Network pharmacological study of Schizonepetae Herba and Saposhnikoviae Radix in treatment of ulcerative colitis / 中国中药杂志

The aim of this paper was to screen the active targets of Schizonepetae Herba and Saposhnikoviae Radix in the treatment of ulcerative colitis by means of network pharmacology,and to investigate their mechanism of action. The effective components of Schizonepetae Herba and Saposhnikoviae Radix were screened out by traditional Chinese medicine systematic pharmacological( TCMSP)database,with oral bioavilability( OB) ≥30% and drug-like( DL) ≥18% selected as the thresholds. Target PPI network was built between the main components and their corresponding targets. One hundred and eighty-two human genes corresponding to the medicine target sites were obtained from Uniprot database; 3 874 genes corresponding to ulcerative colitis were obtained from Genecard database.A total of 115 intersection genes were screened from disease genes and medicine genes,and the PPI interaction analysis was conducted by using String tool. Disease-target PPI network was drawn by using Cytoscape software,and component-target-disease network was constructed. One hundred and eight nodes and 1 882 connections were found,and then Cytoscape software was used to merge the networks and filter the core network for gene GO function analysis and KEGG pathway enrichment analysis. The mechanism of Schizonepetae Herba and Saposhnikoviae Radix was then verified by animal experiment. Gene GO functional analysis suggested that biological process,molecular functions and cell components were involved,and it was found that ulcerative colitis might be related to transcription factor activity,and cytokine receptor binding,etc. Gene KEGG pathway enrichment analysis showed that the mechanism of ulcerative colitis might be associated with TNF and Toll-like receptors( TLRs) signaling pathway-mediated cytoinflammatory factors interleukin-1( IL-1) and interleukin-6( IL6). The possible mechanism of the effective components of Schizonepetae Herba and Saposhnikoviae Radix in treating ulcerative colitis might be related to intervening the cytokine receptor binding of TNF and TLRs signaling pathways,reducing the transcription of nuclear factor-kappaB( NF-κB),and inhibiting the secretion of intestinal inflammatory factors IL-1 and IL-6.

R-apomorphine protects against 6-hydroxydopamine-induced nigrostriatal damage in rat / 神经科学通报·英文版

Objective The aim of the present study was not only to assess the retrograde degenerative changes in the dopaminergic neurons of the substantia nigra (SN) and ventral tegmental area (VTA) after injection of 6-hydroxydopamine (6-OHDA) into the striatum, but also to use this 6-OHDA model of Parkinson's disease to explore the possible neuroprotective effect of R-apomorphine (R-APO). Methods The partial lesion was obtained by intrastriatal administration of 6-OHDA. R-APO administration (10 mg/kg, s.c.) started 15 min prior to lesioning and continued daily for another 22 days post surgery. Testing was carried out 5 weeks after lesioning. We investigated the histology and associated behavior and neurochemical changes. Structural and functional deficits were quantified by tyrosine hydroxylase (TH) / Nissl-staining cell number counting, striatal dopamine (DA) content determination and amphetamine-induced rotation analysis. Results R-APO-treatment attenuated the amphetamine-induced ipsiversive rotation 5 weeks after the lesion induction. R-APO administration for 22 days significantly reduced the size of the lesion at the level of the SN from 50% (control group) to 69%. Moreover, the cell shape resembled that observed in the intact animals. R-APO treatment significantly increased the number of cells in both the lesion and the intact sides of VTA by 60%, suggesting selective neurotrophic effect of R-APO in this area. Finally, R-APO-treatment significantly attenuated the 6-OHDA-induced striatal DA depletion and normalized dihydroxyphenylacetic acid (DOPAC)/DA ratios. Conclusion We conclude that R-APO has neuroprotective and possible neurotrophic effect on a striatal lesion with 6-OHDA, suggesting that this drug may have rescuing properties in patients with early stage Parkinson's disease. These effects are more pronounced in VTA and enhance with duration of treatment.

Experimental study on the prevention of epidural scar adhesion with polycaprolactone/polylactic acid membrane / 中华外科杂志

<p><b>OBJECTIVE</b>To evaluate the ability of a polycaprolactone/polylactic acid (PCL/PLA) membrane to inhibit epidural scar adhesion after laminectomy, and observe the responsive changes of the pain media in the spinal cord.</p><p><b>METHODS</b>L(1), L(3) laminectomies were performed on 96 Wistar rats. The rats were divided into 3 groups: None-implant Control Group (NC), Autologous free fat graft group (AFFG) and PCL/PLA membrane group (PCL/PLAm). The rats were killed at 1, 3, 6, and 12 weeks postoperatively. Epidural scar formation and adhesion were observed grossly and histologically. Reverse transcription polymerase chain reaction (RT-PCR) were used to analyses the expression of Transforming growth factor beta (TGF-beta) in the epidural scar. Immunohistochemistry stain and RT-PCR were performed to evaluate the expression of the substance P and the c-fos gene in the relevant spinal cord, and the results were analyzed statistically.</p><p><b>RESULTS</b>Gross evaluation and histological evaluation showed that in the NC lamina defect site had much scar tissue and had wide and tight adhesions to the dura; in the AFFG, with the fat degrading gradually, the adhesions were increased; whereas in the PCL/PLAm group, there were slightly adhesions to the dura. RT-PCR showed that the expression of the TGF-beta was much less in the PCL/PLAm group than in the NC group. The insertion of the PCL/PLA membrane and the fat patch reduced the expression of the substance P and the c-fos gene in the spinal cord.</p><p><b>CONCLUSION</b>The insertion of the PCL/PLA membrane reduces scar formation and separates fibrosis tissue from the dura, the results indicate that PCL/PLA membrane is an effective way of reducing peridural scar formation and preventing the failed back surgery syndrome.</p>