MicroRNAs (miRNA) are small RNA molecules that negatively regulate gene expression through base pairing interactions between 3'-UTR of the target mRNAs and seed sequence of miRNA. Any changes in the recognition site could destroy binding sites or modify binding affinity, resulting in evasion from miRNA regulation. A putative binding site for miR-491-5p resides in 3'-UTR of MMP9, and a genetic variant (rs1056628 A → C) is present in this region. The role of MMP9 over expression well marked in various cancers. However, whether rs1056628 SNP in miR-491-5p binding site of MMP9 3'-UTR could abrogate its post-transcriptional regulation and affect cancer susceptibility remains largely unknown. To test this, the rs1056628 SNP was genotyped in 300 cases of lung, gastric and breast cancers and 200 age- and sex-matched healthy controls. The results showed that compared with the AA genotype, C was a risk genotype for all three cancers development and was also associated with gastric and breast cancers metastasis and invasion. Based on the base pairing analysis and secondary structure evaluation of MMP9 mRNA and miR-491-5p, we found that miR-491-5p had a higher binding affinity for A genotype than the C genotype. The Luciferase activity of MMP9 3'-UTR indicates differential regulation of two genetic variations of MMP9. Overexpression of miR-491-5p decreased MMP9 mRNA level in cell lines of gastric, breast and lung cancers and thus leads to decreasing of the invasion ability. Therefore, for the first time we imply that the C variant of MMP9 contributes to the likelihood of gastric, breast and lung cancers susceptibility via a novel mechanism of subtle gene regulation through miRNA binding capacity.
Implication for health policy/practice/research/medical education:Thyme daenensis extracts have antioxidant and anti-inflammatory properties and can improve liver injury in mice by decreasing pro-inflammatory TNF and IL-6 cytokines. So, this extract might be used as anti-inflammatory and hepato-protective agent.Please cite this paper as: Soosani B, Sazegar H. Effects of Thymus daenensis on inflammatory factors and liver toxicity induced by thioacetamide in rats.
Background: The purpose of the present study was to produce a pcDNA3.1(+)-ureA recombinant vector and evaluate the capacity of this vector to stimulate the immune response against H. pylori infection in infused BALB/c mice. Materials and methods: The pcDNA3.1(+)-ureA construct was prepared and transformed into E. coli, successfully. The animals we used in the study were allotted into three groups for infusion of 1) recombinant plasmid, 2) pcDNA3.1(+)-ureA + nanoparticles, and 3) pcDNA3.1(+). Blood and tissue specimens from each group of mice were collected at days 15, 30, and 45 after the last infusion and the expression levels of cytokines such as TGF-β1, IL-4, and IFNγ genes comparing to GAPDH as well as the expression of ureA in the mice’s thigh muscle were evaluated. Results: The genes expression analysis showed that the IL4 expression significantly decreased (p<0.001) but IFNγ and TGF-β1 expression increased in the blood of infused mice (p<0.001). Also, the urea expression level in pcDNA3.1(+)-urea and pcDNA3.1(+)-ureA+ nanoparticle 15, 30, and 45 days after the last infusion was significantly different (p<0.001) and its expressions at days 15 and 30 were significantly different (p<0.001), but 45 days after the last infusion it was not significantly different (p>0.05). Conclusion: The pcDNA3.1(+)-ureA recombinant vector with or without chitosan nanoparticles can stimulate the immune response in animal models against H. pylori infection. Also, after combining the recombinant vector with nanoparticles we observed a better immune response was observed. In future studies this recombinant construct can be used as a biomarker and therapeutic approaches in eukaryotic systems.
Background and aims: The positive effects of medicinal herbs on diabetes have been proved in previous studies. The aim of the present study was to evaluate the effect of active Momordica Charantia on the treatment of liver diseases resulting from diabetes and the expression level of the Mcl-1 gene, which is a proapoptotic gene and becomes antiapoptotic in the event of damage. Methods: In this study, 42 adult male Wistar rats were randomly divided into 7 groups including healthy, diabetic, metformin, 150 mg/kg M. charantia controls, and three groups that received the active M. charantia with doses of 50, 100, and 150 mg/kg. All groups became diabetic with streptozotocin injected intraperitoneally except for the control and M. charantia. Afterward, they received the active M. charantia by gavage for four weeks (three times a week). Finally, the Kruskal-Wallis method was used for comparison among the groups. The statistical tests were analyzed using SPSS software, version 22. Results: The level of Mcl-1 expression in the diabetic control group (C) was significantly higher than that in the healthy control (A) and the M. charantia-receiving control group (B, P < 0.05). The group receiving 150 mg/kg dose of M. charantia drug (G) had a better effect compared to the group that received 100 mg/kg (F), and this difference was significant (P < 0.05). This increase indicated that the medication was dose-dependent. Conclusion: In general, a reduction in the level of Mcl-1 gene expression relied on the M. charantia dose. After the development of diabetes, this level significantly increased in the diabetic groups, but decreased after receiving M. charantia, leading to a decrease in the side effects and symptoms associated with diabetes. Receiving 50 mg/kg of metformin 0.9043 ± 0.0002 b Receiving 50 mg/kg of M. charantia 0.77820.1178 ± b Receiving 100 mg/kg of M. charantia 0.541 ± 0.0556 c Receiving 150 mg/kg of M. charantia 0.1672 ± 0.0640 eUnsimilar letters indicate the significance of the groups together (P < 0.05).
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.