scholarly journals A Subpressor Dose of Angiotensin II Elevates Blood Pressure in a Normotensive Rat Model by Oxidative Stress

2015 ◽  
pp. 153-159 ◽  
Author(s):  
M. M. GOVENDER ◽  
A. NADAR
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Mrna Expression ◽  
Rat Model ◽  
Wistar Rat ◽  
Control Group ◽  
Sod Activity ◽  
Male Wistar Rats ◽  
Experimental Group

Oxidative stress is an imbalance between free radicals and antioxidants, and is an important etiological factor in the development of hypertension. Recent experimental evidence suggests that subpressor doses of angiotensin II elevate oxidative stress and blood pressure. We aimed to investigate the oxidative stress related mechanism by which a subpressor dose of angiotensin II induces hypertension in a normotensive rat model. Normotensive male Wistar rats were infused with a subpressor dose of angiotensin II for 28 days. The control group was sham operated and infused with saline only. Plasma angiotensin II and H2O2 levels, whole-blood glutathione peroxidase, and AT-1a, Cu/Zn SOD, and p22phox mRNA expression in the aorta was assessed. Systolic and diastolic blood pressures were elevated in the experimental group. There was no change in angiotensin II levels, but a significant increase in AT-1a mRNA expression was found in the experimental group. mRNA expression of p22phox was increased significantly and Cu/Zn SOD decreased significantly in the experimental group. There was no significant change to the H2O2 and GPx levels. Angiotensin II manipulates the free radical-antioxidant balance in the vasculature by selectively increasing O2− production and decreasing SOD activity and causes an oxidative stress induced elevation in blood pressure in the Wistar rat.

scholarly journals Preliminary Biochemical Description of Brain Oxidative Stress Status in Irritable Bowel Syndrome Contention-Stress Rat Model

Medicina ◽  
2019 ◽  
Vol 55 (12) ◽  
pp. 776 ◽  
Author(s):  
Ioana-Miruna Balmus ◽  
Radu Lefter ◽  
Alin Ciobica ◽  
Sabina Cojocaru ◽  
Samson Guenne ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nervous System ◽  
Irritable Bowel Syndrome ◽  
Rat Model ◽  
Complex Model ◽  
Control Group ◽  
Oxidative Stress Status ◽  
Male Wistar Rats ◽  
Brain Oxidative Stress ◽  
Irritable Bowel

Background and objectives: Oxidative stress and inflammation have been implicated in the etiology of irritable bowel syndrome (IBS), a common gastrointestinal functional disease. This study aimed to further characterize the contention-stress rat model by exploring a possible correlation between oxidative stress markers measured in brain tissues with behavioral components of the aforementioned model. Thus, it is hereby proposed a possible IBS animal model relevant to pharmacological and complementary medicine studies. Materials and Methods: Wild-type male Wistar rats (n = 5/group) were chronically exposed to 6-hour/day contention, consisting of isolating the animals in small, vital space-granting plastic devices, for seven consecutive days. Following contention exposure, temporal lobes were extracted and subjected to biochemical analyses to assess oxidative stress-status parameters. Results: Our results show increased brain oxidative stress in contention-stress rat model: decreased superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde production in the IBS group, as compared to the control group. Furthermore, the biochemical ratios which are used to evaluate the effectiveness of an antioxidant system on oxidative stress could be described in this model. Conclusions: The correlations between the behavioral patterns and biochemical oxidative stress features could suggest that this may be a complex model, which can successfully mimic IBS symptomatology further providing evidence of a strong connection between the digestive system, enteric nervous system, and the central nervous system.

scholarly journals Anticonvulsant Effects of Topiramate and Lacosamide on Pilocarpine-Induced Status Epilepticus in Rats: A Role of Reactive Oxygen Species and Inflammation

