Leonurine protects against ulcerative colitis by alleviating inflammation and modulating intestinal microflora in mouse models

xlomafota13 shared this article with you from Inoreader Leonurine protects against ulcerative colitis by alleviating inflammation and modulating intestinal microflora in mouse models Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1199. doi: 10.3892/etm.2021.10633. Epub 2021 Aug 23. ABSTRACT Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the colon. The aim of the present study was to explore the effects of leonurine (YMJ) on inflammation and intestinal microflora in colonic tissues of a dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) mouse model. Mice were randomly divided into control (n=5), DSS (n=5, treated with DSS) and DSS+YMJ (n=5, treated with DSS and YMJ) groups. Body weight was recorded, disease activity index (DAI) was calculated, and colon histopathology was evaluated using hematoxylin and eosin staining. Serum interleukin (IL)-6, tumor necrosis factor-α (TNF-α) and IL-1β levels were examined using ELISA. Expression levels of nuclear factor-κB (p65) and phosphorylated (p)-p65 were evaluated via western blotting. 16S ribosomal RNA was extracted from mouse feces. Composition or abundan ce changes of intestinal microflora were analyzed. The results indicated that YMJ treatment (DSS+YMJ group) significantly increased body weight, reduced DAI scores and increased colon length in UC mouse models compared with those in the DSS group (P<0.05). YMJ significantly reduced inflammatory infiltration, significantly decreased serum TNF-α, IL-6 and IL-1β levels (P<0.05) and significantly downregulated the p-p65/p65 ratio compared with the DSS group (P<0.05). YMJ increased the quantity of the intestinal flora and improved intestinal microflora diversity in the mice of the DSS group. Specifically, YMJ partly regulated intestinal microflora in feces, including a reduction of Bifidobacterium, and an increase in Parasutterella and Ackermania. In conclusion, YMJ improved disease outcomes of the UC mice, reduced the levels of serum inflammatory factors and increased the ratio of beneficial bacteria in the intestinal tract. PMID:34584544 | PMC:PMC8422400 | DOI:10.3892/etm.2021.10633 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Linc8986 and linc0597 in plasma are novel biomarkers for systemic lupus erythematosus

xlomafota13 shared this article with you from Inoreader Linc8986 and linc0597 in plasma are novel biomarkers for systemic lupus erythematosus Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1210. doi: 10.3892/etm.2021.10644. Epub 2021 Aug 24. ABSTRACT Despite increasing evidence that large intergenic non-coding RNAs (lincRNAs) are widely involved in human disease, the role of lincRNAs in the development of systemic lupus erythematosus (SLE) has remained largely elusive. The purpose of the present study was to investigate the expression of three lincRNAs (linc0597, linc8986 and linc7190) in the plasma of patients with SLE and their potential use as biomarkers for the diagnosis and treatment of SLE. Plasma samples were obtained from 54 patients with SLE, 24 patients with rheumatoid arthritis (RA), 24 patients with Sjogren's syndrome (SS) and 22 healthy controls. LincRNA expression levels were measured by reverse transcription-quantitative PCR. Compared with those in the healthy controls, the plasma levels of linc0597 and linc8986 were significantly increased in the patients with SLE (P<0.001) , while the difference in the level of linc7190 was not significant (P=0.052). In addition, there was no significant difference in the levels of linc0597 and linc8986 among patients with RA, patients with SS and the healthy controls (P>0.05). Compared with patients with SLE without lupus nephritis (LN), the levels of linc0597 were significantly higher in patients with LN (P=0.044). For linc7190 and linc8986, there was no significant difference between patients with and without LN (P>0.05). Furthermore, complement component 3 (C3) levels were used to evaluate whether the expression of linc8986 and linc0597 is related to the activity of SLE. The results indicated that the levels of linc8986 and linc0597 were negatively correlated with the level of C3 (P<0.001 and P=0.004, respectively). Further analysis suggested that linc0597 and linc8986 were able to specifically identify patients with SLE and that a combination of linc0597 and linc8986 may improve the diagnostic accuracy. Therefore, the plasma levels of linc0597 and linc8986 may be suitable biomarkers for diagnosing SLE. PMID:34584555 | PMC:PMC8422381 | DOI:10.3892/etm.2021.10644 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Regulatory role of microRNA-320 during off-pump coronary artery bypass grafting with dexmedetomidine adjunct anesthesia

