scholarly journals Therapeutic efficacy of liraglutide on diabetic nephropathy mice by inhibiting inflammatory factors

2018 ◽  
Vol 16 ◽  
pp. 205873921881928
Author(s):  
WenXing Fan ◽  
Zhang Liang ◽  
Hua Xiao ◽  
QiuPing Yang
Keyword(s):  
Diabetic Nephropathy ◽  
Messenger Rna ◽  
Quantitative Polymerase Chain Reaction ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Renal Tissue ◽  
Inflammatory Factors ◽  
Expression Of Genes ◽  
Polymerase Chain ◽  
Necrosis Factor

This study was to investigate the role and mechanism of liraglutide in the treatment of diabetic nephropathy (DN) mice. A mouse model of streptozotocin-induced DN was established. The mice were intraperitoneally injected with liraglutide at a dose of 200 μg/kg for 6 weeks. The expression of interleukin-6 (IL-6), tumor necrosis factor (TNF), and nuclear factor kappa B (NF-κB) messenger RNA (mRNA) in renal tissue of mice was examined by real-time quantitative polymerase chain reaction (PCR). Meanwhile, the expression of IL-6 and TNF protein in renal tissue of mice was detected by western blot, while the expression of NF-κB protein in renal tissues of each group was detected by immunofluorescence. After 6 weeks of intervention, the blood glucose (GLU), total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), and weight of the liraglutide group were significantly lower than those of the DN group ( P < 0.01 or P < 0.05), whereas high-density lipoprotein (HDL) was significantly increased ( P < 0.05). At the same time, the microscale albuminuria (MAU) and N-acetyl-β-d-glucosaminidase (NAG) in the liraglutide group were significantly lower than those in the DN group ( P < 0.05). Moreover, the urea (UR), creatinine (CR), and uric acid (UA) in the liraglutide group were significantly lower than those in the DN group ( P < 0.01 or P < 0.05). In addition, the mRNA and proteins of IL-6, TNF, and NF-κB in the liraglutide group were significantly lower than those in the DN group ( P < 0.05). In conclusion, the mechanism of liraglutide in the treatment of DN may be related to the inhibition of the expression of genes and proteins of inflammatory factors.

scholarly journals Hyperlipidemia: a factor contributing to diabetic nephropathy development and progress

1993 ◽  
Vol 39 (5) ◽  
pp. 7-9 ◽  
Author(s):  
M. V. Shestakova ◽  
I. I. Dedov ◽  
I. I. Neverov ◽  
E. S. Severghina ◽  
T. G. Dyuzheva ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Nephropathy ◽  
Low Density Lipoprotein ◽  
Renal Involvement ◽  
Density Lipoprotein ◽  
Insulin Dependent Diabetes Mellitus ◽  
Serum Levels ◽  
Renal Tissue ◽  
Dependent Diabetes Mellitus ◽  
Insulin Dependent

Twenty-nine patients with insulin-dependent diabetes mellitus with similarly manifest renal involvement were examined to elucidate the role of dyslipidemia in diabetic nephropathy progress. Clinicolaboratory parameters (urinary albumin excretion, blood serum levels of total cholesterol, triglycerides, low, very low, and high density lipoprotein cholesterol) and morphologic changes in renal tissue biopsy specimens were analyzed. An increment of the number of large lipid incorporations was observed in various cells of renal glomeruli and interstitium, as well as a high prevalence of low density lipoprotein deposition in glomerular basal membranes and canaliculi as the renal process augmented in severity. Since lipids accumulating in glomerular structures may stimulate mesangial cell proliferation and mesangial matrix hyperproduction, the authors believe that dyslipidemia in diabetes mellitus may be conducive to a more rapid progress of renal disease.

