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Luigi Sironi - One of the best experts on this subject based on the ideXlab platform.
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altered iron homeostasis in an animal model of Hypertensive Nephropathy stroke prone rats
Journal of Hypertension, 2013Co-Authors: Paolo Gelosa, Alice Pignieri, Elisabetta Gianazza, Salvatore Criniti, Uliano Guerrini, Maria Domenica Cappellini, Cristina Banfi, Elena Tremoli, Luigi SironiAbstract:BACKGROUND AND AIM Iron is the most abundant metal in mammalian cells, and plays a pivotal role in many metabolic processes. Dysregulated iron homeostasis is involved in the cause of a number of pathological processes including renal diseases. METHODS AND RESULTS Longitudinal MRI scans of salt-loaded spontaneously Hypertensive stroke-prone rats (SHRSP), an animal model that spontaneously develops Hypertensive Nephropathy, showed a decrease in renal and hepatic T2 SI (a sign of iron accumulation) of, respectively, 42.3 ± 2.5% (P < 0.01) and 60.4 ± 15.1% (P < 0.01) in comparison with SHRSP fed a standard diet. This was accompanied by the development of renal inflammation and oxidative stress (as evaluated by immunohistochemical and proteomic analyses), mitochondrial dysfunction, massive proteinuria and sustained intravascular hemolysis with the subsequent depletion of plasma haptoglobin, which was responsible for the renal uptake of hemoglobin and iron accumulation. In order to investigate the role of iron in these pathological processes, we subcutaneously treated the salt-loaded rats with the iron chelator deferoxamine (200 mg/kg per day). The pharmacological treatment prevented iron tissue accumulation, as indicated by the increase in renal and hepatic T2 SI of, respectively, 120.0 ± 10.1% (P < 0.01) and 73.9 ± 4.4% (P < 0.01) in comparison with salt-loaded rats treated with vehicle alone. Deferoxamine also preserved renal morphology and function, the renal infiltration of ED-1-positive macrophages/monocytes, and the expression of MCP-1 and TGF-β mRNA, reduced the level of reactive oxygen species, and improved the activity of mitochondrial cytochrome c oxidase. CONCLUSION These findings suggest that iron dysmetabolism is involved in the development of Hypertensive Nephropathy in SHRSP.
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Altered iron homeostasis in an animal model of Hypertensive Nephropathy: stroke-prone rats.
Journal of hypertension, 2013Co-Authors: Paolo Gelosa, Alice Pignieri, Elisabetta Gianazza, Salvatore Criniti, Uliano Guerrini, Maria Domenica Cappellini, Cristina Banfi, Elena Tremoli, Luigi SironiAbstract:BACKGROUND AND AIM Iron is the most abundant metal in mammalian cells, and plays a pivotal role in many metabolic processes. Dysregulated iron homeostasis is involved in the cause of a number of pathological processes including renal diseases. METHODS AND RESULTS Longitudinal MRI scans of salt-loaded spontaneously Hypertensive stroke-prone rats (SHRSP), an animal model that spontaneously develops Hypertensive Nephropathy, showed a decrease in renal and hepatic T2 SI (a sign of iron accumulation) of, respectively, 42.3 ± 2.5% (P
Zhuyuan Fang - One of the best experts on this subject based on the ideXlab platform.
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Danhong Injection for the Treatment of Hypertensive Nephropathy: A Systematic Review and Meta-Analysis.
Frontiers in pharmacology, 2020Co-Authors: Shihai Yan, Lichao Qian, Yawei Zheng, Zhuyuan FangAbstract:Objective Danhong Injection (DHI) has been widely used to treat various diseases in China for many years. The objective of this systematic review was to evaluate the efficacy of DHI combined with antiHypertensive drugs for treatment of Hypertensive Nephropathy. Methods Seven databases were searched from inception to September 21st, 2019. Randomized controlled trials comparing DHI combined with antiHypertensive drugs versus antiHypertensive drugs alone were extracted. The primary outcome was microalbuminuria (mALB). Secondary outcomes included systolic blood pressure (SBP), diastolic blood pressure (DBP), and serum creatinine (SCr). Results Fifteen studies were included in the meta-analysis, which indicated that DHI combined with antiHypertensive drugs has advantages compared with antiHypertensive drugs alone for reducing mALB [weighted mean difference (WMD) = -12.86, 95% confidence interval (CI) (-14.72, -11.0), P < 0.01], lowering SBP [WMD = -2.84, 95% CI (-4.56, -1.12), P = 0.001] and DBP [WMD = -2.38, 95% CI (-4.34, -0.43), P = 0.017], and decreasing SCr [WMD = -40.45, 95% CI (-55.69, -25.21), P < 0.01]. Conclusion The combination of DHI with antiHypertensive drugs appears to be more effective than antiHypertensive drugs alone for treatment of Hypertensive Nephropathy. A moderate duration (≤4 weeks) of DHI administration is reasonable, and longer treatment with DHI should be avoided, according to the results of subgroup analysis.
