Hatfieldlarson1075
on, the repressed cell proliferation and promoted cell apoptosis abilities in VSMCs with LV-sh circPTPRAs were reversed following with miR-636 inhibitor transfection, which suggested that circPTPRA regulated cell proliferation and apoptosis through miR-636/SP1 axis in AS.
According to the results, we found that circPTPRA was upregulated in serum samples of AS patients, which promoted cell proliferation and inhibited cell apoptosis through repressing miR-636 and upregulating SP1 signaling axis. Our results uncovered a potential role of circPTPRA, which might be a marker and therapeutic target for AS patients.
According to the results, we found that circPTPRA was upregulated in serum samples of AS patients, which promoted cell proliferation and inhibited cell apoptosis through repressing miR-636 and upregulating SP1 signaling axis. Our results uncovered a potential role of circPTPRA, which might be a marker and therapeutic target for AS patients.
To design and evaluate a novel oxyntomodulin (OXM) derivative with albumin-binding helix domain and dual GLP-1 receptor (GLP-1R) and glucagon receptor (GcgR) activation activity to achieve metabolize improvement on the diabetes-related complication.
Mutation (D-Ser2) on OXM was performed and then different helix albumin-binding domains were fused to the mutated OXM via a thrombin-cleavable linker to generate seven fusion peptides, named LM01-LM07. Seven LM peptides were synthesized and screened via in vitro receptor activation test, albumin binding measurement and protease cleavage assay to select potent candidate peptide for further in vivo study. Moreover, acute and chronic efficacy studies were conducted to evaluate the efficacy of selected candidate using db/db mice.
LM06, as selected OXM derivative, exhibited higher albumin-binding affinity, sustained-release efficiency and balanced activation activities on both GLP-1R and GcgR compared with other ones. Moreover, LM06 was demonstrated with improvedultrasound.
This study aims to investigate whether liraglutide can affect proliferation, osteogenic differentiation and serum deprivation-induced apoptosis of preosteoblast cell line MC3T3-E1 through the Notch, Wnt/β-catenin, and Hedgehog (Hh) signaling pathways.
MC3T3-E1 cells were exposed to different treatments (via Notch inhibitor DAPT, an Hh inhibitor cyclopamine, or serum deprivation) or transfections of different siRNAs (targeting glucagon-like peptide-1 receptor (GLP-1R), β-catenin, or Gli1) in the presence or absence of 100 nM liraglutide. Selleck Epigenetic inhibitor Cell proliferation, mRNA levels of osteogenic differentiation-related genes, mRNA and protein levels of the Notch and Hh signaling pathway proteins, and apoptosis-related proteins were assessed.
Liraglutide significantly increased proliferation of MC3T3-E1 cells, expression levels of the Notch and Hh signaling pathway proteins and β-catenin, and mRNA levels of osteogenic differentiation-related genes and TCF7L2. Moreover, liraglutide promoted a translocation of β-catenin signaling pathways involving β-catenin and Gli1. These results provide a therapeutic foundation that patients with diabetes and osteoporosis may be cured with treatments of liraglutide.
To evaluate the protective effect of dexmedetomidine (Dex) against renal ischemia-reperfusion injury (RIRI) in rats through the phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (Akt)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway.
(1) A Sprague- Dawley rat model of RIRI was established. Thirty rats were divided into Sham group, injury (RIRI) group, and Dex treatment (RIRI + Dex) group. Serum was collected to detect renal function-related indexes, and the levels of serum inflammatory factors were examined via enzyme-linked immunosorbent assay (ELISA). (2) The kidney tissues were separated, and the degree of tissue damage was determined using immunohistochemical staining. (3) Ribonucleic acids (RNAs) were extracted from tissues, and the mRNA levels of inflammatory factors were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). (4) The protein expressions of Akt, phosphorylated (p)-Akt, PI3K, p-PI3K, and HIF-1α were detected via Western blotting.
Compared with those in RIRI group, the levels of blood urea nitrogen and creatinine declined (p<0.05), the synthesized mRNAs of inflammatory factors in the kidney tissues were reduced (p<0.05), the secreted serum inflammatory factors was also reduced (p<0.05), and the phosphorylation levels of Akt and PI3K and the HIF-1α level rose (p<0.05) in RIRI + Dex group.
Dex promotes the recovery of renal function and reduces the inflammatory level in RIRI rats through the PI3K/Akt/HIF-1α signaling pathway.
Dex promotes the recovery of renal function and reduces the inflammatory level in RIRI rats through the PI3K/Akt/HIF-1α signaling pathway.
This study aims to evaluate the effect of trans-resveratrol/carboxymethylated (1.3/1.6)-β-d-glucan administered via nasal, after FESS, assessing nasal respiratory distress and nasal mucosa healing.
We enrolled 70 patients, from March 2019 to February 2020, with chronic nasal obstruction not responding to medical therapy and candidates to endoscopic nasal surgery. Patients were divided in two non-randomized groups group A treated with trans-resveratrol/carboxymethylated (1.3/1.6)-β-d-glucan administered via nasal, and group B treated with 0.9% nasal irrigation saline. Patients were clinically evaluated, in post-operative period, at 7 (T0), 15 (T1), and 30 days (T2) with fibroendoscopy. The CRS (chronic rhinosinusitis) questionnaire (Snot 20) was administrated at T0, T1, and T2. The findings were scored with respect to middle turbinate edema. In both Groups, the inferior turbinate's medial aspect was scraped using a sterile disposable Rhino-probe mucosal curette (Arlington Scientific, Inc., Springville, UT, USA) at T0, T1, and T2.
