Kuwanon G protects HT22 cells from advanced glycation end product-induced damage

xlomafota13 shared this article with you from Inoreader Kuwanon G protects HT22 cells from advanced glycation end product-induced damage Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):425. doi: 10.3892/etm.2021.9869. Epub 2021 Feb 25. ABSTRACT The incidence of diabetic encephalopathy is increasing as the population ages. Evidence suggests that formation and accumulation of advanced glycation end products (AGEs) plays a pivotal role in disease progression, but limited research has been carried out in this area. A previous study demonstrated that Kuwanon G (KWG) had significant anti-oxidative stress and anti-inflammatory properties. As AGEs are oxidative products and inflammation is involved in their generation it is hypothesized that KWG may have effects against AGE-induced neuronal damage. In the present study, mouse hippocampal neuronal cell line HT22 was used. KWG was shown to significantly inhibit AGE-induced cell apoptosis in comparison with a control treatment, as determined by both MTT and flow cytometry. Compared with the AGEs group, expression of pro-apoptotic protein Bax was red uced and expression of anti-apoptotic protein Bcl-2 was increased in the AGEs + KWG group. Both intracellular and extracellular levels of acetylcholine and choline acetyltransferase were significantly elevated after KWG administration in comparison with controls whilethe level of acetylcholinesterase decreased. These changes in protein expression were accompanied by increased levels of superoxide dismutase and glutathione peroxidase synthesis and reduced production of malondialdehyde and reactive oxygen species. Intracellular signaling pathway protein levels were determined by western blot and immunocytochemistry. KWG administration was found to prevent AGE-induced changes to the phosphorylation levels of Akt, IκB-α, glycogen synthase kinase 3 (GSK3)-α and β, p38 MAPK and NF-κB p65 suggesting a potential neuroprotective effect of KWG against AGE-induced damage was via the PI3K/Akt/GSK3αβ signaling pathway. The findings of the present study suggest that KWG may be a potential treatment for diabetic encephalopathy. PMID:33747164 | PMC:PMC7967837 | DOI:10.3892/etm.2021.9869 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Expression of histone deacetylase 2 in tracheal stenosis models and its relationship with tracheal granulation tissue proliferation

xlomafota13 shared this article with you from Inoreader Expression of histone deacetylase 2 in tracheal stenosis models and its relationship with tracheal granulation tissue proliferation Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):444. doi: 10.3892/etm.2021.9872. Epub 2021 Mar 1. ABSTRACT The current treatments for benign tracheal stenosis are inefficient. The present study examined the expression of histone deacetylase 2 (HDAC2) in different tracheal stenosis models and explored its association with the proliferation of tracheal granulation tissue and its ability to constitute a potential therapy for tracheal stenosis. Animal tracheal stenosis models were established, as indicated by hematoxylin and eosin (H&E) staining. A total of 24 New Zealand White rabbits were randomly divided into control, erythromycin, budesonide and vorinostat groups. Stenotic tracheal tissues were collected on day 11 after drug administration for 10 days. The degree of tracheal stenosis in each group was calculated, and pathological alterations were observed using H&E staining. The mRNA expression of HDAC2, interleukin-8 (IL-8), transforming growth factor-β1 (TGF-β1) and vascular endothelial growth factor (VEGF) was examined via reverse transcription-quantitative PCR. The protein expression of HDAC2 was examined via immunofluorescence, while the expression of type I and type III collagen was assessed using immunohistochemistry. The results of the present study demonstrated that tracheal epithelial hyperplasia in the erythromycin group was improved, the degree of hyperplasia being the lowest among all groups, and tracheal stenosis was reduced compared with the control group. In the vorinostat group, tracheal epithelial tissue hyperplasia was aggravated and stenosis was increased. The HDAC2 mRNA and protein levels were increased and decreased in the erythromycin and vorinostat groups, respectively. In contrast, the IL-8 mRNA expression levels were decreased and increased in the erythromycin and vorinostat groups, respectively. TGF-β1, VEGF, type I and type III collagen expression was decreased in the erythromycin group, while TGF-β1, VEGF and type III collagen expression was increased in the vorinostat group. Compared with the control, the budesonide group did not exhibit any alterations in all of the indicators examined, including TGF-β1, VEGF, IL-8, HDAC2 and collagen. Erythromycin treatment upregulated the expression of HDAC2, inhibited the inflammatory responses and reduced the proliferation of tracheal granulation tissue. In contrast, vorinostat treatment downregulated HDAC2 expression, promoted the inflammatory responses and increased the proliferation of tracheal granulation tissue. These results suggest that regulating HDAC2 may be used as a potential treatment for benign tracheal stenosis. PMID:33747180 | PMC:PMC7967890 | DOI:10.3892/etm.2021.9872 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Protective effects of dexmedetomidine on the ischemic myocardium in patients undergoing rheumatic heart valve replacement surgery

