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italic>Sophora flavescens is a traditional Chinese medicine rich in flavonoids and has wide application potential in drug development and clinical practice. In this study, a total of 227 flavonoids were detected among five tissues of S. flavescens during anthesis using widely targeted metabolomics techniques. There were 137 flavonoids shared by five S. flavescens tissues and 18 root-specific flavonoids. There were 156, 155, 156 and 150 differentially accumulated metabolites identified in stem, leaf, flower, and young pod, respectively, compared with root. Forty-seven potentially active flavonoid components in S. flavescens were identified using the PubChem and SwissADME databases. The 58 potential target proteins for these potentially active components were predicted to be important in the treatment of type 2 diabetes mellitus (T2DM) based on the SwissTargetPrediction and GeneCards database. These 58 target proteins were used to construct a protein-protein interaction network through the STRING database, from which we performed GO and KEGG functional enrichment analysis. The mechanisms by which S. flavescens flavonoids may be useful in the treatment of T2DM was further explored in a multi-level and systematic way based on a "component-target-pathway" network. Finally, ten key potentially effective components were identified and found to be mainly distributed in the roots, flowers, and pods, and their content varied significantly between tissues. The results predict that the key targets of S. flavescens flavonoids in the treatment of T2DM are AKT1, ESR1, EGFR, PIK3R1, TNF and PTGS2, and that they play a hypoglycemic role through the regulation of endocrine resistance, AGE-RAGE, the PI3K-Akt signaling pathway, EGFR tyrosine kinase inhibitor resistance and other signaling pathways. This analysis of the tissue distribution and network pharmacology of S. flavescens flavonoids provides a theoretical basis for further studies on S. flavescens metabolites, the rational development and utilization of the S. flavescens aboveground parts, and initiates a comprehensive exploration of the mechanisms by which S. flavescens can be used in the treatment of T2DM.
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Smallanthus sonchifolius， a plant resource with both medicinal and edible values， has been taken as fruit for a long history. Studies have proved that phenolic acids， flavonoids， sesquiterpene lactones， and fructooligosaccharides are the major compounds in S. sonchifolius. The extract of S. sonchifolius demonstrates noticeable antioxidant， anti-inflammatory， antimicrobial， and anti-cancer effects， as well as the activities of lowering blood glucose level， regulating intestinal function and so on. The rhizomes and leaves of S. sonchifolius contain abundant phenolic acids， mainly caffeic acid and its derivatives， which endow S. sonchifolius with remarkable antioxidant effect. Moreover， these substances can reduce blood glucose by improving insulin sensitivity. Fructooligosaccharides are abundant in the tuber of this plant， which can improve intestinal function by regulating intestinal flora. The sesquiterpene lactones in glandular trichomes on the leaf surface can inhibit the proliferation of cancer cells， among which uvedafolin and enhydrofolin have particularly strong activities. Furthermore， the sesquiterpene lactones have obvious inhibitory effect on Gram-positive bacteria. In terms of structure， the number of epoxy groups is linked to the strength of anticancer and antimicrobial effects. In addition， S. sonchifolius contains other compounds such as volatile oils， fatty acids， sterols， diterpenes， p-hydroxyacetophenone derivatives， and octulosonic acid derivatives， thereby exhibiting the pharmacological effects of treating Alzheimer's disease， protecting kidney， and lowering blood lipids. However， the isolation and identification of the main compounds in S. sonchifolius need further exploration， and the mechanism of action remains to be studied. Here we summarized the principal chemical components and pharmacological activities of S. sonchifolius， aiming to give a clue for the comprehensive development and utilization of this plant.
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We report a case of giant hysteromyoma and complex pelvic adhesion treated by robotic assisted laparoscopic total hysterectomy and bilateral salpingectomy. The patient was diagnosed with uterine fibroids after physical examination in 1998 but did not receive any treatment, and regular examinations reported progressive growth of the fibroids. Ultrasound suggested multiple uterine fibroids, and pelvic MRI indicated large uterine fibroids with bleeding. Robot-assisted laparoscopic total hysterectomy and bilateral salpingectomy were performed after relevant examinations, and the operation was completed smoothly. The patient was discharged 4 days after surgery with good appearance of the abdominal wall and good recovery during the follow-up. With its unique advantages, robot-assisted laparoscopy provides a minimally invasive surgical approach for giant hysterectomy with complex pelvic adhesions.