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Efficacy and Safety of Sodium Tanshinone IIA Sulfonate Injection on Hypertensive Nephropathy: A Systematic Review and Meta-Analysis
Frontiers in pharmacology, 2019Co-Authors: Chenghua Zhang, Ming Liu, Xiaoqing Shi, Weimin Jiang, Zhuyuan FangAbstract:Background: Sodium tanshinone IIA sulfonate (STS) injection, the extractive of traditional Chinese medicine Danshen, is supposed to be a supplementary treatment in Hypertensive Nephropathy. Objectives: To evaluate the efficacy and safety of STS in treatment of Hypertensive Nephropathy. Methods: We systematically searched China National Knowledge Infrastructure (CNKI), Chinese Scientific Journals Database (VIP), Wan-fang database, Chinese Biomedicine Database (CBM), PubMed, Embase, Web of Science, and Cochrane Library from their inception to December 2018. All studies were screened by two reviewers according to the inclusion and exclusion criteria independently. The Cochrane Collaboration's risk tool was used to assess the methodological quality of the included studies. Reviewer Manager 5.3 was employed for statistical analysis. Results: Sixteen trials involving 1,696 patients were included. The meta-analysis results indicated a combination of STS and angiotensin receptor blockers (ARBs) was more effective than ARB monotherapy in modulating Hypertensive Nephropathy, as represented by improved estimated glomerular filtration rate (eGFR) [mean difference (MD) = 6.87, 95% CI (4.47, 9.28), P < 0.00001] and reduced 24 h urinary protein [MD = -0.23, 95% CI (-0.27, -0.19), P < 0.00001], serum creatinine (SCr) [MD = -21.74, 95% CI (-24.11, -19.38), P < 0.00001], cystatin-C [MD = -0.16, 95% CI (-0.24, -0.07), P = 0.0003], urinary immunoglobulin G (IgG) [MD = -0.85, 95% CI (-1.11, -0.59), P < 0.00001], and urinary transferrin [MD = -0.61, 95% CI (-1.04, -0.17), P = 0.007]. In addition, the combination therapy had better control in systolic blood pressure (SBP) [MD = -6.53, 95% CI (-8.19, -4.87), P < 0.00001] and diastolic blood pressure (DBP) [MD = -4.14, 95% CI (-5.69, -2.59), P < 0.00001]. Only three trials reported adverse events, and no adverse drug reactions were observed. Conclusions: STS combined with ARBs had a stronger effect on improving renal function in patients with primary Hypertensive Nephropathy than ARB monotherapy. The combination therapy also provided auxiliary hypotensive effects. Further large-scale, multicenter, and rigorously designed randomized controlled trials (RCTs) should be conducted to confirm our findings.
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Combined Therapy of Hypertensive Nephropathy with Breviscapine Injection and AntiHypertensive Drugs: A Systematic Review and a Meta-Analysis
Evidence-based complementary and alternative medicine : eCAM, 2018Co-Authors: Ming Liu, Zhuyuan FangAbstract:Objective. To evaluate the beneficial and adverse effects of breviscapine injection in combination with antiHypertensive drugs for treating Hypertensive Nephropathy in clinical practice. Methods. We searched PubMed, the Cochrane Library, Embase, CNKI, Sino Med, VIP, and Wanfang Data for relevant literature. The timeframe of retrieval was set from the founding date of each database to September 28, 2018. Results. Fourteen papers were included in this study. The quality of all the studies included was determined to be low. All studies were conducted with Chinese populations. Meta-analysis showed that, compared with single-use antiHypertensive drugs, using breviscapine injection in combination with antiHypertensive drugs to treat Hypertensive Nephropathy can reduce serum creatinine (Scr) [WMD = –35.16, 95% CI(–50.01, –20.31), ≤ 0.001], blood urea nitrogen (BUN) [WMD = –2.00, 95% CI(–3.07, –0.94), ≤ 0.001], 24-hour urinary total protein (24 h UTP) [WMD = –0.04, 95% CI(–0.05, –0.02), ≤ 0.001], and the beta-2-microglobulin (B2M) [WMD = –0.09, 95% CI(–0.11, –0.07), ≤ 0.001], improve creatinine clearance rate (Ccr) [WMD = 7.84, 95% CI(5.20, 10.49), ≤ 0.001], and increase the clinical efficacy [RR = 1.27, 95% CI(1.05, 1.53), = 0.014], but does not lower systolic blood pressure (SBP) [WMD = –1.02, 95% CI(–2.88, 0.84), = 0.281]. There was no significant difference in adverse events between experimental groups and control groups. Conclusion. Breviscapine injection in combination with antiHypertensive drugs can improve clinical efficacy and Ccr and reduce Scr, BUN, 24 h UTP, and B2M in patients with Hypertensive Nephropathy. The present meta-analysis indicated that breviscapine injection can serve as a renal protective effect to patients with Hypertensive Nephropathy. However, the evidence of methodological quality and sample sizes is weak, and thus, further standardized research is required.