xlomafota13 shared this article with you from Inoreader Protective effects of dexmedetomidine on the ischemic myocardium in patients undergoing rheumatic heart valve replacement surgery Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):427. doi: 10.3892/etm.2021.9844. Epub 2021 Feb 26. ABSTRACT The aim of the present study was to compare the effects of two methods of dexmedetomidine (Dex) administration on myocardial injury, inflammation and stress in ischemic myocardium during rheumatic heart valve replacement. In total, 90 patients were included in the present study and were divided into the following three groups: i) Dex group (1.0 µg/kg Dex pre-administered 10 min prior to anesthesia, then 0.5 µg/kg/h Dex for maintenance); ii) Dex pre-conditioning group (Pre-Dex; 1.0 µg/kg Dex administered 10 min prior to anesthesia, then saline for maintenance); and iii) control group (saline 10 min prior to anesthesia and saline during maintenance), with 30 patients in each group. Heart rate (HR) and mean artery pressure (MAP) were recorded at eight time-points: i) T1, pre-medication; ii) T2, 10 min post-medication; iii) T3, immediately post-intu bation; iv) T4, upon skin incision; v) T5, upon sawing the sternum; vi) T6, immediately post-cardiopulmonary bypass; vii) T7, immediately post-operation; and viii) T8, 24 h post-operation. The serum cardiac troponin I (cTnI), interleukin (IL)-8, IL-10 and malondialdehyde (MDA) levels were also detected at T1, T6, T7 and T8. Blood glucose levels were detected at T1, T5, T6 and T7. In comparison with the control group, patients in the Dex group exhibited a significant increase in cardiac function, as indicated by an increase in HR, MAP and IL-10 levels, and a significant decrease in cTnI, IL-8, MDA and glucose levels. Both Dex perfusion and Dex preconditioning were able to reduce myocardial injury, inflammation, oxidative stress and stress response in rheumatic heart valve replacement surgery. However, Dex perfusion during the whole surgery was more effective than Dex preconditioning treatment. The study was registered with the Chinese Clinical Trial Registry (ChiCTR; no. ChiCTR-INR-1 7011955). PMID:33747166 | PMC:PMC7967827 | DOI:10.3892/etm.2021.9844 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

miR-584 and miR-146 are candidate biomarkers for acute respiratory distress syndrome