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Female , Humans , Hysterectomy , Laparoscopy , Leiomyoma/surgery , Robotics , UterusABSTRACT
Objective:To investigate the effect of analgecine (AGC) on inflammatory response in the cell model of ischemic stroke and its mechanism. Methods:Sodium hydrosulfite (Na2S2O2) combined with sugar-free culture-medium was used to stimulate the model of ischemic stroke in vitro. BV2 cells were divided into six groups: control group, control with 0.5 U/ml AGC group, oxygen deprivation and recovery (OGD/R) group, OGD/R with AGC (0.25 U/ml, 0.5 U/ml, 1 U/ml) groups. After oxygen and glucose deprivation for 1.5 hours, they were changed to normal medium and given different concentrations of AGC in OGD/R with AGC groups. After co-incubation for three hours, the cells were treated. The content of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the supernatant was detected. The expression of M1-type microglia marker CD16+CD32 and M2-type microglia marker CD206 were detected with immunofluorescent staining. BV2 cells were divided into seven groups: control group, control with 0.5 U/ml AGC group, IL-4 group, IL-4 + lipopolysaccharide (LPS) + interferon (IFN)-γ group, IL-4 + LPS + IFN-γ with AGC (0.25 U/ml, 0.5 U/ml, 1 U/ml) groups. After 24 hours of IL-4 treatment, LPS + IFN-γ were added for 18 hours, they were changed to normal medium and given different concentrations of AGC for 24 hours, the expression of CD16+CD32 and CD206 were observed by flow cytometry. Results:Compared with the control group, the IL-6 and TNF-α level increased (P < 0.01), the number of CD16++CD32+ increased and the number of CD206+ decreased in OGD/R group. Compared with the OGD/R group, the IL-6 and TNF-α level decreased (P < 0.01), the number of CD16++CD32+ decreased and the number of CD206+ increased in AGC groups. Compared with the control group, the number of CD206 tended to increase, and the number of CD16+CD32 tended to decrease in IL-4 group; compared with IL-4 group, the number of CD16+CD32 tended to increase, and the number of CD206 tended to decrease in IL-4 + LPS + IFN-γ group; compared with IL-4 + LPS + IFN-γ group, the number of CD16+CD32 tended to decrease, and the number of CD206 tended to increase in IL-4 + LPS + IFN-γ + 0.25 U/ml AGC group and IL-4 + LPS + IFN-γ + 0.5 U/ml AGC group, while the number of CD206 increased in IL-4 + LPS + IFN-γ + 1.0 U/ml AGC group (P < 0.05). Conclusion:AGC could inhibit the secretion of inflammation factors by promoting the polarization of microglia from M1 phenotype to M2 phenotype.
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Objective:To observe the effects of Analgecine (AGC) on middle cerebral artery ischemia-reperfusion injury in rats and its mechanism. Methods:A total of 61 Sprague-Dawley rats were divided into sham group (n = 11), sham-AGC group (n = 11), model group (n = 20) and model-AGC group (n = 19). The model group and the model-AGC group were occluded the middle cerebral arteries for 1.5 hours and reperfused (2 rats in each group unsuccessful). The sham-AGC group and the model-AGC group were injected AGC 20 U/kg through tail-vein, while the sham group and the model group were injected saline of same volume. Four rats in each group were tested heat shock proteins 70 (HSP70), Bcl-2 and Bax in brain with Western blotting 48 hours after injection. The other rats were assessed with Prehensile Traction Test seven days after injection, and then, four of each group were detected ionized calcium binding adapter molecule 1 (Iba1) and glial fibrillary acidic protein (GFAP) expression with immunohistochemistry. Results:The prehensile time increased in the model-AGC group compared with that of the model group (P < 0.01), with the increase of HSP70 and Bcl-2 (P < 0.01) and decrease of Iba1 and GFAP expression (P < 0.05). Conclusion:AGC may promote the recovery of motor function in rats with cerebral ischemia-reperfusion injury, which may associate with inhibiting cell apoptosis and neruoinflammatory response.
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Objective::To observe the intervention effect of Yiqi Huoxue recipe (YQHX) on ventricular remodeling in rats with chronic heart failure, in order to explore its mechanism. Method::Among 40 male SD rats, 10 were randomly selected as the sham operation group. The left anterior descending coronary artery ligation was performed to construct the chronic heart failure(CHF) rat model. After modeling, they were randomly divided into model group, captopril group(13.5 mg·kg-1·d-1) and YQHX group (20 g·kg-1·d-1), and orally given the corresponding drugs. After 8 weeks of intervention, cardiac tissues were collected, body mass and heart mass were weighed, and echocardiography were performed to detect the changes in cardiac structure. Masson staining was performed to determine the myocardial interstitial collagen volume fraction. Western blot was used to detect the expression levels of mitochondrial fusion protein optic atrophy 1 (Opa1) and cleavage protein dynamic-related protein 1 (Drpl). The quantitative real-time fluorescence polymerase chain reaction(Real-time PCR)was applied to detect the expressions of Wnt/β-catenin pathway-related factors such as lipoprotein receptor-related protein 6 (LRP6), glycogen synthase kinase-3β (GSK-3β) and β-catenin. Result::Compared with the sham group, the left ventricular wall of the model group was significantly thickened (P<0.05), the cardiac cavity was significantly enlarged, and the content of collagen in the myocardial interstitium was increased (P<0.01). The expression level of Opal decreased, the expression level of Drp1 increased (P<0.05), the mRNA expression level of LRP6, GSK-3, and β-catenin increased (P<0.01). Compared with the model group, YQHX group can reduce ventricular wall thickening, heart chamber enlargement, myocardial interstitial collagen content, up-regulate the low expression of Opa1, but down-regulate the high expressions of Drpl, LRP6, GSK-3β, β-catenin(P<0.05, P<0.01). Conclusion::YQHX can effectively alleviate ventricular remodeling and improve mitochondrial energy metabolism in rats with CHF. The mechanism may be related to the inhibition of Wnt/β-catenin related factors.
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The discussion on pathophysiological of multiple sclerosis (MS) mainly focuses on T and B cells in adaptive immune response, but less involve in the myeloid cells (dendritic cells, monocytes, macrophages and microglia) in the innate immune system, which also play an important role in the pathogenesis of MS. The myeloid cell population acts as antigen-presenting cells and effector cells in neuroinflammation in the innate immune system. The interactions between T cells and myeloid cells form a vicious cycle which makes the disease continuous deterioration. At present, the studies on the therapeutic drugs for MS mainly are focused on the adaptive immune system, but pay less attention to myeloid cells. In this article, we reviewed the sub-types and functions of myeloid cells, their changes in MS patients and animal models, as well as the effects of some therapeutic drugs for MS on myeloid cells, in the purpose of finding new targets and strategies for development for MS therapy.