ABSTRACT
The research investigated the effect of Patrinia heterophylla Bunge (Valerianaceae) polysaccharides (PHB-P1) on U14-bearing mice. The tumor weight of mice treated with PHB-P1 (30, 60 mg/kg body weight) was significantly lower than that of the control group, a decrease of serum lactate dehydrogenase (LDH) activity was observed, and the serum alkaline phosphatase (AKP) level was increased slightly. The number of apoptotic tumor cells was significantly increased in the mice by treatment of PHB-P1 (30, 60 mg/kgbw). Cell cycle analysis showed the accumulation of tumor cells in the G2/M phase and a relative decrease of the S phase. By the immunohistochemical analysis, PHB-P1 (30, 60 mg/kgbw) might up-regulate the expression of p53 and Bax, and significantly inhibited the expression of Bcl-2 in tumor tissues. In conclusion, PHB-P1 could inhibit tumor growth and induce tumor cell apoptosis.
Subject(s)
Antineoplastic Agents, Phytogenic/therapeutic use , Carcinoma/drug therapy , Patrinia/chemistry , Phytotherapy , Plant Extracts/therapeutic use , Polysaccharides/therapeutic use , Uterine Cervical Neoplasms/drug therapy , Animals , Antineoplastic Agents, Phytogenic/chemistry , Antineoplastic Agents, Phytogenic/isolation & purification , Antineoplastic Agents, Phytogenic/pharmacology , Apoptosis/drug effects , Carcinoma/blood , Carcinoma/pathology , Cell Cycle/drug effects , Cell Line, Tumor , Dose-Response Relationship, Drug , Down-Regulation/drug effects , Drug Screening Assays, Antitumor , Female , Mice , Plant Extracts/chemistry , Plant Extracts/isolation & purification , Plant Extracts/pharmacology , Polysaccharides/chemistry , Polysaccharides/isolation & purification , Polysaccharides/pharmacology , Proto-Oncogene Proteins c-bcl-2/metabolism , Random Allocation , Tumor Burden/drug effects , Tumor Suppressor Protein p53/metabolism , Up-Regulation/drug effects , Uterine Cervical Neoplasms/blood , Uterine Cervical Neoplasms/pathology , bcl-2-Associated X Protein/metabolismABSTRACT
Jinding laying ducks (n = 648) were subjected to one of six dietary treatments (0, 1, 5, 25, 50, or 100 mg of melamine/kg of diet) to investigate the toxicity of melamine and determine the melamine residue in eggs. Ducks were fed melamine-supplemented diets for 21 days followed by a 21 day withdrawal period. Dietary melamine had no adverse effects on laying performance. Renal lesions were correlated with increasing levels of dietary melamine. Melamine residue in eggs increased with dietary melamine during the first 21 days and reached the maximum content (1.35 mg/kg) in the 100 mg of melamine/kg of diet group. Melamine residue in eggs decreased rapidly during the withdrawal period. The depletion time for egg melamine residue increased with dietary melamine level. These results indicated that a dietary level of > or = 50 mg of melamine/kg of feed induces obvious renal injury. The residue level and withdrawal time for melamine clearance in eggs correlated with the dietary melamine level.
Subject(s)
Diet , Ducks , Eggs/analysis , Oviposition/drug effects , Triazines/toxicity , Animals , Dose-Response Relationship, Drug , Female , Kidney/drug effects , Kidney/pathology , Liver/drug effects , Liver/pathologyABSTRACT
The aim of our study was to investigate the effect of Patrinia scabra Bunge polysaccharide (PSB-P2) on cervical cancer cell (U14)-bearing mice. The tumor weight of mice treated with PSB-P2 (40, 80 mg/kg b.w.) was significantly lower than that of the control group and serum lactate dehydrogenase (LDH) activity was decreased, while serum alkaline phosphatase (AKP) level was only changed slightly. Meanwhile, the number of apoptotic tumor cells was significantly increased in the mice by the treatment of PSB-P2 (40, 80 mg/kg b.w.). At the same time, cell cycle analysis showed the accumulation of tumor cells in the G0/G1 phase and a relative decrease in the S phase. On the other hand, using the reverse transcription-polymerase chain reaction (RT-PCR) assay, PSB-P2 (40, 80 mg/kg b.w.) showed the up-regulation of p53 and Bax, and significant inhibition of Bcl-2 in tumor tissues. It suggests a possible mechanism of the inhibitory effect of PSB-P2 on tumor growth.