Combined Modality Therapy ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; methods ; trends ; Neoplasms ; diagnosis ; drug therapy ; therapy ; Phytotherapy ; Treatment Outcome

Dosage Forms ; Drug Carriers ; Drug Delivery Systems ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Nanotechnology

Antineoplastic Agents, Phytogenic ; pharmacology ; therapeutic use ; Apoptosis ; drug effects ; Cyclin-Dependent Kinases ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Gene Expression ; drug effects ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Neoplasms ; drug therapy ; metabolism ; Protein-Tyrosine Kinases ; metabolism ; Signal Transduction

Alkaloids ; pharmacology ; Angiogenesis Inhibitors ; pharmacology ; Antineoplastic Agents, Phytogenic ; pharmacology ; Drugs, Chinese Herbal ; chemistry ; Ginsenosides ; pharmacology ; Humans ; Lymphatic Metastasis ; prevention & control ; Pyrazines ; pharmacology ; Quinolizines

Emodin is one of the main active ingredient of Rheum palmatum, and has anti-inflammatory, anti-bacterial, anti-viral and other effects. In recent years, it arouse concern since it has a significant anti-tumor effect with low toxicity. In this paper we mainly report the anti-cancer effects of emodin according to the studies of the past five years, including four parts such as inhibit tumor growth, inhibit migration and invasion, enhance the efficacy of combination therapy, increase chemosensitivity and attenuated side effects. We hope that our work may provide a reference for further study.
Animals ; Antineoplastic Agents, Phytogenic ; chemistry ; pharmacology ; Emodin ; chemistry ; pharmacology ; Humans ; Neoplasms ; drug therapy

Animals ; Antineoplastic Agents, Phytogenic ; blood ; pharmacology ; Apoptosis ; drug effects ; Breast Neoplasms ; pathology ; Humans ; Liver Neoplasms ; pathology ; Serum ; chemistry ; physiology ; Tumor Cells, Cultured

OBJECTIVETo evaluate the effect of Herba Epimedii Brevicornus (HEB) and prepared Radix Rehmannia (RR), the representative Chinese herbs for warming yang and nourishing yin on glucocorticoid receptor (GR) in GR down-regulated rats.

METHODSThe GR down-regulated model was established by subcutaneous injection of hydrocortisone. Seventy-two SD male rats were randomly divided into four groups: the normal group; the model group (MG) ; the HEB group, and the RR group. And every group was subdivided to 3 batches depending on the time points (the 3rd, 7th and 14th day after modeling) of observation, with 6 rats in each batch. Changes in blood level of corticosterone (GS), as well as protein expression and binding power of GR in splenic lymphocytes at corresponding time points of the batches were determined by RIA and flow cytometry.

RESULTSNo significantly difference was found in blood GS levels of the model group at all the time points, as compared with that of the normal group (P > 0.05), while that in the RR group was significantly lowered at the 14th day, and showed significant difference from that in the model group (P < 0.05). The protein expression and binding power in the model rats were lower than those in normal ones (all P < 0.01), but they were significantly higher on the 7th and 14th day in the RR group (P < 0.01), and on the 14th day in the HEB group higher than those in the model group, respectively (all P < 0.01).

CONCLUSIONBoth HEB and RR, in dosage-form of water decoction, could up-regulate the protein expression and binding power of GR in GR down-regulated model rats, but different in acting time.

Animals ; Corticosterone ; blood ; Disease Models, Animal ; Down-Regulation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Epimedium ; chemistry ; Flow Cytometry ; Hydrocortisone ; pharmacology ; Lymphocytes ; cytology ; drug effects ; metabolism ; Male ; Radioimmunoassay ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, Glucocorticoid ; metabolism ; Rehmannia ; chemistry ; Spleen ; cytology

Animals ; Animals, Newborn ; Brain ; drug effects ; metabolism ; pathology ; Disease Models, Animal ; Excitatory Amino Acid Antagonists ; pharmacology ; therapeutic use ; Female ; Hypoxia-Ischemia, Brain ; drug therapy ; metabolism ; Ketamine ; pharmacology ; therapeutic use ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Treatment Outcome

Clinical trials have demonstrated that arsenic trioxide(As2O3) was effective in the treatment of acute promyelocytic leukemia(APL), based on this facts, studies have been carried out to study its role in the treatment of solid cancer at home and abroad. Primary in vitro study showed that As2O3 could treat the cancer of digestive system such as hepatoma, esophageal carcinoma, gastric cancer, and the cancer of urinary and reproductive system such as cervical cancer, ovarian cancer, bladder transitional carcinoma,as well as lung cancer, breast cancer, prostate cancer, etc. The mechanism of As2O3 actions may be the induction of apoptosis, the inhibition of growth and the promotion of differentiation of solid cancers. This article reviews on As2O3 in treatment of solid cancer.

Objective To observe the expression of bcl-2 gene in cell apoptosis of neonatal rats followed by hypoxic-ischemic brain damage(HIBD) and investigate the mechanism of neuronal apoptosis after HIBD.Methods Fifty-four neonatal SD rats were used in 1 sham-operated group and 8 trial groups. The models of HIBD were established in neonatal rats by inhaling the mixed gases of 92 % N 2 and 8 % O 2, the animals were sacrificed by dislocation their heads at different time points(0.5,1,3,6,12,24,48,72 h), the hippocampus were dissected for morphological analysis. The neuronal apoptosis and the expression of bcl-2 gene in hippocampus were detected by the methods of immunohistochemistry. Results The apoptotic cells appeared at the time point of 3 h, and reached the peak at 48 h, then decreased. The positive cell of bcl-2 protein increased from the time point of 30 min and reached the peak at 6 h and then decreased gradually following HIBD. Conclusion The expression of bcl-2 gene plays a role in the process of neuronal apoptosis following HIBD.