scholarly journals Curcumin and its analog alleviate diabetes-induced damages by regulating inflammation and oxidative stress in brain of diabetic rats​

2021 ◽  
Author(s):  
Chengfeng Miao ◽  
Hanbin Chen ◽  
Yulian Li ◽  
Ying Guo ◽  
Feifei Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Western Blot ◽  
Diabetic Rats ◽  
High Dose ◽  
Diabetic Encephalopathy ◽  
Sprague Dawley ◽  
The Brain ◽  
And Oxidative Stress ◽  
Myelin Staining

Abstract Background: Diabetic encephalopathy is a severe diabetes complication with cognitive dysfunction and neuropsychiatric disability. The mechanisms underlying diabetic encephalopathy is believed to be relevant with oxidative stress, vascular amylin deposition, immune receptors, inflammation, etc. This study wanted to evaluate the ability of curcumin and its analog A13 to alleviate oxidative stress and inflammation in diabetes-induced damages in brain. Methods: Sixty adult male Sprague-Dawley rats were divided into 5 groups: normal control (NC) group, diabetes mellitus (DM) group, curcumin-treated diabetes mellitus (CUR) group, high dose of A13-treated diabetes mellitus (HA) group, low dose of A13-treated diabetes mellitus (LA) group. Activation of the nuclear factor kappa-B (NF-κB p65) pathway was detected by RT-qPCR, immunohistochemical (IHC) staining and Western blot; oxidative stress was detected by biochemical detection kit; brain tissue sections were stained with hematoxylin–eosin (HE) staining and Myelin staining. Results: RT-qPCR, IHC staining and Western blot showed that curcumin and A13 treatment could inhibit the NF-κB p65 pathway. Curcumin and A13 increased the activity of superoxide dismutase and decreased the malondialdehyde level in the brain of diabetic rats. Furthermore, HE staining and Myelin staining demonstrated that the histological lesions of the brain in diabetic rats could be significantly ameliorated by curcumin and A13.Conclusion: Curcumin analog A13 could alleviate the damages in the brain of diabetes rats by regulating the pathways of inflammation and oxidative stress. A13 may be a new potential therapeutic agent for diabetic encephalopathy.

scholarly journals Curcumin and Its Analog Alleviate Diabetes-induced Damages by Regulating Inflammation and Oxidative Stress in Brain of Diabetic Rats​

2020 ◽  
Author(s):  
Chengfeng Miao ◽  
Hanbin Chen ◽  
Yulian Li ◽  
Ying Guo ◽  
Feifei Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Western Blot ◽  
Diabetic Rats ◽  
High Dose ◽  
Diabetic Encephalopathy ◽  
Sprague Dawley ◽  
The Brain ◽  
And Oxidative Stress ◽  
Myelin Staining

Abstract Background: Diabetic encephalopathy is a severe diabetes complication with cognitive dysfunction and neuropsychiatric disability. The mechanisms underlying diabetic encephalopathy is believed to be relevant with oxidative stress, vascular amylin deposition, immune receptors, inflammation, etc. This study wanted to evaluate the ability of curcumin and its analog A13 to alleviate oxidative stress and inflammation in diabetes-induced damages in brain.Methods: Sixty adult male Sprague-Dawley rats were divided into 5 groups: normal control (NC) group, diabetes mellitus (DM) group, curcumin-treated diabetes mellitus (CUR) group, high dose of A13-treated diabetes mellitus (HA) group, low dose of A13-treated diabetes mellitus (LA) group. Activation of the nuclear factor kappa-B (NF-κB p65) pathway was detected by RT-qPCR, immunohistochemical (IHC) staining and Western blot; oxidative stress was detected by biochemical detection kit; brain tissue sections were stained with hematoxylin–eosin (HE) staining and Myelin staining. Results: RT-qPCR, IHC staining and Western blot showed that curcumin and A13 treatment could inhibit the NF-κB p65 pathway. Curcumin and A13 increased the activity of superoxide dismutase and decreased the malondialdehyde level in the brain of diabetic rats. Furthermore, HE staining and Myelin staining demonstrated that the histological lesions of the brain in diabetic rats could be significantly ameliorated by curcumin and A13.Conclusion: Curcumin analog A13 could alleviate the damages in the brain of diabetes rats by regulating the pathways of inflammation and oxidative stress. A13 may be a new potential therapeutic agent for diabetic encephalopathy.

