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

ABSTRACT: 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 ?M, 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.

SUBMITTER: Lee SY

PROVIDER: S-EPMC6836098 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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

Lee Seung Yun SY Hur Sun Jin SJ

Foods (Basel, Switzerland) 20191006 10

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 peptid ...[more]

PMID: 31590451

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Project description:Hypertension is an independent risk factor for the progression of chronic renal failure, and oxidative stress plays a critical role in hypertensive renal damage. Forkbox O1(FoxO1) signaling protects cells against oxidative stress and may be a useful target for treating oxidative stress-induced hypertension. Tongxinluo is a traditional Chinese medicine with cardioprotective and renoprotective functions. Therefore, this study aimed to determine the effects of Tongxinluo in hypertensive renal damage in spontaneously hypertensive rats(SHRs)and elucidate the possible involvement of oxidative stress and FoxO1 signaling in its molecular mechanisms. SHRs treated with Tongxinluo for 12 weeks showed a reduction in systolic blood pressure. In addition to increasing creatinine clearance, Tongxinluo decreased urinary albumin excretion, oxidative stress injury markers including malondialdehyde and protein carbonyls, and expression of nicotinamide adenine dinucleotide phosphate oxidase subunits and its activity in SHR kidneys. While decreasing phosphorylation of FoxO1, Tongxinluo also inhibited the phosphorylation of extracellular signal-regulated kinase1/2 and p38 and enhanced manganese superoxide dismutase and catalase activities in SHR kidneys. Furthermore, histology revealed attenuation of glomerulosclerosis and renal podocyte injury, while Tongxinluo decreased the expression of α-smooth muscle actin, extracellular matrixprotein, transforming growth factor β1 and small mothers against decapentaplegic homolog 3,and improved tubulointerstitial fibrosis in SHR kidneys. Finally, Tongxinluo inhibited inflammatory cell infiltration as well as expression of tumor necrosis factor-α and interleukin-6. In conclusion, Tongxinluo protected SHRs against hypertension-induced renal injury by exerting antioxidant, antifibrotic, and anti-inflammatory activities. Moreover, the underlying mechanisms of these effects may involve inhibition of oxidative stress and functional activation of FoxO1 signaling.

Project description:BackgroundThe combination of systemic arterial hypertension and diabetes mellitus (DM) induces greater cardiac remodeling than either condition alone. However, this association has been poorly addressed in senescent rats. Therefore, this study aimed to analyze the influence of streptozotocin-induced DM on ventricular remodeling and oxidative stress in aged spontaneously hypertensive rats (SHR).MethodsFifty 18 month old male SHR were divided into two groups: control (SHR, n = 25) and diabetic (SHR-DM, n = 25). DM was induced by streptozotocin (40 mg/kg, i.p.). After nine weeks, the rats underwent echocardiography and myocardial functional study in left ventricular (LV) isolated papillary muscle preparations. LV samples were obtained to measure myocyte diameters, interstitial collagen fraction, and hydroxyproline concentration. Gene expression of atrial natriuretic peptide (ANP) and α- and β-myosin heavy chain (MyHC) isoforms was evaluated by RT-PCR. Serum oxidative stress was assessed by measuring lipid hydroperoxide concentration and superoxide dismutase and glutathione peroxidase activities.StatisticsStudent's t test or Mann-Whitney test, p < 0.05.ResultsSHR-DM presented higher blood glucose (487 ± 29 vs. 89.1 ± 21.1 mg/dL) and lower body weight (277 ± 26 vs. 339 ± 38 g). Systolic blood pressure did not differ between groups. Echocardiography showed LV and left atrial dilation, LV diastolic and relative wall thickness decrease, and LV systolic and diastolic function impairment in SHR-DM. Papillary muscle study showed decreased myocardial contractility and contractile reserve in SHR-DM. Myocyte diameters and myocardial interstitial collagen fraction and hydroxyproline concentration did not differ between groups. Increased serum pro-oxidant activity and gene expression of ANP and β/α-MyHC ratio were observed in DM.ConclusionDiabetes mellitus induces cardiac dilation and functional impairment, increases oxidative stress and activates fetal gene program in aged spontaneously hypertensive rats.

Project description:Inflammation and oxidative and dicarbonyl stress play important roles in the pathogenesis of type 2 diabetes. Metformin is the first-line drug of choice for the treatment of type 2 diabetes because it effectively suppresses gluconeogenesis in the liver. However, its "pleiotropic" effects remain controversial. In the current study, we tested the effects of metformin on inflammation, oxidative and dicarbonyl stress in an animal model of inflammation and metabolic syndrome, using spontaneously hypertensive rats that transgenically express human C-reactive protein (SHR-CRP). We treated 8-month-old male transgenic SHR-CRP rats with metformin (5 mg/kg/day) mixed as part of a standard diet for 4 weeks. A corresponding untreated control group of male transgenic SHR-CRP rats were fed a standard diet without metformin. In a similar fashion, we studied a group of nontransgenic SHR treated with metformin and an untreated group of nontransgenic SHR controls. In each group, we studied 6 animals. Parameters of glucose and lipid metabolism and oxidative and dicarbonyl stress were measured using standard methods. Gene expression profiles were determined using Affymetrix GeneChip Arrays. Statistical significance was evaluated by two-way ANOVA. In the SHR-CRP transgenic strain, we found that metformin treatment decreased circulating levels of inflammatory response marker IL-6, TNF? and MCP-1 while levels of human CRP remained unchanged. Metformin significantly reduced oxidative stress (levels of conjugated dienes and TBARS) and dicarbonyl stress (levels of methylglyoxal) in left ventricles, but not in kidneys. No significant effects of metformin on oxidative and dicarbonyl stress were observed in SHR controls. In addition, metformin treatment reduced adipose tissue lipolysis associated with human CRP. Possible molecular mechanisms of metformin action-studied by gene expression profiling in the liver-revealed deregulated genes from inflammatory and insulin signaling, AMP-activated protein kinase (AMPK) signaling and gluconeogenesis pathways. It can be concluded that in the presence of high levels of human CRP, metformin protects against inflammation and oxidative and dicarbonyl stress in the heart, but not in the kidney. Accordingly, these cardioprotective effects of metformin might be especially effective in diabetic patients with high levels of CRP.

Dataset Information

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

Publications

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

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