scholarly journals Antioxidant Potential of Adiponectin and Full PPAR-γ Agonist in Correcting Streptozotocin-Induced Vascular Abnormality in Spontaneously Hypertensive Rats

PPAR Research ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Sheryar Afzal ◽  
Munavvar Abdul Sattar ◽  
Edward James Johns ◽  
Olorunfemi A. Eseyin ◽  
Ali Attiq
Keyword(s):  
Oxidative Stress ◽  
Arterial Stiffness ◽  
Antioxidant Potential ◽  
Oxygen Species ◽  
Hypertensive Rats ◽  
Adiponectin Concentration ◽  
Spontaneously Hypertensive ◽  
Plasma Adiponectin ◽  
Ppar Γ ◽  
Lipid Contents

Oxidative stress, which is associated with metabolic and anthropometric perturbations, leads to reactive oxygen species production and decrease in plasma adiponectin concentration. We investigated pharmacodynamically the pathophysiological role and potential implication of exogenously administered adiponectin with full and partial peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonists on modulation of oxidative stress, metabolic dysregulation, and antioxidant potential in streptozotocin-induced spontaneously hypertensive rats (SHR). Group I (WKY) serves as the normotensive control, whereas 42 male SHRs were randomized equally into 7 groups ( n = 6 ); group II serves as the SHR control, group III serves as the SHR diabetic control, and groups IV, V, and VI are treated with irbesartan (30 mg/kg), pioglitazone (10 mg/kg), and adiponectin (2.5 μg/kg), whereas groups VII and VIII received cotreatments as irbesartan+adiponectin and pioglitazone+adiponectin, respectively. Diabetes was induced using an intraperitoneal injection of streptozotocin (40 mg/kg). Plasma adiponectin, lipid contents, and arterial stiffness with oxidative stress biomarkers were measured using an in vitro and in vivo analysis. Diabetic SHRs exhibited hyperglycemia, hypertriglyceridemia, hypercholesterolemia, and increased arterial stiffness with reduced plasma adiponectin and antioxidant enzymatic levels ( P < 0.05 ). Diabetic SHRs pretreated with pioglitazone and adiponectin separately exerted improvements in antioxidant enzyme activities, abrogated arterial stiffness, and offset the increased production of reactive oxygen species and dyslipidemic effects of STZ, whereas the blood pressure values were significantly reduced in the irbesartan-treated groups (all P < 0.05 ). The combined treatment of exogenously administered adiponectin with full PPAR-γ agonist augmented the improvement in lipid contents and adiponectin concentration and restored arterial stiffness with antioxidant potential effects, indicating the degree of synergism between adiponectin and full PPAR-γ agonists (pioglitazone).

scholarly journals Exogenous adiponectin with full Peroxisome proliferator-activated receptor agonists (pioglitazone) abrogates streptozotocin induced oxidative stress and vascular abnormalities in Spontaneously hypertensive rats.

2020 ◽  
Author(s):  
Sheryar Afzal ◽  
Munavvar Abdul Sattar ◽  
Edward James Johns ◽  
Olorunfemi. A. Eseyin
Keyword(s):  
Oxidative Stress ◽  
Arterial Stiffness ◽  
Peroxisome Proliferator ◽  
Oxygen Species ◽  
Adiponectin Concentration ◽  
Peroxisome Proliferator Activated Receptor ◽  
Spontaneously Hypertensive ◽  
Plasma Adiponectin ◽  
Ppar Γ ◽  
Lipid Contents

