. However, the underlying molecular mechanisms remain to be elucidated. The present study investigated whether emodin suppresses angiogenesis in pancreatic cancer. A nude mouse pancreatic cancer xenograft model was established using SW1990 human pancreatic cancer cells by surgical orthotopic implantation. Different doses of emodin were injected into the abdominal cavities of the tumor­bearing mouse models and controls three times each week for 2 weeks. The tumors were measured and weighed, the expression of cluster of differentiation 34 was detected using immunochemistry, and microvessel densities were calculated. Reverse transcription­quantitative polymerase chain reaction (RT­qPCR) and western blotting were performed to determine the mRNA and protein expression levels of transforming growth factor (TGF)­ß and drosophila mothers against decapentaplegic (Smad) homologs. The angiogenesis­associated microRNAs (miR), miR­20, miR­155 and miR­210 were assessed by RT­qPCR. A negative dose­dependent association was revealed between treatment with emodin and the volume and weight of tumors and microvessel density. Emodin was associated with lower mRNA and protein expression levels of TGF­ß1 and its downstream target, angiopoietin­like 4, and higher mRNA and protein expression levels of TGF­ß receptor (TßR)I, TßRII and Smad4. Notably, treatment with emodin was associated with lower expression levels of miR­155 and miR­210 and higher expression levels of miR­20b. The present study suggested that treatment with emodin may repress angiogenesis in pancreatic cancer by altering the activities of the TGF-ß/Smad pathway and angiogenesis-associated miR-20b, miR-155, and miR-210.

Involvement of endoplasmic reticulum stress in capsaicin-induced apoptosis of human pancreatic cancer cells.

Capsaicin, main pungent ingredient of hot chilli peppers, has been shown to have anticarcinogenic effect on various cancer cells through multiple mechanisms. In this study, we investigated the apoptotic effect of capsaicin on human pancreatic cancer cells in both in vitro and in vivo systems, as well as the possible mechanisms involved. In vitro, treatment of both the pancreatic cancer cells (PANC-1 and SW1990) with capsaicin resulted in cells growth inhibition, G0/G1 phase arrest, and apoptosis in a dose-dependent manner. Knockdown of growth arrest- and DNA damage-inducible gene 153 (GADD153), a marker of the endoplasmic-reticulum-stress- (ERS-) mediated apoptosis pathway, by specific siRNA attenuated capsaicin-induced apoptosis both in PANC-1 and SW1990 cells. Moreover, in vivo studies capsaicin effectively inhibited the growth and metabolism of pancreatic cancer and prolonged the survival time of pancreatic cancer xenograft tumor-induced mice. Furthermore, capsaicin increased the expression of some key ERS markers, including glucose-regulated protein 78 (GRP78), phosphoprotein kinase-like endoplasmic reticulum kinase (phosphoPERK), and phosphoeukaryotic initiation factor-2 α (phospho-eIF2 α ), activating transcription factor 4 (ATF4) and GADD153 in tumor tissues. In conclusion, we for the first time provide important evidence to support the involvement of ERS in the induction of apoptosis in pancreatic cancer cells by capsaicin.

Antiangiogenic effects of oxymatrine on pancreatic cancer by inhibition of the NF-κB-mediated VEGF signaling pathway.

Oxymatrine, the main alkaloid component in the traditional Chinese herbal medicine Sophora japonica (Sophora flavescens Ait), has been reported to have antitumor properties. However, the mechanisms of action in human pancreatic cancer are not well established to date. In the present study, we investigated the antiangiogenic effects of oxymatrine on human pancreatic cancer as well as the possible mechanisms involved. The results of the cell viability assay showed that treatment of PANC-1 pancreatic cancer cells with oxymatrine resulted in cell growth inhibition in a dose- and time-dependent manner. To investigate the possible mechanisms involved in these events, we performed western blotting and reverse transcription-polymerase chain reaction (RT-PCR) analysis. The results revealed that oxymatrine decreased the expression of angiogenesis-associated factors, including nuclear factor κB (NF-κB) and vascular endothelial growth factor (VEGF). Finally, the antiproliferative and antiangiogenic effects of oxymatrine on human pancreatic cancer were further confirmed in pancreatic cancer xenograft tumors in nude mice. In conclusion, our studies for the first time suggest that oxymatrine has potential antitumor effects on pancreatic cancer via suppression of angiogenesis, probably through regulation of the expression of the NF-κB-mediated VEGF signaling pathway.

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential.

