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1.
Zhongguo Zhong Yao Za Zhi ; 31(2): 141-4, 2006 Jan.
Article in Chinese | MEDLINE | ID: mdl-16570804

ABSTRACT

OBJECTIVE: To study the effect of ursolic acid (UA), apentacyclic triterpene acid, on MCF-7 cell apoptosis, and probable mechanism involved by detecting the expressions of caspase-3 and poly ADP-ribose polymerase(PARP) at protein level. METHOD: MCF-7 cells were cultured with different concentrations of UA. Growth inhibition of UA on MCF-7 cells was evaluated by MTT assay. Cell cycle and sub-G1 peak were performed by FCM. Morphologic changes of UA-treated cells were observed by light microscope. Apoptotic cells with condensed or fragmented nuclei were visualized by Ho 33258 staining by a fluorescence microscope (EX: U. V.). The protein expression of caspase-3 and PARP was analyzed by immunofluorescence cell staining (SABC-Cy3). RESULT: 24 hours after UA treatment, inhibition of MCF-7 cell growth was concentration-dependent. The IC50 value for UA was (22.6 +/- 3.0) micromo x L(-1). Cell cycle anaysis by FCM showed that 50 micromol x L(-1) of UA arrested MCF-7 cell cycle at G0 - G1 phase. Morphological changes of MCF-7 Cells exhibited many of the hallmark features of apoptosis, including chromatin clumps and aggregation and DNA fragmentation. UA increased caspase-3 protein expression. CONCLUSION: The results suggest that UA evokes MCF-7 cell apoptosis is correlation with the up-regulation of caspase-3. Our study indicated that UA might be a potential Chinese medical component for breast neoplasm.


Subject(s)
Apoptosis/drug effects , Breast Neoplasms/enzymology , Caspases/metabolism , Poly(ADP-ribose) Polymerases/metabolism , Triterpenes/pharmacology , Antineoplastic Agents, Phytogenic/pharmacology , Breast Neoplasms/pathology , Caspase 3 , Cell Cycle/drug effects , Cell Line, Tumor , Female , Humans , Ursolic Acid
2.
Acta Pharmacol Sin ; 23(2): 124-8, 2002 Feb.
Article in English | MEDLINE | ID: mdl-11866871

ABSTRACT

AIM: To investigate effects of simvastatin (Sim) on the activities of antioxidant enzymes and angiotensin-converting enzyme in rat myocardium with pressure-overload cardiac hypertrophy. METHODS: Left ventricular hypertrophy (LVH) was induced by partly constricting rat abdominal aorta between the left and right renal artery. Rats were given ig Sim 1.8 and 3.6 mg . kg-1 . d-1 for 8 weeks following 6 weeks aortic constriction. Activities of antioxidant enzymes and angiotensin-converting enzyme, and lipid peroxidation of left ventricular (LV) tissue were determined. RESULTS: Contents of angiotensin II and thiobarbituric acid reactive substances (TBARS), and activity of ACE in LVH group (n = 8) were increased by 163 %, 90 %, and 130 %, respectively (P < 0.01)compared with sham-operated group (n = 7), and were decreased by 30 %, 37 %, and 51 %, respectively (P < 0.01) in high dosage Sim treatment group (n = 9) compared with LVH group. Activities of catalase and glutathione peroxidase of LV tissue in LVH group were decreased by 29 % and 23 % (P < 0.01) compared with sham-operated group, and were increased by 32 % and 22 % (P < 0.01) in high dosage Sim treatment group compared with LVH group. Activity of Cu, Zn-superoxide dismutase (SOD) of LV tissue was increased by 33 % in LVH group compared with sham-operated group. Sim treatment did not significantly affect activity of Cu,Zn-SOD. CONCLUSION: Alteration of redox status in myocardium is associated with cardiac hypertrophy and inhibitory effects of Sim on cardiac hypertrophy in rats model might be linked to its antioxidant effects.


Subject(s)
Antioxidants/pharmacology , Heart/drug effects , Hypertrophy, Left Ventricular/pathology , Myocardium/enzymology , Peptidyl-Dipeptidase A/metabolism , Simvastatin/pharmacology , Superoxide Dismutase/metabolism , Animals , Aorta, Thoracic/pathology , Catalase/metabolism , Constriction , Glutathione Peroxidase/metabolism , Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology , Male , Rats , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism
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