scholarly journals LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 117-127
Author(s):  
Hongmei Gao ◽  
Zhaohui Guo
Keyword(s):  
Smooth Muscle ◽  
Muscle Protein ◽  
Umbilical Vein ◽  
Smooth Muscle Actin ◽  
Quantitative Polymerase Chain Reaction ◽  
Density Lipoprotein ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Western Blot Assay ◽  
Lactate Dehydrogenase Activity

Abstract Long noncoding RNAs (lncRNAs) have been verified as vital regulators in human disease, including atherosclerosis. However, the precise role of X-inactive-specific transcript (XIST) in atherosclerosis remains unclear. The proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) exposed to low-density lipoprotein (ox-LDL) were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide, and flow cytometry assays, correspondingly. The western blot assay was used to quantify protein expression. Lactate dehydrogenase activity and the concentrations of inflammatory factors were measured by matched kits. The real-time quantitative polymerase chain reaction (qPCR) was used to determine α-smooth muscle actin, smooth muscle protein 22-α, XIST, miR-98-5p, and pregnancy-associated plasma protein A (PAPPA) levels in HUVECs. The relationship among XIST, miR-98-5p, and PAPPA was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. We found ox-LDL repressed proliferation and induced inflammation and apoptosis in HUVECs. Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5p-induced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. However, silencing of miR-98-5p strengthened the ox-LDL-induced effects on HUVECs by increasing expression of PAPPA. Mechanistically, XIST could regulate PAPPA expression in ox-LDL-induced HUVECs by sponging miR-98-5p, providing understanding for atherosclerosis.

scholarly journals Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and plasma lipoprotein concentrations by defined dietary fats. Comparison of trimyristin, tripalmitin, tristearin and triolein

1995 ◽  
Vol 311 (1) ◽  
pp. 167-173 ◽  
Author(s):  
A J Bennett ◽  
M A Billett ◽  
A M Salter ◽  
E H Mangiapane ◽  
J S Bruce ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Dietary Fats ◽  
Low Density ◽  
Mrna Levels ◽  
Expression Of Genes ◽  
Coa Reductase

Different dietary fatty acids exert specific effects on plasma lipids but the mechanism by which this occurs is unknown. Hamsters were fed on low-cholesterol diets containing triacylglycerols enriched in specific saturated fatty acids, and effects on plasma lipids and the expression of genes involved in hepatic lipoprotein metabolism were measured. Trimyristin and tripalmitin caused significant rises in low-density lipoprotein (LDL) cholesterol which were accompanied by significant reductions in hepatic LDL receptor mRNA levels. Tripalmitin also increased hepatic expression of the apolipoprotein B gene, implying an increased production of LDL via very-low-density lipoprotein (VLDL) and decreased removal of LDL in animals fed this fat. Hepatic levels of 3-hydroxy-3-methylglutaryl-CoA reductase mRNA did not vary significantly between the groups. Compared with triolein, tristearin had little effect on hepatic gene expression or total plasma cholesterol. However, it caused a marked decrease in VLDL cholesterol and a rise in LDL cholesterol such that overall it appeared to be neutral. Lipid analysis suggested a rapid desaturation of much of the dietary stearate. The differential changes in plasma lipids and hepatic mRNA levels induced by specific dietary fats suggests a role for fatty acids or a metabolite thereof in the regulation of the expression of genes involved in lipoprotein metabolism.

scholarly journals Effects of combined use of atorvastatin and losartan in treating patients with diabetic nephropathy

2018 ◽  
Vol 16 ◽  
pp. 205873921879670
Author(s):  
Chao Ding ◽  
Xiaohua Hu
Keyword(s):  
Diabetic Nephropathy ◽  
Endothelial Function ◽  
Cardiovascular Events ◽  
Density Lipoprotein ◽  
Blood Lipid ◽  
Inflammatory Factors ◽  
Control Group ◽  
Vascular Endothelial ◽  
Observation Group ◽  
Vascular Endothelial Function