xlomafota13 shared this article with you from Inoreader Regulatory role of microRNA-320 during off-pump coronary artery bypass grafting with dexmedetomidine adjunct anesthesia Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1201. doi: 10.3892/etm.2021.10635. Epub 2021 Aug 23. ABSTRACT The present study investigated the effects of dexmedetomidine on the expression level of microRNA-320 (miR-320) and neuroglobin (NGB) in patients undergoing off-pump coronary artery bypass grafting (OPCABG). A total of 40 patients undergoing OPCABG were recruited and randomly divided into the dexmedetomidine and normal saline groups (treated before anesthesia), respectively. The NGB levels in the blood samples before and after surgery were analyzed and compared. The CATH.a cells were cultured and induced with dexmedetomidine, and the NGB expression level was detected. CATH.a cells were treated with NGB and lipopolysaccharide (LPS), and the cell survival rate was determined. The miR-320 expression levels in the blood samples and dexmedetomidine-induced cells were detected. Dual-luciferase reporter assay was performed. Compared with control subject s, patients in the dexmedetomidine group had higher NGB levels in the blood. In the CATH.a cells, the dexmedetomidine treatment upregulated the NGB levels. Moreover, upon pre-incubation with NGB and LPS stimulation, dexmedetomidine elevated cell viability. Furthermore, miR-320 expression levels were significantly downregulated in the blood of patients in the dexmedetomidine group, as well as in the dexmedetomidine-induced cells. Dual-luciferase reporter assay confirmed that miRNA-320a directly targeted on NGB, and upregulated miRNA-320a in CATH.a cells decreased cell proliferation activity. Pre-administration of dexmedetomidine can decrease miR-320 expression level in the blood of patients undergoing OPCABG, stimulating the high expression of NGB and increasing the proliferation activity of neuronal cells, which may decrease the postoperative cognitive impairment. PMID:34584546 | PMC:PMC8422394 | DOI:10.3892/etm.2021.10635 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

HBxAg promotes HBV replication and EGFR activation in human placental trophoblasts

xlomafota13 shared this article with you from Inoreader HBxAg promotes HBV replication and EGFR activation in human placental trophoblasts Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1211. doi: 10.3892/etm.2021.10645. Epub 2021 Aug 24. ABSTRACT Hepatitis B virus (HBV) infection is a global epidemic. The main transmission route of chronic HBV infection is from mother to child, yet the mechanisms underlying HBV intrauterine infection remain unclear. In the present study, the effect and the mechanism underlying hepatitis B virus X antigen (HBxAg) on HBV replication and EGFR activation in trophoblasts was investigated. Serum samples from pregnant women with HBV infection were used to infect trophoblasts and HBxAg expression was detected using ELISA. HBV plasmids carrying either full length hepatitis B virus X (HBx) or HBx with a deletion mutation (ΔHBx) were transfected into trophoblasts and expression levels of HBV DNA, hepatitis B e-antigen and pregenomic (pg)RNA, and structural maintenance of chromosomes (Smc) 5/6 were assessed. The association between HBx and EGFR promoters was charact erized using a luciferase reporter assay and EGFR/PI3K/phosphorylated (p)-AKT expression and apoptosis rate were also monitored. The results of the present study indicated that HBxAg expression increased with the increasing titre of HBV DNA (P<0.05). Compared with the wild-type group, the amount of HBV DNA in the supernatant and cells was significantly reduced (P<0.05) in the ΔHBx group and the intracellular HBeAg and pgRNA levels were also significantly decreased (P<0.05). In addition, Smc5/6 expression was also significantly decreased (P<0.05) when the intracellular HBx protein was expressed compared with mock-transfected cells. Co-transfection of HBx and EGFR promoter plasmids in JEG-3 and HTR-8 cells significantly elevated EGFR promoter driven luciferase expression relative to the control group (P<0.01). In EGFR overexpressing cells, the expression of PI3K/p-AKT was significantly increased, whereas the apoptosis rate was significantly decreased (P<0.05). These results were reversed in the EGFR-knockdown group. In conclusion, the present study demonstrated that HBx promotes HBV replication in trophoblasts via downregulation of Smc5/6, activates the EGFR promoter and inhibits trophoblast apoptosis via the PI3K/p-AKT downstream signalling pathway, thereby increasing the risk of HBV intrauterine infection. PMID:34584556 | PMC:PMC8422389 | DOI:10.3892/etm.2021.10645 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Podofilox suppresses gastric cancer cell proliferation by regulating cell cycle arrest and the c-Myc/ATG10 axis

