AIM　DDT1 MF-2 hamster smooth muscle cells were used to investigate the role of α1B-adrenoceptor (AR) in the cell proliferation and its signaling pathway. METHODS　DNA synthesis was measured by ［3H］thymidine (TdR) incorporation and the cell cycle was determined by flow cytometry. The actions of several inhibitors and activators of second messenger on NE-induced DNA synthesis were investigated. RESULTS　NE (0.1～1 μmol*L-1) elicited significant concentration-dependent stimulation of DDT1 MF-2 cell proliferation. The proliferative effect caused by α1B-AR was blocked by PLC inhibitor (U73122, 10 μmol*L-1), Ca2+/ATPase inhibitor (cyclopiazonic acid, 10 μmol*L-1), intracellular Ca2+ chelator (BAPTA/AM, 10 μmol*L-1), PKC inhibitors (RO-31-8220, 0.1 μmol*L-1 and calphostin C, 0.1 μmol*L-1), TK inhibitors (tyrphostin A25, 10 μmol*L-1 and genistein, 10 μmol*L-1), and MEK1/2 inhibitor (PD 98059, 10 μmol*L-1). CONCLUSION　α1B-AR subtypes stimulate DDT1 MF-2 cells growth and its signal pathway is related to the PLC activation、Ca2+ release、PKC、TK and ERKs activation.

The inhibitory effects of total glucosides of Moutan Cortex (TGM) and to talglucosides of Paeony Lactiflora (TGP) on osmotic hemolysis and oxidative hemolysis induced by hydrogen peroxide were studied. TGM at lower concentration and TGP could inhibit osmotic hemolysis significcantly, but higher concentration (100mg ? L-1) of TGM had a hemolytic activity. TGM and TGP could inhibit hemolysis induced by H2O2 significantly,but TGM was more effective than TGP. TGM .TGP and Vit E all could inhibit lipid peroxidation and glutathione depletion, induced by H2O2, on erythrocytes.

AIM DDT1 MF 2 hamster smooth muscle cells were used to investigate the role of ? 1B adrenoceptor (AR) in the cell proliferation and its signaling pathway. METHODS DNA synthesis was measured by [ 3H]thymidine (TdR) incorporation and the cell cycle was determined by flow cytometry. The actions of several inhibitors and activators of second messenger on NE induced DNA synthesis were investigated. RESULTS NE (0 1～1 ?mol?L -1 ) elicited significant concentration dependent stimulation of DDT1 MF 2 cell proliferation. The proliferative effect caused by ? 1B AR was blocked by PLC inhibitor (U73122, 10 ?mol?L -1 ), Ca 2+ /ATPase inhibitor (cyclopiazonic acid, 10 ?mol?L -1 ), intracellular Ca 2+ chelator (BAPTA/AM, 10 ?mol?L -1 ), PKC inhibitors (RO 31 8220, 0 1 ?mol?L -1 and calphostin C, 0 1 ?mol?L -1 ), TK inhibitors (tyrphostin A25, 10 ?mol?L -1 and genistein, 10 ?mol?L -1 ), and MEK1/2 inhibitor (PD 98059, 10 ?mol?L -1 ). CONCLUSION ? 1B AR subtypes stimulate DDT1 MF 2 cells growth and its signal pathway is related to the PLC activation、Ca 2+ release、PKC、TK and ERKs activation.

Objective: To investigate the mechanism of scorpion venom active peptides(SVAPs) on platelet aggregation. Methods: Platelet aggregation in vivo and vitro was determined by turbidimetry. Carotid thrombosis model was induced by electrostimulation. The determination of 6 keto PGF 1 and TXB 2 were performed by radioimmunoassay. Results: SVAPs 0.125,0.25,0.5mg?ml -1 significantly inhibited the rabbit platelet aggregation triggered by thrombase 0.03u.ml -1 , ADP 10u.ml -1 in vitro( P