This study is to investigate the effect of atorvastatin combined with losartan on inflammatory factors, vascular endothelial function, and cardiovascular events in patients with diabetic nephropathy. A total of 128 patients with diabetic nephropathy treated in our hospital from January 2014 to December 2015 were selected as the study subjects, and 64 cases were randomly divided into observation group and 64 cases in the control group. The control group was treated with losartan on the basis of routine treatment, and the observation group was treated with atorvastatin on the basis of the control group. The blood lipid, inflammatory factors, changes in vascular endothelial function and cardiovascular events were compared between the two groups. The levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were not significantly different between the two groups before treatment ( P > 0.05); after treatment, the levels of TC, TG, and LDL-C in the observation group were significantly lower than those of the control group, and the level of HDL-C was significantly higher than that of the control group ( P < 0.05). The levels of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6) were not statistically different between the two groups before treatment ( P > 0.05); after treatment, the levels of hs-CRP, TNF-α, and IL-6 in the observation group were significantly lower than those of the control group ( P < 0.05), the level of HDL-C was significantly higher than that of the control group ( P < 0.05). There were no significant differences in the levels of endothelin-1 (ET-1) and nitric oxide (NO) between the two groups before treatment ( P > 0.05). After treatment, the level of ET-1 in the observation group was significantly lower than that of the control group ( P < 0.05), and the level of NO was significantly higher than that of the control group ( P < 0.05). After treatment, all patients were followed up for 2 years, and the incidence of secondary cardiovascular events in the observation group was 12.50% (8/64), which was significantly lower than 29.69% (19/64) of the control group ( P < 0.05). Combination of atorvastatin and losartan can significantly improve the levels of blood lipid, inflammatory factors, and vascular endothelial function in patients with diabetic nephropathy and can effectively reduce the incidence of cardiovascular events.

scholarly journals Expression of genes encoding IGFBPs, SNARK, CD36, and PECAM1 in the liver of mice treated with chromium disilicide and titanium nitride nanoparticles

2017 ◽  
Vol 51 (2) ◽  
pp. 84-95
Author(s):  
Dmytro O. Minchenko ◽  
D. O. Tsymbal ◽  
O. P. Yavorovsky ◽  
N. V. Solokha ◽  
O. H. Minchenko
Keyword(s):  
Titanium Nitride ◽  
Mouse Liver ◽  
Quantitative Polymerase Chain Reaction ◽  
Down Regulation ◽  
Expression Of Genes ◽  
Genes Expression ◽  
Genes Encoding ◽  
Polymerase Chain ◽  
Working Day ◽  
20 Nm

AbstractObjective. The aim of the present study was to examine the effect of chromium disilicide and titanium nitride nanoparticles on the expression level of genes encoding important regulatory factors (IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK/NUAK2, CD36, and PECAM1/CD31) in mouse liver for evaluation of possible toxic effects of these nanoparticles.Methods. Male mice received 20 mg chromium disilicide nanoparticles (45 nm) and titanium nitride nanoparticles (20 nm) with food every working day for 2 months. The expression of IGFBP1, IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK, CD36, and PECAM1 genes in mouse liver was studied by quantitative polymerase chain reaction.Results. Treatment of mice with chromium disilicide nanoparticles led to down-regulation of the expression of IGFBP2, IGFBP5, PECAM1, and SNARK genes in the liver in comparison with control mice, with more prominent changes for SNARK gene. At the same time, the expression of IGFBP3 and CD36 genes was increased in mouse liver upon treatment with chromium disilicide nanoparticles. We have also shown that treatment with titanium nitride nanoparticles resulted in down-regulation of the expression of IGFBP2 and SNARK genes in the liver with more prominent changes for SNARK gene. At the same time, the expression of IGFBP3, IGFBP4, and CD36 genes was increased in the liver of mice treated with titanium nitride nanoparticles. Furthermore, the effect of chromium disilicide nanoparticles on IGFBP2 and CD36 genes expression was significantly stronger as compared to titanium nitride nanoparticles.Conclusions. The results of this study demonstrate that chromium disilicide and titanium nitride nanoparticles have variable effects on the expression of IGFBP2, IGFBP3, IGFBP4, IGFBP5, SNARK, CD36, and PECAM1 genes in mouse liver, which may reflect the genotoxic activities of the studied nanoparticles.