xlomafota13 shared this article with you from Inoreader miR-584 and miR-146 are candidate biomarkers for acute respiratory distress syndrome Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):445. doi: 10.3892/etm.2021.9873. Epub 2021 Mar 1. ABSTRACT MicroRNAs (miRNAs/miRs) have important roles in inflammation and infections, which are common manifestations of acute respiratory distress syndrome (ARDS). The present study aimed to assess whether serum miRNAs are potential diagnostic biomarkers for human ARDS. For this, two sets of serum samples from healthy individuals and patients with ARDS were analysed by high-throughput sequencing to identify differentially expressed genes in ARDS. A total of 679 valid sequences were identified as differentially expressed (P<0.05). Of these, five differentially expressed miRNAs were subjected to reverse transcription-quantitative PCR validation. Finally, two miRNAs (miR-584 and miR-146a) were successfully verified. These two miRNAs were significantly downregulated in the serum of patients with ARDS. Gene Ontology annotations and Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed that their target transcripts were implicated in a broad range of biological processes and various metabolic pathways, including involvement in the regulation of various inflammatory factors. The present study provided a framework for understanding the molecular mechanisms of ARDS and suggested that miR-584 and miR-146a are associated with ARDS and may be potential therapeutic targets. PMID:33747181 | PMC:PMC7 967848 | DOI:10.3892/etm.2021.9873 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Anti-inflammatory effects of Fritillaria thunbergii Miquel extracts in LPS-stimulated murine macrophage RAW 264.7 cells

xlomafota13 shared this article with you from Inoreader Anti-inflammatory effects of <em>Fritillaria thunbergii</em> Miquel extracts in LPS-stimulated murine macrophage RAW 264.7 cells Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):429. doi: 10.3892/etm.2021.9846. Epub 2021 Feb 26. ABSTRACT The aim of the present study was to demonstrate that Fritillaria thunbergii Miquel extract exerts anti-inflammatory and antioxidant effects on lipopolysaccharide-stimulated RAW 264.7 cells. To confirm the inhibitory effect of ethyl acetate fraction of FTM (EAFM) on inflammation, the expression of nitric oxide (NO) and inflammatory cytokines was assessed by performing ELISA. Expression of intracellular mRNA and protein was confirmed by reverse transcription PCR and western blotting. In addition, the anti-inflammatory and anti-oxidant mechanisms of NF-κB, MAPK and heme oxygenase-1 (HO-1) were also investigated. EAFM significantly inhibited the expression of inflammatory factors including NO, IL-6 and TNF-α at non-toxic concentrations. EAFM also inhibited the mRNA and protein expression of inducible nitric oxide synthase in a concentration-de pendent manner, but did not alter the expression of cyclooxygenase-2. Pre-treatment with EAFM inhibited the nuclear translocation of NF-κB, and suppressed the phosphorylation of ERK and JNK. In addition, EAFM induced 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging activity and an increase in the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1. The results indicated that EAFM inhibited the expression of pro-inflammatory cytokines by inhibiting ERK/JNK phosphorylation and NF-κB translocation. EAFM also exerted antioxidant effects via Nrf2/HO-1 stimulation. Collectively, the results of the present study indicated that EAFM may be a valuable alternative for the treatment of a variety of inflammatory diseases. PMID:33747168 | PMC:PMC7967825 | DOI:10.3892/etm.2021.9846 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Serum NT-proBNP and TUG1 as novel biomarkers for elderly hypertensive patients with heart failure with preserved ejection fraction

xlomafota13 shared this article with you from Inoreader Serum NT-proBNP and TUG1 as novel biomarkers for elderly hypertensive patients with heart failure with preserved ejection fraction Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):446. doi: 10.3892/etm.2021.9874. Epub 2021 Mar 1. ABSTRACT Patients with heart failure with preserved ejection fraction (HFPEF) account for ~50% of all cases of heart failure and their clinical prognosis is poor. The present study attempted to investigate the diagnostic value of circulating long non-coding RNA taurine upregulated gene 1 (TUG1) for HFPEF in subjects with hypertension. Between January 2017 and January 2019, 80 aged/elderly hypertensive patients with or without HFPEF were recruited for the present study. The concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP) in the serum was measured using ELISA and TUG1 expression levels were determined using reverse transcription-quantitative PCR. Echocardiography was used for the determination of cardiac function. The results indicated that the levels of NT-proBNP and TUG1 were increased in the serum of hypertensive patients with HFPEF. P earson analysis demonstrated that NT-proBNP and TUG1 were positively correlated with the left atrial diameter and negatively correlated with the ratio of the peak flow velocity in the early diastolic phase to the peak flow velocity in the late diastolic phase. In addition, a positive correlation was confirmed between TUG1 and NT-proBNP levels. Receiver operating characteristic curve analysis demonstrated that TUG1 and NT-proBNP were useful biomarkers for the diagnosis of HFPEF. In conclusion, it was observed that NT-proBNP and TUG1 were increased in the serum of hypertensive patients with HFPEF. Furthermore, TUG1 and NT-proBNP were indicated to be useful plasma biomarkers for the diagnosis of HFPEF. PMID:33747182 | PMC:PMC7967840 | DOI:10.3892/etm.2021.9874 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