In this study, we investigated the apoptotic effect of emodin on human pancreatic cancer cell line Panc-1 in vitro and in vivo as well as the possible mechanisms involved. In vitro, human pancreatic cancer cell line Panc-1 was exposed to varying concentrations of emodin (0, 10, 20, 40 or 80 µmol/l). Then the mitochondrial membrane potential (MMP) was analyzed by JC-1 staining, cell apoptosis was analyzed by flow cytometry (FCM) and cell proliferation was analyzed by MTT. In vivo, nude mice orthotopically implanted were randomly divided into five groups to receive treatments by different doses of emodin: control group (normal saline 0.2 ml), E10 group (emodin 10 mg/kg), E20 group (emodin 20 mg/kg), E40 group (emodin 40 mg/kg) and E80 group (emodin 80 mg/kg). Each mouse was treated 5 times by intraperitoneal injection of emodin every 3 days. During the treatment, the feeding stuff was recorded. One week after the last treatment, we recorded the body weight and the maximum diameter of tumor in each group before the mice were sacrificed. Then the cell apoptosis of the tumor was tested by TUNEL assay. The results in vitro showed that the MMP of the cells declined and the apoptosis rate increased with the emodin concentration increasing and the cell proliferation of each group was inhibited in a dose- and time-dependent manner by emodin. The feeding stuff curve did not decline significantly in E40 group and the apoptosis rate of the tumor cells in this group was higher than the lower-dose groups. Taken together, our results demonstrate that emodin may induce the pancreatic cancer cell apoptosis via declining the MMP and a moderate dose of emodin improved the living state of the model mice.

Antitumor and apoptosis-promoting properties of emodin, an anthraquinone derivative from Rheum officinale Baill, against pancreatic cancer in mice via inhibition of Akt activation.

Pancreatic adenocarcinoma is one of the most common malignancies worldwide. Gemcitabine is currently the standard first-line chemotherapeutic agent for pancreatic cancer. However, gemcitabine can induce activation of Akt and nuclear factor-κB (NF-κB), which is associated with its chemoresistance. It has been reported that gemcitabine combination therapies result in improved survival outcomes in pancreatic cancer. Therefore, agents that can either enhance the effects of gemcitabine or overcome chemoresistance to the drug are needed for the treatment of pancreatic cancer. Emodin is an active component of Chinese medicinal herbs and can inhibit the activation of Akt and NF-κB. In this study, we investigated whether emodin could enhance the anticancer effect of gemcitabine on pancreatic cancer in vivo. We demonstrated that treatment of gemcitabine combined with emodin efficiently suppressed tumor growth in mice inoculated with pancreatic tumor cells. This treatment paradigm promoted apoptotic cell death and mitochondrial fragmentation. Furthermore, it reduced phosphorylated-Akt (p-Akt) level, NF-κB activation and Bcl-2/Bax ratio, increased caspase-9 and -3 activation, Cytochrome C (CytC) release occurred in combination therapy. Collectively, emodin enhanced the activity of gemcitabine in tumor growth suppression via inhibition of Akt and NF-κB activation, thus promoting the mitochondrial-dependent apoptotic pathway. Therefore, our findings may provide new insights into understanding the pharmacological regulation of emodin on gemcitabine-mediated proapoptosis in pancreatic cancer and may aid in the design of new therapeutic strategies for the intervention of human pancreatic cancers.

[Experimental study on anti-metastasis effect of emodin on human pancreatic cancer].

OBJECTIVE: To investigate the anti-metastasis effect of emodin on the pancreatic cancer in vitro and in vivo. METHOD: Human pancreatic cancer cell line SW1990 was treated with different concentrations of emodin (10, 20, 40 micromol x L(-1)) for 2 h, the effects of emodin on the migration and invasion of SW1990 cells were examined by using wound assay and matrigel counting. Western blot was used to detect the protein expression of NF-kappaB and MMP-9 in SW1990 cells after various concentrations of emodin (10, 20, 40 micromol x L(-1)) treatment for 48 h. Metastatic model simulating human pancreatic cancer was established by orthotropic implantation of histologically intact human tumor tissue into pancreatic wall of nude mice, and then divided into three groups: control group, low-dose emodin group (L-EMO) and high-dose emodin group (H-EMO). Eight weeks after implantation, the presences of metastasis were evaluated respectively after the mice were sacrificed. Immunohistochemistry was used to detect the positive expression of CD34, NF-kappaB and MMP-9 in the tumors. RESULT: Emodin suppressed the migration and invasion of SW1990 cells in a dose-dependent manner. Western bolt assay indicated that emodin down-regulated the expression of NF-kappaB and MMP-9 proteins in SW1990 cells. The incidences of metastasis were decreased significantly in L-EMO group and H-EMO group as compared with that in control group. The percentage of CD34, NF-kappaB and MMP-9-positive cells in the tumors were significantly reduced by the administration of emodin. CONCLUSION: Emodin exerts anti-metastatic activity in pancreatic cancer both in vitro and in vivo, which may be related to down-regulation of NF-kappaB and MMP-9.