scholarly journals Andrographis paniculata and Its Bioactive Diterpenoids Against Inflammation and Oxidative Stress in Keratinocytes

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 530 ◽  
Author(s):  
Eugenie Mussard ◽  
Sundy Jousselin ◽  
Annabelle Cesaro ◽  
Brigitte Legrain ◽  
Eric Lespessailles ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Quantitative Polymerase Chain Reaction ◽  
Andrographis Paniculata ◽  
Ros Production ◽  
Inflammatory Conditions ◽  
Tnf Α ◽  
Dichlorofluorescein Diacetate ◽  
Polymerase Chain ◽  
Factor Α ◽  
Necrosis Factor

Andrographis paniculata was widely used in traditional herbal medicine to treat various diseases. This study explored the potential anti-aging activity of Andrographis paniculata in cutaneous cells. Human, adult, low calcium, high temperature (HaCaT) cells were treated with methanolic extract (ME), andrographolide (ANDRO), neoandrographolide (NEO), 14-deoxyandrographolide (14DAP) and 14-deoxy-11,12-didehydroandrographolide (14DAP11-12). Oxidative stress and inflammation were induced by hydrogen peroxide and lipopolysaccharide/TNF-α, respectively. Reactive oxygen species (ROS) production was measured by fluorescence using a 2′,7′-dichlorofluorescein diacetate (DCFH-DA) probe and cytokines were quantified by ELISA for interleukin-8 (IL-8) or reverse transcription-quantitative polymerase chain reaction (RT-qPCR) for tumor necrosis factor-α (TNF-α). Hyaluronic acid (HA) secretion was determined by an ELISA. Our results show a decrease in ROS production and TNF-α expression by ME (5 µg/mL) in HaCaT under pro-oxidant and pro-inflammatory conditions, respectively. ME protected HaCaT against oxidative stress and inflammation. Our findings confirm that ME can be used for the development of bioactive compounds against epidermal damage.

scholarly journals Effect of dietary eicosapentaenoic and docosahexaenoic acid on expression of rat liver genes controlling cholesterol homeostasis and on plasma cholesterol level

2014 ◽  
Vol 59 (No. 9) ◽  
pp. 391-398 ◽  
Author(s):  
T. Komprda ◽  
G. Zorníková ◽  
A. Knoll ◽  
Z. Vykoukalová ◽  
V. Rozíková ◽  
...  
Keyword(s):  
Docosahexaenoic Acid ◽  
Plasma Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cholesterol Homeostasis ◽  
Ldlr Gene ◽  
Expression Of Genes ◽  
Density Lipoprotein Receptor ◽  
Lower Plasma Cholesterol ◽  
Coa Reductase

A hypothesis that eicosapentaenoic acid + docosahexaenoic acid (EPA+DHA) lower plasma cholesterol via increased expression of the Insig-1 gene with ensuing decrease of expression of genes coding for 3-hydroxy-3-methyl-glutaryl-CoA reductase (Hmgcr) and low density lipoprotein receptor (Ldlr) was tested in rats fed a diet with 3% of fish oil (FO). Expression of the Insig-1 gene in the liver of the FO-fed rats was 730% (P &lt; 0.05) of the control. However, contrary to the hypothesis, expression of the Hmgcr gene and Ldlr gene was 165% and 210% of the control (P &gt; 0.05). Nevertheless, FO in the diet decreased (P &lt; 0.05) plasma cholesterol of rats by 10% (from 1.19 to 1.07 mmol/l); it was therefore concluded that the cholesterol-lowering effect of EPA+DHA is at least partly based on mechanisms other than tested in the present experiment. &nbsp;

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