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The effects of intravenous high mobility group box 1 (HMGB1) on myocardial ischemia/reperfusion (I/R) injury remains to be elucidated. The purpose of the present study was to investigate the effects of intravenous HMGB1 on the expression of hypoxia inducible factor-1α (HIF-1α) in the myocardium of rats following acute myocardial ischemia, and to examine the effects of intravenous HMGB1 on myocardial I/R injury. Male Wistar rats were divided into the following groups: Sham operation group (n=10), a group exposed to ischemia for 30 min and reperfusion for 4 h (I/R group) as a control (n=10), an HMGB group, in which 100 ng/kg HMGB was administered intravenously 30 min prior to ischemia (n=10), an LY group, in which LY294002, an inhibitor of phosphoinositide 3-kinase (PI3K), was administered intravenously (0.3 mg/kg) 40 min prior to ischemia (n=10), and the HMGB1+LY group, in which HMGB1 (100 ng/kg) and LY294002 (0.3 mg/kg) were administered intravenously 30 min and 40 min prior to ischemia, respectively (n=10). The serum levels of cardiac troponin I (cTnI) and tumor necrosis factor-α (TNF-α), and myocardial infarct size were measured. The expression levels of phosphorylated Akt and HIF-1α were investigated using western blot analyses. The results showed that pre-treatment with HMGB1 significantly decreased serum levels of cTnI, and TNF-α, and reduced myocardial infarct size following 4 h reperfusion (all P

The aim of the present study was to investigate whether postconditioning with simvastatin attenuated myocardial ischemia reperfusion injury by inhibiting the expression of high mobility group box 1 (HMGB1) in rat myocardium following acute myocardial ischemia. In total, 30 male Sprague-Dawley rats were divided into sham operation (sham; n=10), acute myocardial infarction (AMI; n=10) and simvastatin (sim; n=10) groups. The AMI and sim groups were subjected to ischemia for 30 min, followed by reperfusion for 180 min. The rats in the sim group were administered 20 mg/kg simvastatin intravenously 5 min prior to reperfusion. Subsequently, the infarct size, serum cardiac troponin (c-TnI), tumor necrosis factor (TNF)-α and myocardial malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were measured. Western blot analysis was used to detect the protein expression of HMGB1. Postconditioning with simvastatin was shown to decrease the infarct size and HMGB1 expression levels in the myocardium following AMI (P

The principle objective of this research was to develop and characterize pH-responsive and biocompatible nanogels as a tumor-targeting drug delivery system. The nanogels were self-assembled from chitosan-based copolymers, chitosan-graft-poly(N-isopropylacrylamide) (CS-g-PNIPAm). The copolymers were synthesized via free radical copolymerization and characterized for their chemical structure by FT-IR and (1)H NMR. These copolymers could be efficiently loaded with oridonin (ORI) and the characteristics of ORI-loaded nanogels were evaluated. Drug release researches indicated that the ORI-loaded nanogels displayed pH-dependent release behaviors. Based on MTT assay and cellular morphological analysis, the anti-tumor activity of ORI-loaded nanogels was higher at pH 6.5 than at pH 7.4. In conclusion, the obtained nanogels appeared to be of great promise in tumor extracellular pH targeting for ORI.

A plasmid pSDK-1 containing the Escherichia coli phosphofructokinase-1 gene (pfkA) was constructed, and transferred into Acidithiobacillus thiooxidans Tt-7 by conjugation. The pfkA gene from E. coli could be expressed in this obligately autotrophic bacterium but the enzyme activity (18 U g-1) was lower than that in E. coli (K12: 86 U g-1; DF1010 carrying plasmid pSDK-1: 97 U g-1). In the presence of glucose, the Tt-7 transconjugant consumed glucose leading to a better growth yield.