xlomafota13 shared this article with you from Inoreader Podofilox suppresses gastric cancer cell proliferation by regulating cell cycle arrest and the c-Myc/ATG10 axis Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1203. doi: 10.3892/etm.2021.10637. Epub 2021 Aug 23. ABSTRACT Gastric cancer (GC) is a malignancy for which effective therapeutic drugs are limited. Podofilox exhibits antitumor effects in various types of cancer; however, whether it may inhibit GC growth remains unknown. The aim of the present study was to investigate the role of podofilox in GC. Cell Counting Kit-8, colony formation and cell cycle assays were used to detect the role of podofilox on cellular proliferation and the cell cycle, respectively. A microarray was used to detect the transcriptional changes induced by podofilox in GC cells. The results of the present study demonstrated that podofilox inhibited GC cell proliferation and colony formation. The half maximal inhibitory concentration of podofilox in AGS and HGC-27 cells was 2.327 and 1.981 nM, respectively. In addition, treatment with podofilox induced G0/G1 cell cyc le arrest. Molecular analysis based on microarray data demonstrated that podofilox altered the expression levels of genes involved in the cell cycle, c-Myc and p53 signaling. Autophagy-related 10 (ATG10), which was highly expressed in GC tissues, was also downregulated by podofilox, as demonstrated by the results of the microarray analysis and immunoblotting. To determine the involvement of ATG10 in GC, ATG10 was knocked down in GC cells by small interfering RNA, which suppressed the proliferation and colony formation of GC cells compared with those observed in the control-transfected cells. Taken together, the results of the present study suggested that podofilox may inhibit GC cell proliferation by preventing the cell cycle progression and regulating the c-Myc/ATG10 signaling pathway. PMID:34584548 | PMC:PMC8422391 | DOI:10.3892/etm.2021.10637 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Overexpression of miR-133b protects against isoflurane-induced learning and memory impairment

xlomafota13 shared this article with you from Inoreader Overexpression of miR-133b protects against isoflurane-induced learning and memory impairment Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1207. doi: 10.3892/etm.2021.10641. Epub 2021 Aug 24. ABSTRACT A number of microRNAs (miRs) have been identified as being involved in the regulation of anesthesia-induced cognitive impairment. The aim of the present study was to investigated the role and potential mechanism of miR-133b in isoflurane-induced learning and memory impairment. An animal model of isoflurane exposure was established using neonatal Sprague-Dawley rats. The rats were trained for Morris water maze (MWM) testing to assess their spatial learning and memory ability. Reverse transcription-quantitative polymerase chain reaction was used for the measurement of miR-133b expression in hippocampal tissues and primary hippocampal neuron cultures. Cell viability was assessed using a Cell Counting Kit-8 assay, and flow cytometric analysis was used to determine the rate of apoptosis. The MWM test results indicated that during the training period, the time required to locate the platform was significantly increased for rats exposed to isoflurane, and this increased time was reduced by the overexpression of miR-133b. The results of a probe trial indicated that isoflurane exposure increased escape latency and decreased the time spent in the platform area for isoflurane-treated rats; however, these effects were reversed by the injection of miR-133b agomir. The in vitro experiments demonstrated that the overexpression of miR-133b attenuated the reduction of neuronal cell viability induced by isoflurane, and inhibited the isoflurane-induced apoptosis of hippocampal neurons. In conclusion, the present study revealed that the overexpression of miR-133b attenuated isoflurane-induced learning and memory impairment in rats. Furthermore, miR-133b overexpression promoted the viability of hippocampal neurons and their resistance to apoptosis when exposed to isoflurane. PMID:34584552 | PMC:PMC8422403 | DOI:10.3892/etm.2021.10641 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Correlation between metabolic status and diabetic retinopathy evolution in type 1 diabetes

xlomafota13 shared this article with you from Inoreader Correlation between metabolic status and diabetic retinopathy evolution in type 1 diabetes Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1214. doi: 10.3892/etm.2021.10648. Epub 2021 Aug 26. ABSTRACT Out of the multiple vascular complications of diabetes, retinopathy is the easiest to diagnose and monitor as the examination of the eye fundus is an easy investigation to perform, does not require expensive medical equipment and can be repeated without any risk to the patient. The appearance of the retinal vessels, the optic nerve and the retina can provide useful information on the coronary and cerebral circulation, plasma lipid levels, renal function, and the quality of the arteries of the lower limbs. It is known that visual acuity changes variably depending on the macular alteration and may decrease when edema is installed in the macular region or is altered by the appearance of hemorrhages or the presence of foveolar neovascular tissues resulting from traction retinal detachment. In the absence of proper treatment, diabetes leads to blindne ss. The lesions that appear are not specific to diabetes, but by combining them they create a clinical picture characteristic of this disease. PMID:34584559 | PMC:PMC8422396 | DOI:10.3892/etm.2021.10648 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.