2021 ◽  
Vol 22 (5) ◽  
pp. 2264
Author(s):  
Michaela Shishmanova-Doseva ◽  
Lyudmil Peychev ◽  
Lyubka Yoanidu ◽  
Yordanka Uzunova ◽  
Milena Atanasova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Status Epilepticus ◽  
Control Level ◽  
Epileptic Activity ◽  
Control Group ◽  
Anticonvulsant Effect ◽  
Sod Activity ◽  
Inflammatory Damage ◽  
Male Wistar Rats ◽  
Early Effects

Background: Status epilepticus (SE) is a neurological disorder characterized by a prolonged epileptic activity followed by subsequent epileptogenic processes. The aim of the present study was to evaluate the early effects of topiramate (TPM) and lacosamide (LCM) treatment on oxidative stress and inflammatory damage in a model of pilocarpine-induced SE. Methods: Male Wistar rats were randomly divided into six groups and the two antiepileptic drugs (AEDs), TPM (40 and 80 mg/kg, i.p.) and LCM (10 and 30 mg/kg, i.p.), were injected three times repeatedly after pilocarpine administration. Rats were sacrificed 24 h post-SE and several parameters of oxidative stress and inflammatory response have been explored in the hippocampus. Results: The two drugs TPM and LCM, in both doses used, succeeded in attenuating the number of motor seizures compared to the SE-veh group 30 min after administration. Pilocarpine-induced SE decreased the superoxide dismutase (SOD) activity and reduced glutathione (GSH) levels while increasing the catalase (CAT) activity, malondialdehyde (MDA), and IL-1β levels compared to the control group. Groups with SE did not affect the TNF-α levels. The treatment with a higher dose of 30 mg/kg LCM restored to control level the SOD activity in the SE group. The two AEDs, in both doses applied, also normalized the CAT activity and MDA levels to control values. In conclusion, we suggest that the antioxidant effect of TPM and LCM might contribute to their anticonvulsant effect against pilocarpine-induced SE, whereas their weak anti-inflammatory effect in the hippocampus is a consequence of reduced SE severity.

scholarly journals FXR expression in a rat model of hilar cholangiocarcinoma

2020 ◽  
Author(s):  
Meng-yu Zhang ◽  
Jie-ping Wang ◽  
Kai he ◽  
Xian-ming Xia
Keyword(s):  
Bile Duct ◽  
Rat Model ◽  
Hilar Cholangiocarcinoma ◽  
Tumor Formation ◽  
Pathological Examination ◽  
Control Group ◽  
Standard Diet ◽  
Male Wistar Rats ◽  
Hilar Bile Duct ◽  
Experimental Group

Abstract Background: To develop a rat model of hilar cholangiocarcinoma and detect Farnesyl X receptor (FXR) expression in hilar cholangiocarcinoma tissues of this model, in order to provide a new method for the treatment of hilar cholangiocarcinoma.Methods: Forty male Wistar rats (body weight, 185 ± 5 g) were randomly divided into two groups (n = 20 each) as follows: The control group was fed a standard diet, and the experimental group was injected by cholangiocarcinoma QBC939 cell suspension along the hilar bile duct into the bile duct bifurcation with microsyringe. Every day note the rats’ mental state, diet, and fur condition. At 4 weeks, one rat of the experimental group was sacrificed, and we recorded changes in hilar bile duct size, texture, and form. This procedure was repeated at 6 weeks. After 6 weeks, hilar cholangiocarcinoma developed only in the experimental group, thereby establishing an experimental model for studying QBC939-induced hilar cholangiocarcinoma. Tumor formation was confirmed by pathological examination, and hilar bile duct tissues were harvested from both the groups. A real-time polymerase chain reaction assay and an immunohistochemical assay were used to analyze the expression of FXR in hilar cholangiocarcinoma and normal hilar bile duct tissues.Results: From the second week, the rats in experimental group began to eat less, and their body mass decreased compared with controls. After 6 weeks, we detected hilar cholangiocarcinoma in 17 rats (85%) in the experimental group. In the experimental group, we found that the levels of total cholesterol, total bilirubin, and direct bilirubin were higher compared with those of the control group. Simultaneously, muddy stones emerged from the bile ducts of rats in the experimental group. The FXR/Gapdh mRNA ratio in hilar cholangiocarcinoma and normal hilar bile duct tissues differed markedly. Light microscopy revealed a granular pattern of FXR expression which reacted with the anti-FXR antibody. Each section was randomly divided into six regions, with 80 cells were observed in every region. Sections with >10% positive cells were designated positive,Sections with <10% positive cells were designated negative. Each group included 4,800 cells. In the experimental group, 1,196 cells (24.9%) were positive and 3,538 cells (73.7%) were positive in the control group, and this difference was statistically significant.Conclusion: FXR expression significantly decreased in hilar cholangiocarcinoma of rats than in those of controls, suggesting that drugs targeting FXR may be a new strategy for hilar cholangiocarcinoma.