Abstract Background Oxidative stress, associates with metabolic and anthropometric perturbations, leads to reactive oxygen species production and decrease in plasma adiponectin concentration. We investigated pharmacodynamically the pathophysiological role and potential implication of exogenously administered adiponectin with full and partial peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonists on modulation of oxidative stress, metabolic dysregulation and antioxidant potential in streptozotocin induced Spontaneously hypertensive rats (SHR).Methods Group I (WKY) serve as normotensive control, whereas 42 male SHRs were randomized equally into 7 groups (n = 6), group II: SHR control, groups III: SHR diabetic control, group IV, V and VI treated with irbesartan (30 mg/kg), pioglitazone (10 mg/kg) and adiponectin (2.5 µg/kg), whereas, groups VII and VIII received co-treatments as irbesartan + adiponectin), (pioglitazone + adiponectin) respectively. Diabetes was induced using an intra-peritoneal injection of Streptozotocin (40 mg/kg). Plasma adiponectin, lipid contents, arterial stiffness with oxidative stress bio-markers were measured using an in-vitro and in-vivo analysis.Results Diabetic SHRs exhibited hyperglycaemia, hypertriglyceridemia, hypercholesterolemia, increased arterial stiffness with reduced plasma adiponectin and antioxidant enzymatic levels (P < 0.05). Diabetic SHRs pre-treated with pioglitazone and adiponectin separately exerted improvements in antioxidant enzyme activities, abrogated arterial stiffness, offset the increased production of reactive oxygen species and dyslipidaemic effects of STZ, except for blood pressure values which were more pronounced with irbesartan treated groups (all P < 0.05).Conclusions The combined treatment of exogenously administered adiponectin with full PPAR-γ agonist augmented the improvement in lipid contents and adiponectin concentration, restores arterial stiffness with antioxidant potential effects, indicating degree of synergism between adiponectin and full PPAR-γ agonists (pioglitazone).

scholarly journals Effect of Treatment with Peptide Extract from Beef Myofibrillar Protein on Oxidative Stress in the Brains of Spontaneously Hypertensive Rats

Foods ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 455
Author(s):  
Lee ◽  
Hur
Keyword(s):  
Oxidative Stress ◽  
Spontaneously Hypertensive Rats ◽  
Myofibrillar Protein ◽  
Oxygen Species ◽  
Hypertensive Rats ◽  
Sod Activity ◽  
Spontaneously Hypertensive ◽  
Hypertension Therapy ◽  
Effect Of Treatment ◽  
Gpx Activity

This study was conducted to determine the effect of beef peptide extract on oxidative stress in the brains of spontaneously hypertensive rats (SHRs). A 3-kDa peptide extract was obtained from beef myofibrillar protein using alkaline-AK (AK3K). Oxidative stress in SHR brains was measured by assessing malondialdehyde (MDA) and reactive oxygen species (ROS) concentrations and superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) activity. The SHR brains treated with the AK3K peptide extract (400 mg/kg body weight, AK3K400) showed a significant decrease in MDA and ROS contents by 0.33 and 23.92 μM, respectively (p < 0.05) compared to the control. The SOD activity for AK3K400 was 61.26%, around 20% higher than the control. Furthermore, the SHRs treated with the AK3K peptide extract showed results similar to those obtained using captopril, a hypertension drug, except for the MDA level. The study demonstrates that the beef peptide extract inhibits the generation of oxidative stress in the SHR brain and could possibly be used for neuronal hypertension therapy.

In Vivo Evidence for Microvascular Oxidative Stress in Spontaneously Hypertensive Rats

Hypertension ◽  
1995 ◽  
Vol 25 (5) ◽  
pp. 1083-1089 ◽  
Author(s):  
Hidekazu Suzuki ◽  
Allen Swei ◽  
Benjamin W. Zweifach ◽  
Geert W. Schmid-Schönbein
Keyword(s):  
Oxidative Stress ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Pioglitazone Attenuates Vascular Fibrosis in Spontaneously Hypertensive Rats

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Dengfeng Gao ◽  
Ning Ning ◽  
Guanghua Hao ◽  
Xiaolin Niu
Keyword(s):  
Real Time ◽  
Immunohistochemical Staining ◽  
Spontaneously Hypertensive Rats ◽  
Pcr Analysis ◽  
Rt Pcr ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Ppar Γ ◽  
Collagen Iii ◽  
Wistar Kyoto

