Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.23 (MMP)
 4,246 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined whether single nucleotide polymorphisms (SNP) of the matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 4 (TIMP-4) genes are associated with risk of intracranial hemorrhage (ICH) among patients with brain arteriovenous malformation (BAVM). For 311 Chinese patients with BAVM, we performed genotyping analysis for 11 selected SNP of MMP-9 and TIMP-4 using the MassARRAY genotyping system (Sequenom, San Diego, CA, USA). Associations between each genotype and risk of hemorrhage were evaluated using logistic regression analysis. Multivariate logistic regression analysis revealed that MMP-9_rs9509 was significantly associated with ICH among patients with BAVM with adjustments for BAVM size, venous drainage type, age and sex (adjusted odds ratio [OR]=0.19; 95% confidence interval [CI]=0.05-0.66; p=0.009 for CC compared with TT genotype). However, the association was not significant (p=0.072) after Bonferroni correction and was not significant (p=0.064) in the univariate model. The TIMP-4_rs3755724 polymorphism did not have a statistically significant effect in the multivariate model (adjusted OR=0.57; 95% CI=0.32-1.01; p=0.055 for CT compared with TT genotype). The global score test did not reveal any statistically significant differences in haplotype frequency distributions for these two genes. Our findings suggest that the MMP-9_rs9509 polymorphism may be associated with ICH in patients with BAVM.
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PMID:The rs9509 polymorphism of MMP-9 is associated with risk of hemorrhage in brain arteriovenous malformations. 2279 76

Yu Ping Feng San (YPFS), an ancient Chinese herbal decoction composed of Astragali Radix, Atractylodis Macrocephalae Rhizoma and Saposhnikoviae Radix, has been used in the clinic for treating immune deficiency. In cancer therapy, YPFS is being combined with chemotherapy drugs to achieve improved efficacy; however, scientific evidence to illustrate this combination effect is lacking. The present study aims to demonstrate the anti-drug resistance of YPFS in cisplatin (DDP)-resistant non-small cell lung cancer cells (A549/DDP). The application of YPFS exhibited a synergistic enhancement of DDP-induced cytotoxicity as well as of the apoptotic signalling molecules. DDP-induced expression of the multi-drug-resistance efflux transporters was markedly reduced in the presence of YPFS, resulting in a higher intracellular concentration of DDP. In addition, the application of YPFS increased DDP-induced ROS accumulation and MMP depletion, decreased p62/TRAF6 signalling in DDP-treated A549/DDP cells. The co-treatment of DDP and YPFS in tumour-bearing mice reduced the tumour size robustly (by more than 80%), which was much better than the effect of DDP alone. These results indicate that YPFS can notably improve the DDP-suppressed cancer effect, which may be a consequence of the elevation of intracellular DDP via the drug transporters as well as the down regulation of p62/TRAF6 signalling.
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PMID:Yu Ping Feng San reverses cisplatin-induced multi-drug resistance in lung cancer cells via regulating drug transporters and p62/TRAF6 signalling. 2755 12

Jiawei Foshou San (JFS) is the new formula originated from classic Foshou San formula, composed with ligustrazine, ferulic acid, and tetrahydropalmatine. Previously JFS inhibited the growth of endometriosis (EMS) with unclear mechanism, especially in metastasis, invasion, and epithelial-mesenchymal transition. In this study, network pharmacology was performed to explore potential mechanism of JFS on EMS. Through compound-compound target and compound target-EMS target networks, key targets were analyzed for pathway enrichment. MMP-TIMP were uncovered as one cluster of the core targets. Furthermore, autologous transplantation of EMS rat's model were used to evaluate in vivo effect of JFS on invasion, metastasis and epithelial-mesenchymal transition. JFS significantly suppressed the growth, and reduced the volume of ectopic endometrium, with modification of pathologic structure. In-depth study, invasion and metastasis were restrained after treating with JFS through decreasing MMP-2 and MMP-9, increasing TIMP-1. Meanwhile, JFS promoted E-cadherin, and attenuated N-cadherin, Vimentin, Snail, Slug, ZEB1, ZEB2, Twist. In brief, anti-EMS effect of JFS might be related to the regulation of epithelial-mesenchymal transformation, thereby inhibition of invasion and metastasis. These findings reveal the potential mechanism of JFS on EMS and the benefit for further evaluation.
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PMID:Anti-endometriosis Mechanism of Jiawei Foshou San Based on Network Pharmacology. 3009 62