David I. Min - One of the best experts on this subject based on the ideXlab platform.
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Gene polymorphism of vascular endothelial growth factor -1154 G>A is associated with Hypertensive Nephropathy in a Hispanic population.
Molecular biology reports, 2010Co-Authors: Jae Wook Yang, Ian V. Hutchinson, Tariq Shah, Jianwen Fang, David I. MinAbstract:The aim of this study was to determine the association between Hypertensive Nephropathy and gene polymorphisms of vascular endothelial growth factor (VEGF) in a self-reported Hispanic patient group. A total of 155 Hispanic living kidney donors as controls and a total of 86 Hispanic kidney transplant patients, whose renal failure was attributed to Hypertensive Nephropathy after ruling out diabetes mellitus or other causes, were genotyped for four different single nucleotide polymorphisms of VEGF: −2578 C>A (rs699947), −1154 G>A (rs1570360), −460 C>T (rs833061), and +936 C>T (rs3025039). The homozygous mutant type (AA) of VEGF −1154 G>A (rs1570360) was found with significantly higher frequency in the Hypertensive Nephropathy patients than in controls. On the other hand, homozygous wild type (GG) was found less frequently in the Hypertensive Nephropathy patient group than in the control group. Linkage disequilibrium (LD) analyses revealed a high degree of LD among VEGF −2578 C>A (rs699947), VEGF −1154 G>A (rs1570360), and VEGF −460 C>T (rs833061). The haplotype analysis revealed that two haplotypes, CGTC and CATC (in the order of VEGF −2578 C>A (rs699947), −1154 G>A (1570360), −460 C>T (rs833061), and +936 C>T (3025039)), were significantly associated with Hypertensive Nephropathy in Hispanic patients. Hence, the −1154 G>A polymorphism (rs1570360) and two haplotypes (CGTC and CATC) of VEGF appear to be associated with Hypertensive Nephropathy in Hispanic patients who developed end-stage renal disease requiring kidney transplant.
Paolo Gelosa - One of the best experts on this subject based on the ideXlab platform.
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altered iron homeostasis in an animal model of Hypertensive Nephropathy stroke prone rats
Journal of Hypertension, 2013Co-Authors: Paolo Gelosa, Alice Pignieri, Elisabetta Gianazza, Salvatore Criniti, Uliano Guerrini, Maria Domenica Cappellini, Cristina Banfi, Elena Tremoli, Luigi SironiAbstract:BACKGROUND AND AIM Iron is the most abundant metal in mammalian cells, and plays a pivotal role in many metabolic processes. Dysregulated iron homeostasis is involved in the cause of a number of pathological processes including renal diseases. METHODS AND RESULTS Longitudinal MRI scans of salt-loaded spontaneously Hypertensive stroke-prone rats (SHRSP), an animal model that spontaneously develops Hypertensive Nephropathy, showed a decrease in renal and hepatic T2 SI (a sign of iron accumulation) of, respectively, 42.3 ± 2.5% (P < 0.01) and 60.4 ± 15.1% (P < 0.01) in comparison with SHRSP fed a standard diet. This was accompanied by the development of renal inflammation and oxidative stress (as evaluated by immunohistochemical and proteomic analyses), mitochondrial dysfunction, massive proteinuria and sustained intravascular hemolysis with the subsequent depletion of plasma haptoglobin, which was responsible for the renal uptake of hemoglobin and iron accumulation. In order to investigate the role of iron in these pathological processes, we subcutaneously treated the salt-loaded rats with the iron chelator deferoxamine (200 mg/kg per day). The pharmacological treatment prevented iron tissue accumulation, as indicated by the increase in renal and hepatic T2 SI of, respectively, 120.0 ± 10.1% (P < 0.01) and 73.9 ± 4.4% (P < 0.01) in comparison with salt-loaded rats treated with vehicle alone. Deferoxamine also preserved renal morphology and function, the renal infiltration of ED-1-positive macrophages/monocytes, and the expression of MCP-1 and TGF-β mRNA, reduced the level of reactive oxygen species, and improved the activity of mitochondrial cytochrome c oxidase. CONCLUSION These findings suggest that iron dysmetabolism is involved in the development of Hypertensive Nephropathy in SHRSP.
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Altered iron homeostasis in an animal model of Hypertensive Nephropathy: stroke-prone rats.