scholarly journals FXR expression in a rat model of hilar cholangiocarcinoma

2020 ◽  
Author(s):  
Meng-yu Zhang ◽  
Jie-ping Wang ◽  
Kai he ◽  
Xian-ming Xia
Keyword(s):  
Bile Duct ◽  
Rat Model ◽  
Hilar Cholangiocarcinoma ◽  
Tumor Formation ◽  
Pathological Examination ◽  
Control Group ◽  
Standard Diet ◽  
Male Wistar Rats ◽  
Hilar Bile Duct ◽  
Experimental Group

Abstract AIM: To develop a rat model of hilar cholangiocarcinoma and detect Farnesyl X receptor (FXR) expression in hilar cholangiocarcinoma tissues of this model, in order to provide a new method for the treatment of hilar cholangiocarcinoma. METHODS: Forty male Wistar rats (body weight, 185 ± 5 g) were randomly divided into two groups (n = 20 each) as follows: The control group was fed a standard diet, and the experimental group was injected by cholangiocarcinoma QBC939 cell suspension along the hilar bile duct into the bile duct bifurcation with microsyringe. Every day note the rats’ mental state, diet, and fur condition. At 4 weeks, one rat of the experimental group was sacrificed after it was administered anesthesia, and we recorded changes in hilar bile duct size, texture, and form. This procedure was repeated at 6 weeks. After 6 weeks, , hilar cholangiocarcinoma developed only in the experimental group, thereby establishing an experimental model for studying QBC939-induced hilar cholangiocarcinoma. Tumor formation was confirmed by pathological examination, and hilar bile duct tissues were harvested from both the groups. A real-time polymerase chain reaction assay and an immunohistochemical assay were used to analyze the expression of FXR in hilar cholangiocarcinoma and normal hilar bile duct tissues. RESULTS: From the second week, the rats in experimental group began to eat less, and their body mass decreased compared with controls. After 6 weeks, we detected hilar cholangiocarcinoma in 17 rats (85%) in the experimental group. In the experimental group with hilar cholangiocarcinoma, we found that the levels of total cholesterol, total bilirubin, and direct bilirubin were higher compared with those of the control group. Simultaneously, muddy stones emerged from the bile ducts of rats in the experimental group. The FXR /Gapdh mRNA ratio in hilar cholangiocarcinoma and normal hilar bile duct tissues differed markedly (16 and 35, respectively). Light microscopy revealed a granular pattern of FXR expression which reacted with the anti- FXR antibody. Each section was randomly divided into six regions, with 80 cells were observed in every region. Sections with >10% positive cells were designated positive, Sections with <10% positive cells were designated negative. Each group included 4,800 cells. In the experimental group, 1,196 cells (24.9%) were positive and 3,538 cells (73.7%) were positive in the control group, and this difference was statistically significant (χ2 = 10.35, P < 0.05). CONCLUSION: FXR expression significantly decreased in hilar cholangiocarcinoma of rats than in those of controls, suggesting that drugs targeting FXR may be a new strategy for hilar cholangiocarcinoma.

scholarly journals ELECTRIC CIGARETTES’S EFFECT TO THE MDA LEVELS IN BLOOD OF WISTAR RAT

