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Osteosarcoma (OS) is the most common primary malignant bone tumor in pediatric and adolescent patients. The calcyclin-binding protein/Siah-1-interacting protein (CacyBP/SIP) performs an essential function in cell proliferation and apoptosis. The present study investigated the effect of CacyBP/SIP in OS cell proliferation and apoptosis. CacyBP/SIP mRNA expression levels were evaluated in four OS cell lines by quantitative PCR. CacyBP/SIP expression was downregulated in Saos-2 cells using a lentivirus transfection system and the transfection efficiency was analyzed. The effects of CacyBP/SIP downregulation on Saos-2 cell proliferation and colony-formation ability were evaluated by MTT and colony-formation assays. The effect of CacyBP/SIP knockdown on Saos-2 cell cycle and apoptosis was analyzed by flow cytometry cell sorting. The Cancer Genome Atlas (TCGA) data was analyzed for validation. Human OS cell lines Saos-2, MG-63, HOS and U20S expressed CacyBP/SIP mRNA. CacyBP/SIP knockdown significantly inhibited cell proliferation and colony-formation ability. G1/S phase arrest was induced by CacyBP/SIP downregulation, which also resulted in the downregulation of CDK and cyclins and the upregulation of p21. In addition, CacyBP/SIP downregulation induced Saos-2 cell apoptosis mediated by Bax and Bcl-2. High expression of CacyBP/SIP was significantly associated with poor prognosis in TCGA sarcoma database. Thus, CacyBP/SIP performs important functions in the proliferation and apoptosis of human OS cells.Hyperglycemia-induced oxidative stress and inflammation are hallmarks of liver damage in diabetes mellitus. Accumulating evidence has demonstrated that Pluchea indica leaf ethanol extract (PILE) possesses strong antioxidant and anti-inflammatory properties. However, studies of its effects on liver damage in streptozotocin (STZ)-induced diabetic animals remain insufficient. To the best of our knowledge, the present study was the first to illustrate that PILE mitigated liver injury in STZ animals. Mice were first pretreated with PILE at either 50 mg/kg (PILE 50) or 100 mg/kg (PILE 100) 2 weeks prior to the induction of hyperglycemia by multiple low doses of STZ. The mice were then fed with PILE 50 or PILE 100 for 4 or 8 weeks, following which liver weight, pathological changes, oxidative stress parameters, inflammation-related markers and caspase-mediated apoptosis were measured at each time point. Untreated STZ mice exhibited abnormal increases in liver weight and severe pathological changes. selleck chemicals llc However, PILE 100 reduced the severity of the STZ-induced diabetic phenotype at both time points. A significant decrease in the levels of superoxide dismutase and catalase, in addition to an increase in malondialdehyde, were observed in the livers of untreated STZ mice, all of which were significantly reversed by treatment with PILE 100 for 8 weeks. Western blot analysis revealed reduced levels of liver inflammatory markers, including interleukin-6, tumor necrosis factor-α, NF-κB p65, transforming growth factor-β1 and protein kinase C following PILE 100 treatment. Additionally, changes in the levels of apoptotic markers indicated that PILE 100 significantly attenuated caspase-9 and -3 expression, whilst preserving that of the Bcl-2 protein. In conclusion, the present study revealed that PILE alleviates hyperglycemia-induced liver injury by normalizing the various mediators of oxidative stress, inflammation and apoptosis.Effect of micro ribonucleic acid (miR)-30 on the proliferation of trophoblasts in preeclampsia (PE) rats through the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway was studied. The miR-30 mimic was transfected into the trophoblast HTR8/SVNEO cell lines. The effects of expression level of miR-30 on the proliferation and hypoxia-induced apoptosis of HTR8/SVNEO cells were detected via methyl thiazolyl tetrazolium (MTT) assay and Annexin V/propidium iodide staining, respectively, using the flow cytometer. A total of 30 pregnant Sprague-Dawley rats were randomly divided into control group (CTL group, n=10), PE rat group (PE group, n=10) and PE + miR-30 Mimic group (PE+agomiR-30 group, n=10) using a random number table. The protein expression levels of phosphorylated ERK (p-ERK)1/2, ERK1/2, proliferating cell nuclear antigen (PCNA) and tubulin were determined using western blot analysis, and the mRNA expression level of ERK1/2 was detected via reverse transcription-quantinhibiting cell apoptosis and promoting cell proliferation.Asarum is frequently applied in combination with other agents for prescriptions in practices of Traditional Chinese Medicine. A number of studies have previously indicated that asarum treatment induces lung toxicity by triggering inflammation. However, the potential effects of asarum in the liver and the underlying mechanisms have remained largely elusive. Therefore, transcriptomics and metabolomics approaches were used in the present study to examine the mechanisms of the hepatotoxicity of asarum. Specifically, mRNA and metabolites were obtained from rat liver samples following intragastric administration of asarum powder. RNA sequencing analysis was subsequently performed to screen for differentially expressed genes (DEGs), and a total of 434 DEGs were identified in liver tissue samples, 214 of which were upregulated and 220 were downregulated. Pathway enrichment analysis found that these genes were particularly enriched in processes including the regulation of p53 signaling, metabolic pathways and bile secretion. To investigate potential changes to the metabolic profile as a result of asarum treatment, a metabolomics analysis was performed, which detected 14 significantly altered metabolites in rat liver samples by gas chromatography-mass spectrometry. These metabolites were predominantly members of the taurine, hypotaurine and amino acid metabolic pathways. Metscape network analyses were subsequently performed to integrate the transcriptomics and metabolomics data. Integrative analyis revealed that the DEGs and metabolites were primarily associated with bile acid biosynthesis, amino acid metabolism and the p53 signaling pathway. Taken together, these results provide novel insight into the mechanism of asarum-mediated hepatotoxicity, which may potentially aid the clinical diagnosis and future therapeutic intervention of asarum poisoning.