ABSTRACT
Objective To observe NLS-KALA-SA-PTX (NKSP) for lung adenocarcinoma cell line A549 in vitro with paclitaxel monotherapy, and the mechanism thereof. Methods MTT assay was used to detect A549 cell proliferation influ-enced by different concentrations of NKSP (20, 40, 80, 100μg/L) and paclitaxel monotherapy (20, 40, 80, 100μg/L) for 24 h, 48 h and 72 h.. Subsequent experiments were divided into four groups, namely, group A (without any drug treatment), group B (added polypeptide 80μg/L of self-assembled nanoparticles, NKS), group C (80μg/L paclitaxel monotherapy) and group D (80μg/L NKSP). Flow cytometry was used to detect the cell apoptotic rates after 48 h and 72 h treatment in four groups. Western blot assay was used to analyse the protein expressions of bax and caspase-3 after 48 h and 72 h treatment in four groups. Results Both paclitaxel monotherapy and NKSP can inhibit the proliferation of A549 cells. The inhibitory rates of paclitaxel monotherapy group at 48 h and 72 h and NKSP group at 72 h showed an increasing trend in a dose-depen-dent manner (P<0.05). After treatment for 48 hours, the apoptotic rate was significantly higher in D group than that of C group (P<0.05). But the apoptotic rate at 72 h was lower in D group than that of C group (P<0.05). The protein expressions of bax and caspase-3 at 48 h were significantl lower in D group than those of C group, which were higher at 72 h in D group than those of C group (P<0.05). Conclusion Compared to paclitaxel monotherapy group, NKS promotes slow release of pa-clitaxol, which reduces the cytotoxicity and extends the antitumor effects.
ABSTRACT
Objective To observe the effect of naloxone(Naloxone,NAL) on myocardial ischemia-reperfusion injury in rats,and to explore its mechanism.Methods 36 male SD rats were randomly divided into blank control group (Con group),ischemia-reperfusion group (I/R group),ischemic preconditioning group (IPC group) and naloxone pretreatment group (Nal+I/R group).Changes of cardiac function,myocardial infarct size and occurrence of arrhythmias after ischemia-reperfusion in each roup were observed.Changes of myocardium under light microscope ultrastructural in each group were also observed.Apoptosis situation in each group was detected by TUNEL assay.Results Compared with th IR group,IPC group and Nal+I/R group showed significantly improvement in cardiac function after ischemia-reperfusion (P
ABSTRACT
Objective To investigate the relationship of the activation of nuclear factor kappa B(NF-kB) with myocardial neutrophil infiltration and injury in human open heart surgery,and to observe the inhibiting effect on the activation of NF-kB and protecting effect on myocardium of the coenzyme Q10,a scavenger of oxygen free radicals.Methods Forty-seven adult patients undergoing open heart surgery were randomly divided into two groups,the control and the treatment.CoenzymeQ10 tablets were given to the treatment group 5 days before operation.Biopsy of right atrium for myocardial pathology,activated NF-kB detection and ultrastructure observation were done prior to cardiopulmonary bypass,45 minutes of ischemia and 45 minutes of reperfusion.The dynamic indexes,vasomotor drug dosage,and outcomes were observed postoperatively.Results Upon 45 minutes of ischemia and 45 minutes of reperfusion,in control group there were neutrophil accumulation and adhesion of vascular endothelium,ultrastructural damages,and positive expression of NF-kB both in nuclei and cytoplasm,in myocardium.In treatment group,there were only mild neutrophil infiltration and ultrastructural damages,and weak positive expression of NF-kB both in nuclei and cytoplasm.However,the dynamic indexes,vasomotor drug dosage,and outcomes of two groups were not significantly different.Conclusion NF-kB plays an important role in pathophysiological process of myocardial ischemia and reperfusion in open heart surgery.CoenzymeQ10 has obvious inhibiting effect on activation of NF-kB and protecting effect on myocardium.