Effect of emodin in suppressing acute rejection following liver allograft transplantation in rats.

OBJECTIVE: To investigate the mechanism of action of emodin for suppressing acute allograft rejection in a rat model of liver transplantation. METHODS: Brown Norway (BW) recipient rats of orthotopic liver transplantation (OLT) were divided into three groups, Group A receiving isografting (with BW rats as donor), Group B receiving allografting (with Lewis rats as donor), Group C receiving allografting and emodin treatment (50 mg/kg daily). They were sacrificed on day 7 of post-transplantation, and their hepatic histology, plasma cytokine levels, and T-cell subset expression were detected. RESULTS: Compared with those in Group A, rats: in Group B exhibited severe allograft rejection with a rejection activity index (RAI) of 7.67+/-0.98, extensive hepatocellular apoptosis with an apoptosis index (AI) of 35.83+/-2.32, and elevated plasma levels of interleukin-2 (IL-2), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-alpha), CD4(+) and CD4 CD4(+)/CD8(+) ratio. However, recipients in Group C showed a decrease in histological grade of rejection and hepatocellular apoptosis, as well as a decrease in plasma levels of IL-2, TNF-alpha, CD4(+) and CD4(+)/CD8(+) ratio, but elevated levels of IL-10 as compared with the allograft group. CONCLUSION: Post-OLT acute rejection could be attenuated by emodin, its mechanism of action may be associated with protecting hepatocytes from apoptosis, polarizing the Th 1 paradigm to Th2, and inhibiting the proliferation of CD4(+) T cell in plasma.

[Emodin enhances antitumor effect of gemcitabine in model of SW1990 cell xenograft on athymic mouse].

OBJECTIVE: To evaluate the enhanced effect of gemcitabine by emodin and the possible mechanisms of the enhancement. METHOD: Based on the model of SW1990 cell xenograft on athymic mouse, the mice were randomized to four groups with intraperitoneal (IP) injections of different drugs: group N (injecting 0.9% sodium chloride), group E (emodin, 40 mg x kg(-1)), group G (gemcitabine, 125 mg x kg(-1)), and group E + G (emodin 40 mg x kg(-1) and gemcitabine 80 mg x kg(-1) in combination). The tumor volume, tumor weight and body weight of mice were measured during the drug therapy. The mice were sacrificed one week after last injection of drug. Tunel assay were used used to detect the apoptosis of tumor cells. And immunohistochemistry (IHC) and Western blot (WB) were used to detect the variance of the apoptosis relative protein expression of Bax, Bcl-2, and Cytochrome C . RESULT: One week after the last administration, the mean tumor volume and tumor weight in group E + G were significantly decreased compared to the other groups. Tunel assay showed group E + G presented apparently more apoptosis than the other groups. Immunohistochemistry (IHC) and Western blot (WB) analysis showed the expression of Cytochrome C in cytoplasmin and Bax in group E + G was apparently upregulated while the expression of Bcl-2 was apparently downregulated compared to the other groups. As a result, Bcl-2/Bax ratio was significantly decreased in group E + G. CONCLUSION: Emodin can significantly improve the antitumor effect of gemcitabine on transplanted tumor of SW1990 cell line through apparently enhancing the tumor cell apoptosis by gemcitabine. Downregulation of Bcl-2/Bax ratio and promoting release of Cytochrome C from mitochondria is possibly one of the mechanisms of the augmented apoptosis.

[Inhibitory effect of emodin on the differentiation and maturation of dendritic cells in vitro].

OBJECTIVE: To study the effect of emodin on the differentiation, maturation and function of human dendritic cells (DC) in vitro. METHODS: Cells isolated from human peripheral blood mononuclear cells (PBMCs) were induced to dendritic cells (DC) with recombinant interleukin-4 and recombinant granulocyte-macrophage colony stimulating factor (GM-CSF). Lipopolysaccharide (LPS) and different concentrations of emodin were added respectively in the cultured cells on the 5th and the 7th to obtain mature or immature DCs. The phenotype of DCs ( HLA-DR, CD80, CD86, CD83, CD14, CD11c) and the secretion of interleukin-12 (IL-12) were analyzed by flow cytometry, and the immune-stimulating function of DCs was evaluated by co-culture of DCs and self-T-lymphocytes. RESULTS: The expression rate of CD80 and CD83 in the emodin group were 13.4% +/- 6.6% and 9.3% +/- 2.2% respectively; which were significantly lower than those in the control group (39.3% +/- 8.6% and 30.7% +/- 5.6%), respectively (P<0.05). IL-12 secretion of DCs was lower (1700.44 +/- 1000.21 microg/L vs 4500.60 +/- 1200.6 microg/L) but IL-10 secretion was higher (350.6 +/- 150.2 microg/L vs 230.7 +/- 90.1 microg/L) in the emodin group than in the control group (P<0.05). Mixed lymphocyte culture (MLR) examination showed that emodin could significantly inhibit the stimulation of DCs on self-T-lymphocyte proliferation. CONCLUSION: Emodin could evidently suppress the maturation and immune stimulating function of DCs during their in vitro conversion process.