miR-135a-5p inhibitor protects glial cells against apoptosis via targeting SIRT1 in epilepsy

xlomafota13 shared this article with you from Inoreader miR-135a-5p inhibitor protects glial cells against apoptosis via targeting SIRT1 in epilepsy Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):431. doi: 10.3892/etm.2021.9848. Epub 2021 Feb 26. ABSTRACT Epilepsy is a common neurological disease that can induce severe physiological brain damage, including nerve cell apoptosis. MicroRNAs (miRs) have been widely investigated in epilepsy therapy. miR-135a-5p expression levels in children with temporal lobe epilepsy were found to be significantly increased. However, whether miR-135a-5p participates in epilepsy-induced cell apoptosis is not completely understood. In the present study, an in vitro model of epilepsy in BV2 microglia cells was induced using 6-µm kainic acid (KA). Reverse-transcription quantitative PCR was performed to analyze miR-135a-5p and sirtuin 1 (SIRT1) mRNA expression levels. Western blotting was performed to measure SIRT1 protein expression levels. BV2 cell proliferation and apoptosis were assessed by performing MTT assays and flow cytometry, respectively. A BCA protein ass ay kit was used to detect caspase-3 and caspase-9 activities. TargetScan and dual luciferase reporter assays were performed to investigate the interaction between miR-135a-5p and the 3'-untranslated region (UTR) of SIRT1. miR-135a-5p expression was significantly increased in the KA-induced in vitro model of epilepsy in BV2 microglia. miR-135a-5p inhibitor effectively promoted BV2 microglia proliferation and inhibited microglia apoptosis, whereas small interfering RNA targeting SIRT1 significantly repressed BV2 microglia proliferation and induced microglia apoptosis. In addition, the results demonstrated that the 3'-UTR of SIRT1 mRNA was targeted by miR-135a-5p, and SIRT1 knockdown attenuated miR-135a-5p inhibitor-mediated effects on epilepsy. In summary, the results of the present study identified the role of miR-135a-5p inhibitor pretreatment in protecting nerve cells against epilepsy-induced apoptosis and provided a novel strategy for the treatment of neural damage in seizu res. PMID:33747170 | PMC:PMC7967866 | DOI:10.3892/etm.2021.9848 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Magnolol may contribute to barrier function improvement on imiquimod-induced psoriasis-like dermatitis animal model via the downregulation of interleukin-23

