title: Emodin induces Panc-1 cell apoptosis via declining the mitochondrial             membrane potential.
abstract: 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.
authors.affiliation: Department of Hepatobiliary-Pancreatic Surgery, The Second Affiliated Hospital of Wenzhou Medical College,Wenzhou 325027, PR China.
authors.forename: Jin-Xiang
authors.initials: JX
authors.lastname: Liu
authors.forename: Jian-Hong
authors.initials: JH
authors.lastname: Zhang
authors.forename: Hong-Hai
authors.initials: HH
authors.lastname: Li
authors.forename: Fu-Ji
authors.initials: FJ
authors.lastname: Lai
authors.forename: Kang-Jie
authors.initials: KJ
authors.lastname: Chen
authors.forename: Hui
authors.initials: H
authors.lastname: Chen
authors.forename: Jiang
authors.initials: J
authors.lastname: Luo
authors.forename: Hong-Chun
authors.initials: HC
authors.lastname: Guo
authors.forename: Zhao-Hong
authors.initials: ZH
authors.lastname: Wang
authors.forename: Sheng-Zhang
authors.initials: SZ
authors.lastname: Lin
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D004435:Eating; D004642:Emodin / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D010190:Pancreatic Neoplasms / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D004365:Drugs, Chinese Herbal; D047428:Protein Kinase Inhibitors; D004642:Emodin