[Effect of emodin on rejection of liver transplantation in rats].

OBJECTIVE: To investigate the mechanism of Emodin on the role of acute rejection in rat liver transplantation. METHOD: Forty-eight pairs of orthotopic liver transplantation model were established with inbred rats which were randomly divided into 3 groups: Control group (BN --> BN), acute rejection group (Lewis --> BN) and emodin group (Lewis --> BN). Six recipients in each group were randomly collected and contents of TNF-alpha and IL-10 in the peripheral blood were detected with ELISA on Day 1, 3, 5 and 7 separately after transplantation and histopathological evaluation was made to detect the differences among groups after the livers were taken out on day 7. The other 10 in each group were protected to evaluate the animation and life time. RESULT: The average meso-life time in emodin group (25.6 days) is significantly longer (P < 0.05) than acute rejection group (10.9 days). Compared with the acute rejection group, Emodin group shows up less rejection in the histopathological evaluation (P < 0.01), less TNF-alpha (P < 0.05) and a significant up-regulation of IL-10 in the peripheral blood (P < 0.05 after day 3). CONCLUSION: Emodin can inhibit the acute rejection of liver transplantation in rats model effectively and it may play the role with reduction of TNF-alpha and upregulation of IL-10.

[Synergistic effect of emodin and cyclosporine A on rejective reaction against liver graft in rats].

OBJECTIVE: To evaluate the effect of emodin in combination with cyclosporine A (CsA) on rejective reaction against liver graft in rats. METHODS: The LEW-->BN orthotopic liver transplantation rat model was used in the study. A total of 48 rats were divided into 4 groups randomly and equally, after operation they were intraperitoneally injected respectively with normal saline (0.5 mL d(-1), group A); CsA (10.0 mg kg(-1) d(-1), group B); emodin (50.0 mg kg(-1) d(-1), group C); and CsA plus emodin (group D, at the same dose as in B and C). Six rats taken from each group were sacrificed on the 8th day after operation to calculate the rejection active index (RAI) and hepatocyte apoptosis index (AI). The remainder were stopped medication and used for observing the survival time. RESULTS: The inter-group comparisons in mean survival time, RAI and AI showed significant difference in comparing group A with group B, C and D (P <0.01), and those in group D were more obvious than in group B and C (P < 0.05, but showed no significant difference between group B and group C (P > 0.05). CONCLUSION: Administering of emodin combined with CsA after liver transplantation shows a synergistic effect for suppressing acute rejective reaction in rats.

[Effect of emodin on hepatocellular apoptosis following orthotopic liver transplantation in rats].

OBJECTIVE: To evaluate the effect of emodin on hepatocellular apoptosis following orthotopic liver transplantation (OLT) in rats. METHOD: The LEW --> BN OLT models were established. A total of 24 rats were divided randomly and equally into 4 groups. Group A was treated with normal saline at dose of 0.5 mL x d(-1) intraperitoneally from 1st day to 8 th day after operation. Group B, CsA at dose of 10.0 mg x kg(-1) x d(-1). Group C, emodin at dose of 50.0 mg x kg(-1) x d(-1). Group D, CsA at dose of 10.0 mg x kg(-1) x d(-1) and emodin at dose of 50.0 mg x kg(-1) x d(-1). Fifteen days after operation, rejection active index (RAI) and hepatocellular apoptosis index (AI) was confirmed after observing the pathologic change of transplanted liver in recipients. RESULT: Respectively, the RAI of group A, B, C, D was 7.67 +/- 0.98, 5.17 +/- 0.40, 5.83 +/- 0.75, 3.83 +/- 0.75 and the AI of group A, B, C, D was 35.83 +/- 2.320, 15.83 +/- 1.33, 16.50 +/- 2.35, 11.50 +/- 1.05. The RAI and AI of group B, C, D was significantly lower than group A (P < 0.01) and group D was significantly lower than group B, C too (P < 0.05). There was no significant distinction between group B and C in RAI and AI. CONCLUSION: Emodin has the effect of reduce the hepatocellular apoptosis following OLT in rats and the effect can stronger by CsA.

[Experimental advance of applying emodin for prevention and treatment of liver diseases].

The experimental researches of applying emodin for prevention and treatment of liver diseases in recent years were reviewed. Emodin can inhibit the growth of liver tumor cells in vitro and in vivo, inducing cell apoptosis is one of its mechanisms. Emodin also has the effects of liver protection, anti-liver fibrosis, and so on, the mechanisms for those effects still need more studies.