scholarly journals Curcumin and its analog alleviate diabetes-induced damages by regulating inflammation and oxidative stress in brain of diabetic rats

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Chengfeng Miao ◽  
Hanbin Chen ◽  
Yulian Li ◽  
Ying Guo ◽  
Feifei Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Western Blot ◽  
Diabetic Rats ◽  
High Dose ◽  
Diabetic Encephalopathy ◽  
Sprague Dawley ◽  
The Brain ◽  
And Oxidative Stress ◽  
Myelin Staining

Abstract Background Diabetic encephalopathy is a severe diabetes complication with cognitive dysfunction and neuropsychiatric disability. The mechanisms underlying diabetic encephalopathy is believed to be relevant with oxidative stress, vascular amylin deposition, immune receptors, inflammation, etc. This study wanted to evaluate the ability of curcumin and its analog A13 to alleviate oxidative stress and inflammation in diabetes-induced damages in brain. Methods Sixty adult male Sprague–Dawley rats were divided into 5 groups: normal control (NC) group, diabetes mellitus (DM) group, curcumin-treated diabetes mellitus (CUR) group, high dose of A13-treated diabetes mellitus (HA) group, low dose of A13-treated diabetes mellitus (LA) group. Activation of the nuclear factor kappa-B (NF-κB p65) pathway was detected by RT-qPCR, immunohistochemical (IHC) staining and Western blot; oxidative stress was detected by biochemical detection kit; brain tissue sections were stained with hematoxylin–eosin (HE) staining and Myelin staining. Results RT-qPCR, IHC staining and Western blot showed that curcumin and A13 treatment could inhibit the NF-κB p65 pathway. Curcumin and A13 increased the activity of superoxide dismutase and decreased the malondialdehyde level in the brain of diabetic rats. Furthermore, HE staining and Myelin staining demonstrated that the histological lesions of the brain in diabetic rats could be significantly ameliorated by curcumin and A13. Conclusion Curcumin analog A13 could alleviate the damages in the brain of diabetes rats by regulating the pathways of inflammation and oxidative stress. A13 may be a new potential therapeutic agent for diabetic encephalopathy.

scholarly journals Liraglutide protects cardiac function in diabetic rats through the PPARα pathway

2018 ◽  
Vol 38 (2) ◽  
Author(s):  
Qian Zhang ◽  
Xinhua Xiao ◽  
Jia Zheng ◽  
Ming Li ◽  
Miao Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Cardiac Dysfunction ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Serum Adiponectin ◽  
Diabetic Rat ◽  
Lv Function ◽  
High Dose ◽  
And Oxidative Stress

Increasing evidence shows that diabetes causes cardiac dysfunction. We hypothesized that a glucagon-like peptide-1 (GLP-1) analog, liraglutide, would attenuate cardiac dysfunction in diabetic rats. A total of 24 Sprague–Dawley (SD) rats were divided into two groups fed either a normal diet (normal, n=6) or a high-fat diet (HFD, n=18) for 4 weeks. Then, the HFD rats were injected with streptozotocin (STZ) to create a diabetic rat model. Diabetic rats were divided into three subgroups receiving vehicle (diabetic, n=6), a low dose of liraglutide (Llirag, 0.2 mg/kg/day, n=6), or a high dose of liraglutide (Hlirag, 0.4 mg/kg/day, n=6). Metabolic parameters, systolic blood pressure (SBP), heart rate (HR), left ventricular (LV) function, and whole genome expression of the heart were determined. Diabetic rats developed insulin resistance, increased blood lipid levels and oxidative stress, and impaired LV function, serum adiponectin, nitric oxide (NO). Liraglutide improved insulin resistance, serum adiponectin, NO, HR, and LV function and reduced blood triglyceride (TG), total cholesterol (TC) levels, and oxidative stress. Moreover, liraglutide increased heart nuclear receptor subfamily 1, group H, member 3 (Nr1h3), peroxisome proliferator activated receptor (Ppar) α (Pparα), and Srebp expression and reduced diacylglycerol O-acyltransferase 1 (Dgat) and angiopoietin-like 3 (Angptl3) expression. Liraglutide prevented cardiac dysfunction by activating the PPARα pathway to inhibit Dgat expression and oxidative stress in diabetic rats.