Journal of hypertension, 2013Co-Authors: Paolo Gelosa, Alice Pignieri, Elisabetta Gianazza, Salvatore Criniti, Uliano Guerrini, Maria Domenica Cappellini, Cristina Banfi, Elena Tremoli, Luigi SironiAbstract:BACKGROUND AND AIM Iron is the most abundant metal in mammalian cells, and plays a pivotal role in many metabolic processes. Dysregulated iron homeostasis is involved in the cause of a number of pathological processes including renal diseases. METHODS AND RESULTS Longitudinal MRI scans of salt-loaded spontaneously Hypertensive stroke-prone rats (SHRSP), an animal model that spontaneously develops Hypertensive Nephropathy, showed a decrease in renal and hepatic T2 SI (a sign of iron accumulation) of, respectively, 42.3 ± 2.5% (P
Haihua Huang - One of the best experts on this subject based on the ideXlab platform.
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mir 101a ameliorates angii mediated Hypertensive Nephropathy by blockade of tgfβ smad3 and nf κb signalling in a mouse model of hypertension
Clinical and Experimental Pharmacology and Physiology, 2019Co-Authors: Hong Ding, Ying Zhou, Haihua HuangAbstract:Hypertensive Nephropathy, clinically characterized by progressive renal fibrosis and inflammation, is a severe complication of hypertension. The objectives of this study were to investigate the roles of miR-101a in relieving angiotensin II (Ang II)-mediated Hypertensive Nephropathy and uncover the possible underlying mechanisms. A Hypertensive mouse model was established via continuous 28-day AngII infusion. Systolic blood pressure (SBP), ratio of urine albumin to creatinine, blood urea nitrogen (BUN), serum creatinine (Scr) and glomerular filtration rate (GFR) were evaluated. Dual luciferase reporter assay was used to explore the target of miR-101a. mRNA levels of miR-101a, TGFβRI, fibrotic markers (Collagen I and α-SMA) and pro-inflammatory cytokines (IL-1β and TNF-α) were determined by real-time PCR. Protein levels of TGFβRI, Collagen I, α-SMA, IL-1β, TNF-α, t-p65, P-p65, t-Smad3, P-Smad3, t-IκBα and P-IκBα were detected by western blot. MiR-101a mimics significantly improved GFR and inhibited AngII-induced increase in the ratio of urine albumin to creatinine, BUN and Scr. MiR-101a mimics partially abolished AngII-induced increase in the mRNA and protein level of fibrotic markers by targeting TGFβRI and inhibiting TGFβ/Smad3 pathway. Moreover, TGFβRI inhibitor galunisertib inhibited AngII-mediated renal injury in mice with Hypertensive Nephropathy. Additionally, miR-101a overexpression blocked AngII-induced up-regulation of pro-inflammatory markers via suppressing NF-κB pathway. MiR-101a exhibited protective effects against Hypertensive Nephropathy via inhibiting TGFβ/Smad3 and NF-κB signalling pathways.
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MiR-101a ameliorates AngII-mediated Hypertensive Nephropathy by blockade of TGFβ/Smad3 and NF-κB signalling in a mouse model of hypertension.
Clinical and experimental pharmacology & physiology, 2018Co-Authors: Hong Ding, Ying Zhou, Haihua HuangAbstract:Hypertensive Nephropathy, clinically characterized by progressive renal fibrosis and inflammation, is a severe complication of hypertension. The objectives of this study were to investigate the roles of miR-101a in relieving angiotensin II (Ang II)-mediated Hypertensive Nephropathy and uncover the possible underlying mechanisms. A Hypertensive mouse model was established via continuous 28-day AngII infusion. Systolic blood pressure (SBP), ratio of urine albumin to creatinine, blood urea nitrogen (BUN), serum creatinine (Scr) and glomerular filtration rate (GFR) were evaluated. Dual luciferase reporter assay was used to explore the target of miR-101a. mRNA levels of miR-101a, TGFβRI, fibrotic markers (Collagen I and α-SMA) and pro-inflammatory cytokines (IL-1β and TNF-α) were determined by real-time PCR. Protein levels of TGFβRI, Collagen I, α-SMA, IL-1β, TNF-α, t-p65, P-p65, t-Smad3, P-Smad3, t-IκBα and P-IκBα were detected by western blot. MiR-101a mimics significantly improved GFR and inhibited AngII-induced increase in the ratio of urine albumin to creatinine, BUN and Scr. MiR-101a mimics partially abolished AngII-induced increase in the mRNA and protein level of fibrotic markers by targeting TGFβRI and inhibiting TGFβ/Smad3 pathway. Moreover, TGFβRI inhibitor galunisertib inhibited AngII-mediated renal injury in mice with Hypertensive Nephropathy. Additionally, miR-101a overexpression blocked AngII-induced up-regulation of pro-inflammatory markers via suppressing NF-κB pathway. MiR-101a exhibited protective effects against Hypertensive Nephropathy via inhibiting TGFβ/Smad3 and NF-κB signalling pathways.