ABSTRACT
Nanotechnology has shown obvious advantages in the field of medical treatment and diagnosis. Through the encapsulation of nano carriers, drugs not only enhance the therapeutic effect and reduce toxic and side effects, but also become intelligent responsive targeted drug systems through the modification on the surface of nano carriers. However, due to the obstacles in relevant basic research, production conditions, cost, clinical trials, and the lack of pharmacokinetic research on various drug loading systems, few nano systems have been used in therapy. In order to solve the above problems, this paper reviewed and analyzed the research progress of nano carriers in drug delivery, including their auxiliary role and characteristics, types and functions, pharmacokinetics, application prospects and challenges.
ABSTRACT
<p><b>AIM</b>To probe the related proteins to stress-induced myocardium injury.</p><p><b>METHODS</b>After establishment of a myocardium injury model induced by restraint stress in rats, myocardium proteins of restraint stress-treated and untreated rats were extracted, and the two-dimensional polyacrylamide gel electrophoresis (2-DE) maps of the extracted proteins were established by using the immobilized pH gradient (IPG) and SDS-PAGE two-dimensional electrophoresis respectively. The alterative protein spots were analyzed by Image Master 3.01 software and identified with assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF-MS) and database searching.</p><p><b>RESULTS</b>Proteomics analysis showed that there were 10 proteins were significantly influenced by restraint stress in rat myocardium. After stress, proteins, including cardiac myosin heavy chain, dihydrolipoamide succinyltransferase component of 2-oxoglutarate dehydrogenase complex, similar to dihydrolipoamide S-succinyltransferase, mitochondrial aldehyde dehydrogenase, H (+)-transporting ATP synthase, albumin, myosin heavy chain and apolipoprotein A-I precursor showed increased expression. Mitochondrial aconitase and uncoupling protein UCP-3 showed decreased expression.</p><p><b>CONCLUSION</b>These differential expressive proteins might be involved in stress-induced injury to myocardium.</p>
Subject(s)
Animals , Male , Rats , Disease Models, Animal , Heat-Shock Proteins , Metabolism , Myocardium , Metabolism , Proteomics , Rats, Wistar , Restraint, Physical , Stress, PhysiologicalABSTRACT
To investigate the effect of stress on homocysteine metabolism in the rat and explore the mechanism as well as the key regulatory link of stress-induced hyperhomocysteinemia, male Wistar rats were treated with restraint stress while control rats received routine treatment. By HPLC-fluorometry, the homocysteine level in rat plasma was determined. Cystathionine beta-synthase (CBS) activity in blood, heart, liver and kidney was measured by radioisotope assay using [(14)C]-serine as the labeled substrate. Total RNA was isolated from rat liver after restraint stress. RT-PCR and Northern blot were used to estimate the level of CBS mRNA. The results showed that hyperhomocysteinemia was induced by restraint stress. The highest CBS enzyme activity was seen in rat livers. A decrease in hepatic activities of CBS was found in restraint stress rats. The 29.4% +/-2.5% reduction in the activity of CBS was accompanied by a 44.1% +/-3.4% decrease in its mRNA level. CBS enzyme activity was slightly elevated in the kidney of stressed rats while it was almost undeterminable in the cardiovascular system. The study suggests that stress leads to an inhibition of the transsulfuration pathway in homocysteine metabolism. The hepatic CBS influenced by stress at the level of transcription exerts a profound effect on the circulating levels of homocysteine. The liver is the key organ where stress affects homocysteine metabolism.
Subject(s)
Animals , Male , Rats , Down-Regulation , Homocysteine , Metabolism , Hyperhomocysteinemia , Blood , Rats, Wistar , Restraint, Physical , Stress, Physiological , MetabolismABSTRACT
<p><b>AIM</b>To observe the injured effect of homocysteine (HCY) on cardiomyocytes and investigate its signal transduction mechanism as well as the key regulatory link.</p><p><b>METHODS</b>Cardiomyocytes were isolated from neonatal Wistar rats. After incubation with HCY, the survival rate of cardiomyocytes was determined by trypan blue stained assay, while the apoptosis rate was measured by TUNEL and FCM. Western blot and EMSA were used to tested ERK2 protein phosphorylation and NF-kappaB active expression in cardiomyocytes, respectively.</p><p><b>RESULTS</b>The survival rate of cardiomyocytes treated with HCY was reduced significantly in dose- and time- dependent manner. It was found that 10(-3) mol/L HCY could increase the apoptosis rate of cardiomyocytes to the peak (7.65%) at 4 h stress. Several HCY levels revealed the strong inhibitory effect on ERK2 protein phosphorylation, especially, 10(-3) mol/L HCY decreased the level of active ERK2 expression to 3.04% of control at 4 h (P < 0.01). NF-kappaB activation was also inhibited significantly by several HCY level for different time in cardiomyocytes.</p><p><b>CONCLUSION</b>HCY plays an important role in injury of cardiomyocytes and apoptosis is a form of HCY-induced injury to cardiomyocytes. HCY can block ERK2 protein phosphorylation and NF-kappaB activation, which contribute to the injury of cardiomyocytes.</p>