scholarly journals Comparative Study of the Antioxidant Effects of Metformin, Glibenclamide, and Repaglinide in Alloxan-Induced Diabetic Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Bonaventure Chukwunonso Obi ◽  
Theophine Chinwuba Okoye ◽  
Victor Eshu Okpashi ◽  
Christiana Nonye Igwe ◽  
Edwin Olisah Alumanah
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Diabetic Complications ◽  
Significant Proportion ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Control Group ◽  
Diabetic Control Group ◽  
Antioxidant Effects ◽  
And Oxidative Stress

Diabetes mellitus is one of the serious global health problems affecting a significant proportion of both developed and developing countries. Overproduction of free radicals and oxidative stress has been associated with the development of diabetic complications. In the present study, the antioxidant effects of metformin (MET), glibenclamide (GLI), and repaglinide (REP) were evaluated in alloxan-induced diabetic rats. The findings from this study may possibly help in understanding the efficacy of these standard drugs in managing the complications arising from diabetes mellitus (DM). Alloxan (130 mg/kg BW) was administered as a single dose to induce diabetes. Four (4) groups of rats (n=6) were used; group 1 served as diabetic control while groups 2, 3, and 4 were the diabetic test groups that received MET (25 mg/kg), GLI (2.5 mg/kg), and REP (0.5 mg/kg), respectively. The result of the study showed significant (p<0.05) improvement in the altered antioxidant enzymes (SOD, CAT) and GSH concentration in diabetic treated rats compared with the diabetic control group. MET and REP produced significant effect on the MDA concentration while GLI showed insignificant reduction in the MDA concentration compared with the diabetic control. Findings from this study suggest that the administration of MET, GLI, and REP exerts significant antioxidant effects in alloxan-induced diabetic rats, thus contributing to the protective effect against oxidative stress-induced damage during diabetic complications.

Protective effects of quercetin on traumatic brain injury induced inflammation and oxidative stress in cortex through activating Nrf2/HO-1 pathway

2021 ◽  
Vol 39 (1) ◽  
pp. 73-84
Author(s):  
Jianqiang Song ◽  
Guoliang Du ◽  
Haiyun Wu ◽  
Xiangliang Gao ◽  
Zhen Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Inflammatory Responses ◽  
Enzyme Linked Immunosorbent Assay ◽  
Heme Oxygenase 1 ◽  
The Brain ◽  
And Oxidative Stress ◽  
Quercetin Treatment

Background: Traumatic brain injury (TBI) has been a serious public health issue. Clinically, there is an urgent need for agents to ameliorate the neuroinflammation and oxidative stress induced by TBI. Our previous research has demonstrated that quercetin could protect the neurological function. However, the detailed mechanism underlying this process remains poorly understood. Objective: This research was designed to investigate the mechanisms of quercetin to protect the cortical neurons. Methods: A modified weight-drop device was used for the TBI model. 5, 20 or 50 mg/kg quercetin was injected intraperitoneally to rats at 0.5, 12 and 24 h post TBI. Rats were sacrificed three days post injury and their cerebral cortex was obtained from the injured side. The rats were randomly assigned into three groups of equal number: TBI and quercetin group, TBI group, and Sham group. The brain water content was calculated to estimate the brain damage induced by TBI. Immunohistochemical and Western blot assays were utilized to investigate the neurobehavioral status. Enzyme-linked immunosorbent assay and reverse transcription polymerase chain reaction were performed to evaluate the inflammatory responses. The cortical oxidative stress was measured by estimating the activities of malondialdehyde, superoxide dismutase, catalase and glutathione-Px. Western blot was utilized to evaluate the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1). Results: Quercetin attenuated the brain edema and microgliosis in TBI rats. Quercetin treatment attenuated cortical inflammatory responses and oxidative stress induced by TBI insults. Quercetin treatment activated the cortical Nrf2/HO-1 pathway in TBI rats. Conclusions: Quercetin ameliorated the TBI-induced neuroinflammation and oxidative stress in the cortex through activating the Nrf2/HO-1 pathway.

scholarly journals Melatonin Attenuates Contrast-Induced Nephropathy in Diabetic Rats: The Role of Interleukin-33 and Oxidative Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Didem Onk ◽  
Oruc Alper Onk ◽  
Kultigin Turkmen ◽  
Huseyin Serkan Erol ◽  
Tulin Akarsu Ayazoglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Potential ◽  
Kidney Tissue ◽  
Diabetic Rats ◽  
Sprague Dawley ◽  
Contrast Induced Nephropathy ◽  
Interleukin 33 ◽  
Sprague Dawley Rats ◽  
And Oxidative Stress

