ABSTRACT
Self-assembly refers to the spontaneous process where basic units such as molecules and nanostructured materials form a stable and compact structure. Peptides can self-assemble by non-covalent driving forces to form various morphologies such as nanofibers, nano layered structures, and micelles. Peptide self-assembly technology has become a hot research topic in recent years due to the advantages of definite amino acid sequences, easy synthesis and design of peptides. It has been shown that the self-assembly design of certain peptide drugs or the use of self-assembled peptide materials as carriers for drug delivery can solve the problems such as short half-life, poor water solubility and poor penetration due to physiological barrier. This review summarizes the formation mechanism of self-assembled peptides, self-assembly morphology, influencing factors, self-assembly design methods and major applications in biomedical field, providing a reference for the efficient use of peptides.
Subject(s)
Pharmaceutical Preparations , Peptides/chemistry , Amino Acid Sequence , Nanostructures/chemistry , Drug Delivery SystemsABSTRACT
This paper was aimed to summarize functional and morphologic changes of neurogliocytes exposure to stress,and the regulating effect of traditional Chinese medicine (TCM) on functional and morphologic changes of neurogliocytes,in order to provide new ideas for mechanism development of stress pathogenesis and TCM regulating effect.
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Objective To investigate hippocampal neuronal damage and dynamic change of α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor subunit GluR2 in status epilepticus, to find out whether GluR2/glyceral dehyde-3-phosphate dehydrogenase (GAPDH) interaction has any change.Methods Male Wistar rats (62 cases) were induced to status epilepticus by using LiC1-pilocarpine.The 62 rats were divided into 1 h (6 cases),6 h (12 cases), 24 h (12 cases),72 h (12 cases)and 7 d (20 cases)after status epilepticus.At the same time, the healthy control group (12 cases) was established.Morphologic changes of hippocampus and the amount of apoptotic cells in healthy control and SE model groups at different time points (6 h, 24 h, 72 h, 7 d) (6 cases each group) after status epilepticus were quantified by adopting Nissl staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling staining respectively.Expressions of GluR2 in healthy control and SE model groups at 1 h,6 h,24 h,72 h and 7 d (6 cases each group) after status epilepticus were detected by using Western blot.Co-precipitation and Western blot techniques were used to investigate whether the GluR2/GAPDH interaction in the hippocampus was increased.Results Compared with the healthy control group, the number of nerve cells in the hippocampal CA1 and CA3 regions was significantly reduced at all studied time points(F =30.866,24.043, all P ＜0.05).Apoptotic cells in hippocampal CA1 and CA3 regions were significantly increased at 24 h,72 h and 7 d after status epilepticus (F =84.762,52.574, all P ＜ 0.01).GluR2 at 1 h,6 h after status epilepticus was equal to that of the control group (P ＞ 0.05), but it was shown to be significantly down-regulated at other studied time points (F =76.506,P ＜ 0.01);when compared with the healthy control group,the GluR2/GAPDH interaction was significantly up-regulated in the hippocampus at 72 h after status epilepticus (t =7.029, P ＜ 0.05).Conclusions Status epilepticus can lead to neuronal damage in the hippocampus.Down-regulation of GluR2 and increase of the GluR2/GAPDH complex formation might be one of the mechanisms involved in hippocampal neuronal damage.
ABSTRACT
<p><b>OBJECTIVE</b>To assess the anxiolytic effect of Anshenfang granules (ASF), a compound traditional Chinese medicinal preparation, on anxiety in rats and the mechanism of its actions.</p><p><b>METHODS</b>Male Wistar rats with anxiety induced by chronic emotional stress were randomized to receive treatments with diazepam or ASF at high, medium or low doses. The behavioral changes of the rats were evaluated using plus-maze test, after which the rats in normal control group, model group, and medium AFS dose group were sacrificed to measure the hippocampal contents of glutamic acid and γ-aminobutyric acid (GABA) using high-performance liquid chromatography (HPLC); immunohistochemistry was employed to evaluate the expressions of GABAA receptor and N-methyl-D-aspartate receptor 1 (NMDAR1).</p><p><b>RESULTS</b>Plus-maze test showed obvious anxiety behaviors in the model group, which were significantly meliorated by diazepam and ASF, especially at the medium dose. Hippocampal glutamate levels increased and GABA decreased significantly in the model group, and such changes were obviously attenuated, by comparable amplitudes, by treatments with diazepam and medium-dose ASF. The model group showed significantly diminished GABAA receptor-positive cells and increased NMDAR1-positive cells, which were improved by diazepam and ASF at the medium dose.</p><p><b>CONCLUSION</b>ASF produces strong anxiolytic effect in rats by increasing the content of GABA in the brain, enhancing GABAA receptor expression, reducing glutamic acid content, and decreasing NMDAR1 expression.</p>