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Outcomes of anatomical and nongenetic components about hyperuricemia in Oriental individuals with vascular disease.
Furthermore, a co‑expression network was constructed based on the co‑expression pairs between 44 DELs and 297 DEGs, in which Pvt1 and Bst1 were overlapped with the ceRNA network. Thus, Bst1‑associated ceRNA (Pvt1‑mmu‑miR‑181a‑Bst1) and co‑expression (Pvt‑Bst1) axes were also pivotal for MI. Accordingly, Pvt1 may be a crucial lncRNA for modification of cardiac remodeling in the IBZ after MI and may function by acting as a ceRNA for miR‑181a to regulate TNF/Met/Itgam/Bst1 or by co‑expressing with Bst1.The aim of the present study was to identify novel antibody markers for the early diagnosis of atherosclerosis in order to improve the prognosis of patients at risk for acute ischemic stroke (AIS) and acute myocardial infarction (AMI). A first screening involved the serological identification of antigens by recombinant cDNA expression cloning and identified additional sex combs‑like 2 (ASXL2) as a target antigen recognized by serum IgG antibodies in the sera of patients with atherosclerosis. Antigens, including the recombinant glutathione S‑transferase‑fused ASXL2 protein and its synthetic peptide were then prepared to examine serum antibody levels. Amplified luminescence proximity homogeneous assay‑linked immunosorbent assay, which incorporates glutathione‑donor beads and anti‑human‑IgG‑acceptor beads, revealed significantly higher serum antibody levels against the ASXL2 protein and its peptide in the patients with AIS, diabetes mellitus, AMI, chronic kidney disease, esophageal squamous cell carcinoma, or colorectal carcinoma compared with those in healthy donors. The ASXL2 antibody levels were well associated with hypertension complication, but not with sex, body mass index, habitual smoking, or alcohol intake. These results suggest that the serum ASXL2 antibody marker can discriminate between hypertension‑induced atherosclerotic AIS and AMI, as well as a number of digestive organ cancers.Currently, microglia are considered as crucial factors in suppressing inflammatory reactions, but the specific molecular mechanism remains unknown. To elucidate whether peroxisome proliferator‑activated receptor‑γ (PPAR‑γ) can inhibit neuroinflammatory cytokine expression via the mTOR signal pathway, the BV‑2 cell line was incubated with lipopolysaccharide (10 mM/ml) to induce an inflammatory injury. PPAR‑γ was activated by rosiglitazone, and was inhibited by GW9662. The mTOR signal pathway was activated by phosphatidic acid (P.A.), while it was inhibited by rapamycin. learn more Western blotting and reverse transcription‑quantitative PCR were used to evaluate the expression levels of PPAR‑γ/mTOR signal pathway related proteins and neuroinflammatory cytokines, including NF‑κB, tumor necrosis factor (TNF)‑α and interleukin (IL)‑1β. When treated with P.A., the expression levels of phosphorylated (p)mTOR and p‑ribosomal protein S6 kinase (pS6K) were significantly increased and the expression levels of TNF‑α and IL‑1β were significantly lower. However, the expression of PPAR‑γ was similar in P.A. link2 treated cells and cells treated with rapamycin. When PPAR‑γ was activated, pmTOR and pS6K protein expression levels were significantly decreased, and the mRNA expression levels of TNF‑α and IL‑1β were significantly reduced, but this inhibition could be alleviated by administrating GW9662. Collectively, it was indicated that the mTOR signal pathway may be located downstream of PPAR‑γ. Furthermore, neuroinflammatory reactions could be inhibited via the activation of PPAR‑γ by suppressing the mTOR signal pathway in microglia.Gastric cancer is one of the most common types of cancer worldwide, with a high incidence and mortality rate. MicroRNAs (miRs) play an important role in tumorigenesis, cell proliferation, migration, apoptosis and metastasis of cancer. The present study aimed to investigate the role and potential mechanism of miR‑204‑5p in gastric cancer. The mRNA expression levels of miR‑204‑5p in gastric cancer were determined by reverse transcription‑quantitative PCR. Cell proliferation was determined using Cell Counting Kit‑8 and colony formation assays. Flow cytometry analysis was performed to detect the cell apoptosis rate. link3 Wound healing and Transwell assays were carried out to determine the cell migration and invasion rates, respectively. A putative binding site of miR‑204‑5p in the 3' untranslated region of human epidermal growth factor receptor 2 (HER‑2) was predicted using a bioinformatics algorithm and confirmed using a dual‑luciferase reporter assay. miR‑204‑5p levels were downregulated in gastric cancer cells. Overexpression of miR‑204‑5p significantly inhibited cell proliferation and decreased cell colony formation. Additionally, miR‑204‑5p decreased the migration and invasion rates of gastric cancer cells. Furthermore, an increased apoptotic rate was detected following overexpression of miR‑204‑5p, along with increased expression levels of Bax and decreased expression levels of Bcl‑2. HER‑2 was a direct target of miR‑204‑5p, and inhibition of HER‑2 acted as a tumor suppressor by inhibiting cell proliferation, migration and invasion, and promoting cell apoptosis, which was reversed by the inhibition of miR‑204‑5p expression. These results suggested that miR‑204‑5p could exert its anti‑tumor function by inhibiting cell proliferation, migration and invasion, and promoting cell apoptosis via regulation of HER‑2, which may be a potential therapeutic target for gastric cancer.Aberrant expression of microRNAs (miRs) has been reported in various types of cancer. The aim of the present study was to investigate the role and underlying molecular mechanism of miR‑130a‑3p in cervical cancer (CC). The expression of miR‑130a‑3p in CC tissues and cell lines (CaSki and SiHa) was measured via reverse transcription‑quantitative