Background.Inflammation and oxidative stress (OxS) contribute to the pathogenesis of diabetic kidney disease (DKD) and contrast-induced nephropathy (CIN). Patients with DKD were found to be more prone to CIN. Interleukin-33 (IL-33) is a proinflammatory cytokine, but its role in DKD and CIN is unknown.Methods.Thirty male Sprague-Dawley rats were enrolled. The first group was comprised of healthy rats (HRs), whereas the other four groups were made up of diabetic rats (DRs), diabetic rats with contrast-induced nephropathy (CIN + DRs), melatonin-treated diabetic rats (MTDRs), and melatonin-treated CIN + DRs (MTCIN + DRs). All groups except the HRs received 50 mg/kg/day streptozotocin (STZ). CIN + DRs were constituted by administrating 1.5 mg/kg of intravenous radiocontrast dye on the 35th day. MTDRs and MTCIN + DRs were given 20 mg/kg/day of intraperitoneal injection of melatonin (MT) from the 28th day for the constitutive seven days.Results.We observed increased IL-33 in the kidney tissue following induction of CIN in DRs. To determine whether MT is effective in preventing CIN, we administered MT in CIN + DRs and demonstrated that kidney tissue levels of OxS markers, inflammatory cytokines, and IL-33 were significantly diminished in MTCIN + DRs compared with other groups without MT treatment (p<0.05).Conclusion.Inhibition of IL-33 with MT provides therapeutic potential in DKD with CIN.

scholarly journals Status of Antioxidants Molecules and Lipid Peroxidation in the Diabetic Testes

2018 ◽  
Vol 26 (1) ◽  
Author(s):  
Kishwor Bhandari ◽  
Sanju Acharya ◽  
AK Srivastava
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Lipid Peroxidation ◽  
Molecular Study ◽  
Epidemiological Studies ◽  
Diabetic Rats ◽  
Enzymatic Antioxidants ◽  
Chronic Hyperglycemia ◽  
Diabetic Model ◽  
And Oxidative Stress

Introduction: According to the epidemiological studies, diabetes mellitus has become a potential cause of male infertility. Knowledge regarding how diabetes mellitus interferes with the process of spermatogenesis and results in infertility needs the molecular study in the testis in diabetic condition. Enhanced oxidative stress and changes in antioxidant capacity are considered to play an important role in the pathogenesis of chronic diabetes mellitus. So, this study was established to investigate the activity of enzymatic antioxidants and oxidative stress in the testis of diabetic model rats. Material & Methods: Diabetes mellitus was induced in the rat by intraperitoneal injection of Streptozotocin. The rats were sacrificed and the dissection was done to take out the testis. The testes were processed for the activity of enzymatic antioxidants. Results: It was found that oxidative stress was increased in the testes of diabetic rats. The sperms were also affected by the chronic hyperglycemia.

Comparative study of cholinergic and oxidative stress biomarkers in brains of diabetic and hypercholesterolemic rats

2015 ◽  
Vol 35 (3) ◽  
pp. 251-258 ◽  
Author(s):  
AM Hegazy ◽  
AS Abdel Azeem ◽  
EM Shahy ◽  
EM El-Sayed
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rats ◽  
High Cholesterol Diet ◽  
Iron Level ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
Total Antioxidant ◽  
Increased Activity ◽  
The Brain ◽  
And Oxidative Stress

Objective: Diabetes mellitus (DM) and hypercholesterolemia (HC) when poorly controlled lead to debilitating central nervous system complications including cognitive deficits and memory impairment. In the present study, we investigated the mechanisms that may be responsible for such deficits. Methods: Both diabetes and HC were induced in two groups of rats independently using alloxan and high cholesterol diet, respectively. Results: Acetyl cholinesterase was significantly increased in brain of diabetic rats. Also, brain malondialdehyde level was extremely elevated in both diabetic and hypercholesterolemic groups. Meanwhile, brain albumin was markedly decreased in both of them. However, the brain iron level was significantly increased in DM with concomitant increase in total antioxidant capacity in the same group as compared to the normal control. The concentration of brain calcium was noticeably increased in HC group. Our results were confirmed by the increased activity of lactate dehydrogenase in both DM and HC groups, indicating major brain cytotoxicity. Conclusions: Overall, our results suggested that both DM and HC have deleterious effects on the brain which may be attributed to oxidative stress and dysregulation of both cholinergic function and calcium level. Administration of antioxidant is recommended in both cases.

