An exploratory study on the mechanism of Huangqi Guizhi Wuwu Decoction in the treatment of neuropathic pain.

Huangqi Guizhi Wuwu Decoction (HGWD) has a definite effect on neuropathic pain (NP), whereas the specific mechanism has not been elucidated. The components and targets in HGWD were collected and identified through System Pharmacology Database (Traditional Chinese Medicine Database and Analysis Platform). Genecards and Online Mendelian Inheritance in Man databases were used to search for NP-related genes. The Venn diagram was drawn to get the intersection target. Cytoscape 3.8.0 software was used to construct the compound-disease-target-pathway networks. STRING database was applied to analyze protein-protein interaction of potential targets. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were used to identify the function of genes related to NP. Finally, molecular docking was performed to visualize the binding mode and affinity between proteins and active ingredients. According to the intersection target of the Venn diagram, the network graph is constructed by Cytoscape and the results show the five compounds, ß-sitosterol, (+)-catechin, quercetin, Stigmasterol, kaempferol, and 15 genes (CASP3, FOS, GSK3B, HSP90AA1, IKBKB, IL6, MAPK8, RELA, ICAM1, SELE, ELK1, HSPB1, PRKACA, PRKCA, RAF1) were highly correlated with NP. KEGG and GO of 15 genes results that TNF, IL-17 and MAPK signaling pathway were Significantly related to the pathological mechanism of NP. Molecular docking showed that core genes in this network were IL-6 (TNF and IL-17 signaling pathways), ICAM1 (TNF signaling pathway), and CASP3 (three signal pathways). This study found that the five active compounds, three core genes, and three signaling pathways may be the key to the treatment of NP by HGWD.

The neuroprotective effects of Lutongkeli in traumatic brain injury rats by anti-apoptosis mechanism

Purpose: To explore the neuroprotective effects of Lutongkeli (LTKL) in traumatic brain injury (TBI) and detect the related mechanism. Methods: TBI model was established with LTKL administration (2 and 4 g/kg/d, p.o.). Motor function of rats was examined by Rotarod test. Nissl staining was used to show neuron morphology. Furthermore, the disease-medicine common targets were obtained with the network pharmacology and analyzed with Kyoto Encyclopedia of Genes and Genomes. Lastly, the predicted targets were validated by real-time polymerase chain reaction. Results: After LTKL administration, neural behavior was significantly improved, and the number of spared neurons in brain was largely increased. Moreover, 68 bioactive compounds were identified, corresponding to 148 LTKL targets; 2,855 genes were closely associated with TBI, of which 87 overlapped with the LTKL targets and were considered to be therapeutically relevant. Functional enrichment analysis suggested LTKL exerted its pharmacological effects in TBI by modulating multiple pathways including apoptosis, inflammation, etc. Lastly, we found LTKL administration could increase the mRNA level of Bcl-2 and decrease the expression of Bax and caspase-3. Conclusions: This study reported the neuroprotective effect of LTKL against TBI is accompanied with anti-apoptosis mechanism, which provides a scientific explanation for the clinical application of LTKL in the treatment of TBI.

LncRNA-MYL2-2 and miR-124-3p Are Associated with Perioperative Neurocognitive Disorders in Patients after Cardiac Surgery.

BACKGROUND: Perioperative neurocognitive disorders (PND) resulting from cardiac surgery is a complication with high morbidity and mortality. However, the pathogenesis is unknown. METHODS: For the sake of investigating the risk factors and mechanism of PND, we collected the characteristics and neurological scores of patients undergoing cardiac surgery in the Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University and Affiliated Hospital of Southwest Medical University from Jan 1, 2016 to Dec 11, 2018. RESULTS: We found that age and left atrial thrombus are independent risk factors for PND after cardiac surgery. Furthermore, the serum of 29 patients was collected on the 7th day after cardiac surgery for detecting the expression of lncRNA-MYL2-2 and miR-124-3p. Increased lncRNA-MYL2-2 and decreased miR-124-3p in serum were associated with the decline of patients' cognition. CONCLUSIONS: LncRNA-MYL2-2 and miRNA-124-3p may jointly participate in the occurrence and development of PND after cardiac surgery. These important findings are advantaged to further understand the pathogenesis of PND and prevent it, provide new biomarkers for the diagnosis and monitoring of PND.

Protective effect of Shengmai injection on myocardial endothelial cell glycoprotein detachment after myocardial ischemia-reperfusion injury in isolated rat hearts.

OBJECTIVE: To investigate effects of Shengmai injection (SMI) postconditioning on myocardial ischemia-reperfusion injury (MIRI) in isolated rat hearts. MATERIALS AND METHODS: A total of thirty isolated hearts were randomly divided into three groups: Sham group, I/R group and SMI group. Sham group was continuously perfused with K-H solution for 120 minutes. I/R group and SMI group were given balanced perfusion for 30 min followed by reperfusion for 60 min, with an interval of 30 min, and those in the SMI group were given postconditioning with 1% SMI during the first 10 min of reperfusion. The left ventricular function, markers of myocardial injury, endothelial cell injury and oxidative stress injury were measured at 30 minutes after equilibration (t0), 30 minutes after ischemia (t2) and 60 minutes after reperfusion (t3). RESULTS: The results showed that there was no significant difference for all observation indexes at t0. Compared with the Sham group, real portfolio project and coronary arterial flow rate and the activity of superoxide dismutase were significantly decreased in the I/R group, whereas those in the SMI group were significantly higher. Left ventricular end-diastolic pressure, the concentrate of malondialdehyde, lactate dehydrogenase, cTn-I, hyaluronic acid, heparin sulphate, syndecan-1 in the I/R group were markedly higher than those in the Sham group, whereas those in the SMI group were significantly lower. CONCLUSION: In summary, the present study indicated that 1% SMI postconditioning can alleviate the detachment of endothelial cell glycoprotein envelope induced by myocardial ischemia-reperfusion injury, and its mechanism is probably related to the inhibition of the oxidative stress injury.