Objective. We sought to investigate whether the peroxisome proliferator-activated receptor-γ (PPAR-γ) ligand pioglitazone can attenuate vascular fibrosis in spontaneously hypertensive rats (SHRs) and explore the possible molecular mechanisms.Methods. SHRs (8-week-old males) were randomly divided into 3 groups (n=8each) for treatment: pioglitazone (10 mg/kg/day), hydralazine (25 mg/kg/day), or saline. Normal male Wistar Kyoto (WKY) rats (n=8) served as normal controls. Twelve weeks later, we evaluated the effect of pioglitazone on vascular fibrosis by Masson’s trichrome and immunohistochemical staining of collagen III and real-time RT-PCR analysis of collagen I, III and fibronectin mRNA.Vascular expression of PPAR-γ and connective tissue growth factor (CTGF) and transforming growth factor-β (TGF-β) expression were evaluated by immunohistochemical staining, western blot analysis, and real-time RT-PCR.Results. Pioglitazone and hydralazine treatment significantly decreased systolic blood pressure in SHRs. Masson’s trichrome staining for collagen III and real-time RT-PCR analysis of collagen I, III and fibronectin mRNA indicated that pioglitazone significantly inhibited extracellular matrix production in the aorta. Compared with Wistar Kyoto rats, SHRs showed significantly increased vascular CTGF expression. Pioglitazone treatment significantly increased PPAR-γ expression and inhibited CTGF expression but had no effect on TGF-β expression.Conclusions. The results indicate that pioglitazone attenuated vascular fibrosis in SHRs by inhibiting CTGF expression in a TGF-β-independent mechanism.

scholarly journals Immunohistochemical Analysis of 4-HNE, NGAL, and HO-1 Tissue Expression after Apocynin Treatment and HBO Preconditioning in Postischemic Acute Kidney Injury Induced in Spontaneously Hypertensive Rats

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1163
Author(s):  
Sanjin Kovacevic ◽  
Milan Ivanov ◽  
Maja Zivotic ◽  
Predrag Brkic ◽  
Zoran Miloradovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Spontaneously Hypertensive Rats ◽  
Kidney Injury ◽  
Immunohistochemical Analysis ◽  
Tissue Expression ◽  
Pure Oxygen ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Renal Expression

Oxidative stress has been considered as a central aggravating factor in the development of postischemic acute kidney injury (AKI). The aim of this study was to perform the immunohistochemical analysis of 4-hydroxynonenal (4-HNE), neutrophil gelatinase-associated lipocalin (NGAL), and heme oxygenase-1 (HO-1) tissue expression after apocynin (APO) treatment and hyperbaric oxygenation (HBO) preconditioning, applied as single or combined protocol, in postischemic acute kidney injury induced in spontaneously hypertensive rats (SHR). Twenty-four hours before AKI induction, HBO preconditioning was carried out by exposing to pure oxygen (2.026 bar) twice a day, for 60 min in two consecutive days. Acute kidney injury was induced by removal of the right kidney while the left renal artery was occluded for 45 min by atraumatic clamp. Apocynin was applied in a dose of 40 mg/kg body weight, intravenously, 5 min before reperfusion. We showed increased 4-HNE renal expression in postischemic AKI compared to Sham-operated (SHAM) group. Apocynin treatment, with or without HBO preconditioning, improved creatinine and phosphate clearances, in postischemic AKI. This improvement in renal function was accompanied with decreased 4-HNE, while HO-1 kidney expression restored close to the control group level. NGAL renal expression was also decreased after apocynin treatment, and HBO preconditioning, with or without APO treatment. Considering our results, we can say that 4-HNE tissue expression can be used as a marker of oxidative stress in postischemic AKI. On the other hand, apocynin treatment and HBO preconditioning reduced oxidative damage, and this protective effect might be expected even in experimental hypertensive condition.

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