scholarly journals Attenuation of Apoptosis and Oxidative Stress by Endurance Training in the Cerebellum of Diabetic Rats

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Asma Taheri ◽  
Abdolhamid Habibi ◽  
Saeid Shakerian ◽  
Mohammad Reza Tabandeh ◽  
Masoud Nikbakht
Keyword(s):  
Oxidative Stress ◽  
Endurance Training ◽  
Exercise Group ◽  
Diabetic Rats ◽  
Moderate Intensity ◽  
Control Group ◽  
Diabetic Patients ◽  
The Brain ◽  
And Oxidative Stress ◽  
Training Protocol

Objectives: Identifying the effective exercise protocol that attenuates the functional and molecular disturbances in different regions of the brain, in particular the cerebellum, can help the proper management of neuropathies in diabetic patients. Methods: Twenty rats were randomly divided into four groups: (1) Normal control group (CON), (2) normal exercise group (TH), (3) diabetes control group (DC), and (4) diabetes exercise group (TD). Diabetes was induced by i.p injection of a single dose of streptozotocin (50 mg/kg). The endurance training protocol was performed on a treadmill for five days a week for six weeks with moderate intensity. The activities of antioxidant enzymes and the expression or release of apoptotic factors were analyzed based on data from rat cerebellum tissue at the end of the experiments. Results: Six weeks of endurance training improved the oxidative defense system by increasing the activities of SOD (from 3.70 ± 0.64 to 6.55 ± 0.56), GPx (from 3.42 ± 0.73 to 4.84 ± 0.62), and catalase (from 1.36 ± 0.23 to 3.59 ± 0.37) and reducing the MDA concentration (from 6.81 ± 1.34 to 4.33 ± 1.03) in the cerebellum of diabetic rats. Increased expression or cytosolic release of apoptotic effectors such as bax, caspase 3, and cytochrome c in the cerebellum of diabetic rats were attenuated following exercise training. Conclusions: Our research results showed that six weeks of endurance training may be helpful for the attenuation of neuropathies in diabetic patients by the attenuation of apoptosis and oxidative stress in the cerebellum.

scholarly journals Effect of moderate exercise on renal changes and oxidative stress in ovariectomized rats with type 1 diabetes mellitus

2019 ◽  
Vol 6 (13) ◽  
pp. 331-345 ◽  
Author(s):  
Mayane Oliveira Rebouças da Silveira ◽  
Liliany Souza de Brito Amaral ◽  
Samira Itana de Souza ◽  
Halanna Rocha Ferraz ◽  
Jéssica Alves Dias ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Renal Function ◽  
Aerobic Exercise ◽  
Type 1 Diabetes Mellitus ◽  
Diabetic Rats ◽  
Ovariectomized Rats ◽  
And Oxidative Stress

This study evaluated the aerobic exercise effects of moderate and progressive intensity on renal function and structure, and oxidative stress in ovariectomized rats with type 1 diabetes mellitus induced by streptozotocin (STZ). Eighteen Wistar rats were divided into 3 groups: OSC - ovariectomized and sedentary control rats; OSD - ovariectomized and sedentary diabetic rats; and OTD - ovariectomized and trained diabetic rats. After induction of diabetes, the OTD group was submitted to eight weeks of exercise. Twenty-four hours after the last training session urine samples were collected. Blood samples and kidneys were collected after euthanasia for renal function analysis, histology, morphometry and oxidative stress. Our results have shown a reduction of the weight gain, increase of kidney weight and postprandial glycemia in diabetic rats. However, exercise decreased glycosuria and prevented the proteinuria in OTD group rats. Focal segmental glomerulosclerosis (FSGS), juxtamedullary glomerular tuft area, tubulointerstitial lesions (TIL), brush border loss and tubular cell debridement were reduced in OTD rats. In addition, exercise training decreased urinary and plasma concentrations of thiobarbituric acid reactive substance (TBARS). Our results demonstrate the beneficial effect of progressive aerobic exercise on proteinuria, glycosuria, and renal structure in ovariectomized diabetic rats, which may be mediated in part by reduction of oxidative stress.

Sign in / Sign up

Export Citation Format

Share Document