To investigate the expression of NOS III mRNA and protein in cultured porcine cerebral arterial endothelial cells (CAEC) during hypoxia and reoxygenation and the effects of L-Tetrahydropalmatine (L-THP) on the gene expression of NOS III in CAEC during hypoxia and reoxygenation. The cultured CAEC were divided into 5 groups; control, hypoxia, hypoxia+reoxygenation, hypoxia +L-THP and reoxygenation +L-THP groups. NOS III mRNA expression was detected by reverse transcription-polymerase chain reaction (RT-PCR). Immunocytochemistry was used to detect the level of NOS III protein. The expression of NOS III mRNA and protein were increased when CAEC were exposed to hypoxia for 1 h, and significantly decreased during reoxygenation 2, 6 and 12 h after 1-h of hypoxia. L-THP from 10⁻⁸ mol/L to 10⁻³ mol/L could inhibit the up-regulation of NOS III gene expression during hypoxia and down-regulation of NOS III gene expression during reoxygenation.

To obeserve the effect of oxidized low density lipoprotein (OxLDL) on arterial endothelial cells apoptosisin vivo, we established a model in which Sprague-Dawley rats were given intraperitoneal and intravenous injection of unmodified LDL (8 mg/kg every day) via the tail vein. Seven days after the injection, the aortic endothelial cells specimens were prepared by anen face preparation of rat aorta. The apoptotic cells were identified and counted byin situ nick and labelling (TUNEL) method and light microscopy. The numbers of the apoptotic cells were 12.52±4.71/field in the intraperitoneal injection control group, 11.41±2.94/field in the intravenous injection control group, 22.98±8.01/field in the intraperitoneal injection LDL group and 103.8±11.5/field in the intravenous injection LDL group, respectively. The difference was significant between injection LDL group and control (P<0.01), and the difference was also significant between two LDL injection groups (P<0.01). These findings suggest that injection of LDL can induce apoptosis in arterial endothelial cells and the effect is especially significant with intravenous injection LDL. After injection, oxidative modification of LDL may occur in local arteries and causes injury to the endothelial cells.

The enzymatic synthesis of a tetrapeptide Phac-Met-Gly-Trp-Met-OEt, a fragment of the cholecystokinin C-terminal octapeptide CCK-8, was reported. This fragment was synthesized by coupling Phac-Met-OEt with Gly-OMe, Trp-OMe and Met-OEf successively. These three steps were catalyzed by α-chymotrpsin, Papain and α-chymotrpsin respectively. The results of FAB-MS showed that all the products had the correct molecular mass.

To investigate the effect of costimulatory factors in the pathogenesis of chronic idiopathic thrombocytopenic purpura (CITP), we examined the expression of CD80 on platelets and megakaryocytes in patients with CITP and the controls by FACS. By using CD80 monoclonal antibody (McAb) to inhibit interaction among cells which is mediated by costimulatory factors, we observed the effect of CD80 McAb on the growth and maturation of megakaryocytic progenitors of patients with CITPin vitro. The results showed the expression of CD80 on platelets and megakaryocytes in CITP group was significantly higher than that in controls (P<0.01). There was a significantly positive correlation between the expression of CD80 on platelets and serum PAIgG in CITP (r=0.86,P<0.05). The mean of various clone numbers (CFU-MK, BFU-MK and mCFU-MK) in CITP were all lower than those in controls (P<0.05). In megakaryocytes co-cultured with CD80 McAb, there was an increasing tendency of the number of CFU-MK and big CFU-MK (the number of megakaryocyte with GP III_a positive was more than 20) and mediate CFU-MK (the number megakaryocyte with GP III_a positive was 11–20). When the concentration of CD80 McAb was 10 μg/L, there was a significant difference in the number of megakaryocytic colony formation (CFU-MK, BFU-MK and mCFU-MK) between the group with CD80 McAb and that without it (P<0.05). These showed the abnormality of costimulatory factors had important effect in the pathogenesis of CITP.