Group A showed an improvement in Snot 20 in T1 and T2 both. The reduction of the mucosal edema and nasal secretion has been statistically significant in the Group A. A slight cell reduction was observed at T2 with respect to T1. This decreased pattern is more evident in nasal scraping from Group A. The appearance of epithelial cells at T2 of Group A is consistent with the reduction of inflammatory cells.
We can assert that in Group A it appears less evident the presence of edema, nasal congestion and crusts, resulting in a quick recover.
We can assert that in Group A it appears less evident the presence of edema, nasal congestion and crusts, resulting in a quick recover.
Several chronic illnesses, including HIV infection are associated with oxidative stress. In addition to HIV itself, some antiretrovirals also increase oxidative stress while decreasing viral replication. To investigate the alterations in oxidative stress parameters and thiol-disulphide homeostasis in people living with HIV who were receiving integrase inhibitor-based antiretroviral therapy.
Thirty treatment-naive adult people living with HIV were prospectively enrolled in the study. Sera were collected from patients twice at the beginning of antiretroviral therapy (group 1) and 6 months later (group 2). Thirty age-matched healthy volunteers were enrolled in the study as the control group (group 3). Serum levels of total antioxidant status (TAS) and total oxidative status (TOS) were determined using an automated measurement method. Serum malondialdehyde (MDA) and protein carbonyl (PC) levels were measured spectrophotometrically. CD4+ T-cells were counted flow cytometrically. A mathematical equation was useople living with HIV.
Acute kidney injury (AKI) is a common critical illness in clinic, which seriously threatens the life of patients. The aim of this study was to validate the anti-apoptotic effect of hydroxytyrosol (HT) in ischemia/reperfusion (I/R)-induced AKI.
The cell model of AKI was established by hypoxia/reoxygenation (H/R), and the animal model of AKI was established by I/R. The apoptosis was observed by Caspase-3 activity assay, flow cytometry and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining. Cell viability was detected by cell counting kit-8 (CCK-8) assay. Protein expression was measured by Western blot and mRNA level was analyzed by quantitative real-time polymerase chain reaction (RT-PCR). Renal function was assessed by measuring serum creatinine (Cr) and blood urea nitrogen (BUN).
H/R induced apoptosis of HK-2 cells and reduced cell viability. When HK-2 cells were pretreated with HT, apoptosis was markedly inhibited, and cell viability was greatly increased. In addition, HT could inhibit I/R-induced apoptosis of rat kidney cells and could notably improve rat kidney function. H/R promoted Sonic Hedgehog (SHH) expression in HK-2 cells, while HT treatment further enhanced SHH expression. Similarly, I/R induces SHH expression in kidney tissue, and HT could further promote SHH expression.
These results indicated that HT could inhibit apoptosis in I/R-induced AKI via activating SHH signaling pathway.
These results indicated that HT could inhibit apoptosis in I/R-induced AKI via activating SHH signaling pathway.
To investigate the effects and mechanism of metformin (Met) combined the interleukin-12 (IL-12) on inhibiting hepatoma HepG2 cell proliferation via in vitro and in vivo assays.
MTT assay was used to detect inhibitory effects of Met, IL-12 alone or combination on HepG2 cells proliferation. Half inhibitory concentration (IC50) and combination index (CI) were also calculated. Anti-tumor effects of combination or monotherapy on the HepG2-bearing mice were investigated and protein expression levels of apoptosis, as well as the Akt/mTOR/STAT3 signaling pathway-related factors were detected by Western blot.
MTT results showed that the inhibitory effect of Met combined with IL-12 on HepG2 cell proliferation was significantly enhanced (both p<0.01) compared with monomer therapy group with a significant synergistic effect (CI<1). The apoptosis rate of HepG2 cells treated with Met combined with IL-12 were 88.12±7.15% and significantly higher than the others (all p<0.01). Moreover, combination treatment significantly suppressed hepatoma growth and increased the survival rate of HepG2-bearing mice without evident body weight loss. Western blot analysis showed that Met combined with IL-12 significantly increased the expression of autophagy-related marker proteins, downregulated the protein expression levels of Bcl-2, p-Akt, p-mTOR, p-STAT3, upregulated the expression level of BAX in both HepG2 cells and tumor tissues.
Met combined with IL-12 exhibited a synergistic antitumor effect on hepatoma HepG2 cells, and the mechanism may be related to its common inhibition of Akt/mTOR/STAT3 signaling pathway and increase of autophagy in HepG2-bearing mice.
Met combined with IL-12 exhibited a synergistic antitumor effect on hepatoma HepG2 cells, and the mechanism may be related to its common inhibition of Akt/mTOR/STAT3 signaling pathway and increase of autophagy in HepG2-bearing mice.
The purpose of this study was to conduct a systematic review and meta-analysis analyzing the efficacy of zoledronic acid in improving outcomes with percutaneous vertebroplasty (PVP) and percutaneous kyphoplasty (PKP) surgeries for osteoporotic vertebral compression fracture (OVCF).
We electronically searched the databases of PubMed, Embase, ScienceDirect, CENTRAL, and Google Scholar up to 15th September 2020. All types of studies assessing the use of zoledronic acid with PKP/PVP surgeries were included.
Seven studies were included. On meta-analysis of data from five studies reporting bone mineral density (BMD) as g/cm2, we found a statistically significant increase in BMD in the zoledronic group (MD 0.14; 95% CI 0.07, 0.21, I2=97%; p<0.001). On pooled analysis of two studies reporting T scores, a similar result in favour of the zoledronic acid group was noted (MD 0.60; 95% CI 0.23, 0.98, I2=76%; p=0.002). We also found a statistically significant reduction in pain scores (MD -1.23; 95% CI -1.59, -0.86, I2=97%; p<0.