xlomafota13 shared this article with you from Inoreader Magnolol may contribute to barrier function improvement on imiquimod-induced psoriasis-like dermatitis animal model via the downregulation of interleukin-23 Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):448. doi: 10.3892/etm.2021.9876. Epub 2021 Mar 1. ABSTRACT Psoriasis is a chronic, recurrent, immune-mediated disease involving the skin and joints. Epidermal hyperproliferation, abnormal keratinocyte differentiation, angiogenesis with blood vessel dilatation, and excess T helper type-1 (Th-1) and Th-17 cell infiltration are the main histopathological features of psoriasis. Magnolol is a polyphenolic compound that exerts its biological properties through a variety of mechanisms such as the NF-κB/MAPK, Nrf2/HO-1 and PI3K/Akt pathways. Magnolol has been demonstrated to exert a number of therapeutic effects on dermatological processes, including acting as an anti-inflammation, antiproliferation and antioxidation agent. However, few studies have been published on the effect of magnolol on psoriasis. Therefore, the present study aimed to elucidate the mechanism of action of magnolol on psoriasis. BALB/c mice we re treated topically with imiquimod (IMQ) to induce psoriasis-like dermatitis, and were randomly assigned to the control, vehicle control, low- and high-dose magnolol, and 0.25% desoximetasone ointment treatment groups in order to investigate skin barrier function, any changes in the levels of cytokines and for the histological assessment. High doses of magnolol were indicated to be able to improve the barrier function following IMQ-induced barrier disruption. Magnolol activated peroxisome proliferator-activated receptor-γ, and also significantly inhibited the protein expression of interleukin (IL)-23, IL-1β, IL-6, tumor necrosis factor-α and interferon-γ. However, administering a high dose of magnolol did not lead to any improvement in the clinical and pathological features of the psoriasis severity Taken together, these results demonstrated that downregulation of IL-23 may contribute to barrier function improvement in a psoriatic skin model. PMID:33747183 | PMC:PMC7967813 | DOI:10.3892/etm.2021.9876 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Drug-coated balloons in the treatment of acute myocardial infarction (Review)

xlomafota13 shared this article with you from Inoreader Drug-coated balloons in the treatment of acute myocardial infarction (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):464. doi: 10.3892/etm.2021.9895. Epub 2021 Mar 5. ABSTRACT Drug-eluting stents are the standard revascularization strategy for the treatment of symptomatic coronary artery disease. However, in-stent restenosis (ISR), stent thrombosis and reinfarction of target lesions following stent implantation present challenges. Drug-coated balloons (DCBs), which deliver antiproliferative drugs into the vessel wall without stent implantation, are a novel treatment option for percutaneous coronary intervention and have been proven to act as a promising strategy in the treatment of ISR and coronary small vessel disease. However, their role in acute myocardial infarction (AMI) remains unclear. The present review discusses current evidence for the treatment of AMI with DCBs. PMID:33747196 | PMC:PMC7967819 | DOI:10.3892/etm.2021.9895 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Meta-analysis of laboratory results in patients with severe coronavirus disease 2019

xlomafota13 shared this article with you from Inoreader Meta-analysis of laboratory results in patients with severe coronavirus disease 2019 Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):449. doi: 10.3892/etm.2021.9877. Epub 2021 Mar 1. ABSTRACT The aim of the present study was to analyze the differences in laboratory results between patients with severe and moderate coronavirus disease 2019 (COVID-19) for clinical intervention. The laboratory results of patients with COVID-19 between December 2019 and May 2020 were assembled from the Medline, Embase and Cochrane Library databases. A meta-analysis was conducted, calculating the individual and pooled odds ratios (ORs) with relative 95% confidence intervals (95% CIs) using Review Manager 5.3. The available data of 1,534 patients from 6 studies were included in this analysis. The results demonstrated that the incidence of leukocytosis, lymphocytopenia, increased procalcitonin (PCT), C-reactive protein (CRP), aspartate aminotransferase (AST) and lactic dehydrogenase (LDH) levels was associated with a nearly 3-fold (OR=3.44; 95% CI: 2.15-5.49), 4-fold (OR=4.39; 95% CI: 1.82-10.60), 5-fold (OR=5.28; 95% CI: 3.42-8.15), 4-fold (OR=3.99; 95% CI: 2.61-6.12), 3-fold (OR=3.02; 95% CI: 2.13-4.26) and 8-fold (OR=8.33; 95% CI: 1.75-39.69) higher risk of severe COVID-19 infection, respectively. These findings indicated that serial white blood cell count, lymphocyte count, CRP, PCT, LDH and AST measurements may be useful for predicting progression towards a more severe form of COVID-19. PMID:33747184 | PMC:PMC7967851 | DOI:10.3892/etm.2021.9877 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.