The mechanism for anti-tumor activity of oridonin (ORI) nanosuspension, prepared by the high pressure homogenization method, was studied using MCF-7 human breast carcinoma cells in vitro. MTT assay, observation of morphologic changes, flow cytometric analysis, and western blot analysis indicated that ORI nanosuspension could significantly intensify the in vitro anti-tumor activity to MCF-7 cells, as compared with ORI solution. Furthermore, ORI nanosuspension induced G2/M stage proliferation arrest and apoptosis in MCF-7 cells depending on its concentration. In addition, western blot analysis indicated that the pro-caspase-3 protein was not cleaved into the activated form and the expression of anti-apoptotic Bcl-2 protein decreased, on the contrary, the expression of pro-apoptotic Bax protein increased in a dose-dependent manner in ORI nanosuspension-treated cells. These observations indicated that the anti-tumor activity of ORI nanosuspension was intensified by cell-cycle arrest and apoptosis induction.

To study the effects of 9-cis-retinoic acid (9-cis-RA) on cell cycle and expression of cyclin D1 and cdk4 in lung cancer cells.9-cis-RA (1 x 10(-6) mol.L-1) was used to treat lung cancer cells for 24 h; Flow cytometry (FCM) was used to detect the percent of G0/G1 phase and S phase cells of three groups including blank control, DMSO control and 9-cis-RA groups; RT-PCR was used to analyze the expression changes of cyclin D1 and cdk4 before and after treatment with 9-cis-RA in lung cancer cells.The percent of G0/G1 phase cells of 9-cis-RA groups was significantly higher than that of the control groups (P0.01 or P0.05) and the percent of S phase cells of 9-cis-RA groups was lower than that of the control groups (P0.01 or P0.05); the expression of cyclin D1 of PG, SPC-A1 and L78 cells was decreased (P0.01) and the expression of cdk4 of PG, A549 and L78 cells was also decreased (P0.01) after treatment with 9-cis-RA.Most of the proliferation and the expression of cyclin D1 and cdk4 of PG, A549, SPC-A1 and L78 were inhibited by 9-cis-RA.

A plasmid pSDK-1 containing the Escherichia coli phosphofructokinase-1 gene (pfkA) was constructed, and transferred into Acidithiobacillus thiooxidans Tt-7 by conjugation. The pfkA gene from E. coli could be expressed in this obligately autotrophic bacterium but the enzyme activity (18 U g-1) was lower than that in E. coli (K12: 86 U g-1; DF1010 carrying plasmid pSDK-1: 97 U g-1). In the presence of glucose, the Tt-7 transconjugant consumed glucose leading to a better growth yield.

AIM: To investigate the levels of D-dimer (DD) and von Willebrand factor (vWF) and the relationship between DD and vWF in ulcerative colitis (UC) patients. METHODS: A total of 29 plasma specimens were obtained from patients with ulcerative colitis (male 13, female 16), aged 21-47 years (33 ± 11). Disease activity was assessed by Truelove-Writeria. Patients with a score of above 5 were regarded as having active colitis. Twenty healthy people (male 12, female 8), aged 19-53 years (31 ± 14), served as normal controls. Blood samples were taken from an antecubital vein puncture. Blood (1.8 mL) was injected into the tubes containing sodium citrate (0.13 mmol/L). The plasma was obtained by centrifugation at 3000 r·min-1 for 10 min, and stored at -80 °C until assayed by ELISA. RESULTS: The mean plasma levels of DD and vWF in active UC patients were significantly higher than those of the controls (0.69 ± 0.41 vs 0.27 ± 0.11, P < 0.01; 143 ± 46 vs 103 ± 35, P < 0.01). The mean plasma levels of DD in the patients with active disease were higher than those with inactive disease (0.69 ± 0.41 vs 0.48 ± 0.29, P < 0.05). The levels of vWF were not different between active and inactive patients. DD levels were positively related to vWF levels (r = 0.574, P < 0.01). There was no significant difference between levels of DD and vWF and the scope of disease and sex of the patients. CONCLUSION: vWF is an important feature and a good marker of UC; intravascular thrombus and endothelial cell dysfunction were found in UC patients; and the combined test of DD and vWF is helpful to distinguish the activity of the UC patients.