PCR. SiHa and CaSki cells were transfected with miR‑130a‑3p mimics and a miR‑130a‑3p inhibitor, respectively. The proliferation, apoptosis and migration and invasion abilities of CC cells were then measured using MTT, flow cytometry, wound‑healing and Transwell assays, respectively. TargetScan and dual‑luciferase reporter gene assays were performed to analyze the association between miR‑130a‑3p and its predicted target gene Runt‑related transcription factor 3 (RUNX3). In addition, a xenograft tumor model was established in mice to evaluate the impact of miR‑130a‑3p on tumor growth in vivo. The expression of miR‑130a‑3p was markedly upregulated in CC tissues and cell lines compared with normal tissues and cells. Transfection with miR‑130a‑3p mimics significantly promoted the proliferation, migration and invasion, and inhibited the apoptosis of SiHa cells. Treatment of CaSki cells with a miR‑130a‑3p inhibitor resulted in opposite effects to those of miR‑130a‑3p mimics. RUNX3 was identified as the target gene of miR‑130a‑3p, and overexpression of RUNX3 eliminated the tumor‑promoting effect of miR‑130a‑3p mimics on CC cells. Overexpression of miR‑130a‑3p also promoted tumor growth in mice. In conclusion, miR‑130a‑3p promoted proliferation, migration and invasion, and inhibited the apoptosis of CC cells via targeting RUNX3, suggesting a novel treatment target for CC.α‑glucosidase is a key enzyme that plays a role in glucose absorption in the gastrointestinal tract, and the inhibition of its activity induces the prevention of postprandial hyperglycemia. Several α‑glucosidase inhibitors have been used as medicines for type 2 diabetes, but a similar effect is observed in natural resources, including traditional herbs and their phytochemicals. To identify the presence of the α‑glucosidase inhibitory activity in herbs, in which various functional effects have been known to occur, the present study investigated the effects of hot‑water extracts of 26 types of herbs on α‑glucosidase activity in an in vitro assay. The results indicated significant increases in the inhibition of α‑glucosidase activity in 1,000 µg/ml olive (P less then 0.01), white willow (P less then 0.01) and red rooibos hot‑water extracts. Furthermore, ≥50% inhibition of α‑glucosidase activity was determined to be significant in 1,000 µg/ml coltsfoot, green tea and bearberry hot‑water extracts. In addition, the effects of bearberry, green tea and coltsfoot hot‑water extracts on α‑glucosidase activity in vivo were evaluated according to the blood glucose levels (BGLs) in maltose and glucose load model rats. It was indicated that the administration of these three herb extracts significantly reduced the increasing BGLs after maltose loading until 0.5 h compared with the control group. However, only coltsfoot extract significantly reduced the increasing BGLs after glucose loading until 0.5 h compared with the control group. Thus, the present results may facilitate the understanding of a novel functionality in traditional herbs, which could be useful for the prevention of disease onset and progression, such as in hyperglycemia and type 2 diabetes.MicroRNA (miR)‑130a has been reported to promote cancer growth; however, its role during acute myeloid leukemia (AML) is not completely understood. In the present study, the effects of miR‑130a on the sensitivity of AML cells to Adriamycin (Adr) were investigated. 5‑Aza‑2'‑deoxycytidine (5‑Aza‑dC) was used to stimulate Adr resistance in AML cells, and cell viability and miR‑130a expression were determined using the Cell Counting Kit‑8 (CCK‑8) assay and reverse transcription‑quantitative PCR, respectively. miR‑130a overexpression and knockdown in Adr‑resistant AML cells was performed to investigate the proliferative and invasive abilities of the cells using CCK‑8 and Transwell assays, respectively. Furthermore, the effects of miR‑130a on the expression of epithelial‑mesenchymal transition (EMT)‑related proteins in Adr‑resistant AML cells were detected using western blot analysis. Pre‑treatment with 5‑Aza‑dC enhanced the cell viability and miR‑130a expression of Adr‑treated AML cells. Adr and miR‑130a expression showed a dose‑dependent relationship, with miR‑130a expression decreasing with increasing Adr concentrations. Moreover, miR‑130a overexpression alleviated the inhibitory effects of Adr on cell viability and invasion, while miR‑130a knockdown enhanced the sensitivity of AML cells to Adr. Furthermore, Adr exerted an inhibitory effect on EMT in AML cells, which was rescued by miR‑130a overexpression and enhanced by miR‑130a knockdown. miR‑130a knockdown also increased the sensitivity of AML cells to Adr by decreasing cell viability, invasion and EMT. Therefore, miR‑130a knockdown is a potential therapeutic strategy for Adr‑resistant AML.Cisplatin‑induced cytotoxicity, such as nephrotoxicity, neurotoxicity and ototoxicity, restricts the clinical application of this compound. Panax notoginseng Saponins (PNS) exhibit potent free radical scavenging and antioxidant activity. PNS have been demonstrated to reduce cisplatin‑induced nephrotoxicity and neurotoxicity. The present study investigated the ability of PNS to protect the auditory HEI‑OC1 cell line against ototoxicity induced by cisplatin. PNS induced activation of the AKT/nuclear factor erythroid 2‑related factor 2 (Nrf2) signaling pathway. Following pretreatment with PNS, HEI‑OC1 cells were treated with cisplatin and cultured for 24 h. The viability of HEI‑OC1 cells was examined using a Cell Counting Kit‑8 assay. Double staining analysis was used to measure cell apoptosis. The ability of PNS to reduce reactive oxygen species (ROS) levels was assessed by flow cytometry. The levels of phosphorylated (p)‑AKT, heme oxygenase 1 (HO‑1), NAD(P)H quinone dehydrogenase 1 (NQO1), glutamate‑cysteine ligase catalytic (GCLC) and Nrf2 were measured by western blotting.
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