2020 ◽  
Vol 5 (1) ◽  
pp. 233
Author(s):  
Etha Rambung
Keyword(s):  
Oxidative Stress ◽  
Electronic Cigarettes ◽  
Wistar Rat ◽  
Control Group ◽  
Blood Levels ◽  
Control Group Design ◽  
Treatment Groups ◽  
Group Design ◽  
Male Wistar Rats ◽  
The Difference

<p class="AbstractText"><em>The use of electronic cigarettes (e-cigarettes) has spread widely and increased dramatically among young people aroud the world. Variations in product design, taste, and marketing patterns increase the young people's interest in electronic cigarettes. Even many electric cigarettes are sold in shoppinng cebters and online, so they are easy to reach by teenagers. This study aims to analyze oxidative stress due to exposure to e-cigarettes by assessing the difference in blood MDA levels in the control and treatment groups. The method used is the Posttest Only Control Group Design.</em> <em>Thirty two male wistar rats divided into four treatments goups: K1 (SC (-), EE (-)), K2 (SC (-), EE(-)), P1 (SC(-),  EE (+) 15 times), and P2 (SC (-), EE (+) 30 times). The treatment is given for 5 minutes/ day for 50 days. Termination was carried out on the 50<sup>th</sup> day using ketamine. Intracardial blood sampling for examination of MDA levels by the TBARS method. The data obtained were tested by Kruskal Wallis with a significance of p &lt;0.05. MDA blood levels in P2 were significantly higher than P1 (p =0,035), K2 (p =0,001) and K1 (p =0,001). This study shows that e-cigarettes can cause oxidative stress in experimental animals.</em></p>

Paradoxical sleep deprivation induces oxidative stress in the submandibular glands of Wistar rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Taye J. Lasisi ◽  
Shehu-Tijani T. Shittu ◽  
Jude I. Abeje ◽  
Kehinde J. Ogunremi ◽  
Seyyid A. Shittu
Keyword(s):  
Oxidative Stress ◽  
Sleep Deprivation ◽  
Wistar Rats ◽  
Paradoxical Sleep ◽  
Salivary Secretion ◽  
Control Group ◽  
Paradoxical Sleep Deprivation ◽  
Sod Activity ◽  
Submandibular Glands ◽  
Male Wistar Rats

Abstract Objectives Paradoxical sleep deprivation has been associated with impaired salivary secretion in rats. However, the mechanism that underlies this is not known. Therefore, this study assessed salivary and serum oxidative stress levels following paradoxical sleep deprivation in rats. Methods Twenty-one male Wistar rats randomly divided into three groups of seven rats each as; Control (C); partial sleep-deprived (PSD); and total sleep-deprived (TSD) were used. Malondialdehyde (MDA) concentration, Superoxide dismutase (SOD), and catalase activities were evaluated in saliva, serum, and submandibular glands after seven days of sleep deprivation. Data were expressed as mean ± standard error of the mean and analyzed using one-way ANOVA, Tukey HSD post hoc, and Pearson’s correlation tests. Results Serum MDA levels were significantly higher in both the TSD and PSD groups compared to the control group whereas only the TSD group showed higher submandibular MDA levels compared to the PSD group and the control group. Submandibular SOD activity was significantly lower in both the TSD and PSD groups compared to the control group. Serum catalase activity was significantly lower in the TSD group only compared to the control group. Conclusions These results have demonstrated for the first time that paradoxical sleep deprivation was associated with changes in the oxidant/antioxidant defense system in the submandibular salivary glands of male Wistar rats which may contribute to impairment in salivary secretion.

Abstract 060: Role of Mir-214 in the Regulation of Perivascular Fibrosis in Angiotensin II Induced Hypertension

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Ryszard Nosalski ◽  
Mateusz Siedlinski ◽  
Aurelie Nguyen Dinh Cat ◽  
Dominik Skiba ◽  
Eilidh Mcginnigle ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Angiotensin Ii ◽  
Mrna Expression ◽  
Vascular Function ◽  
Gene Expression Regulation ◽  
Mesenteric Arteries ◽  
Control Group ◽  
Regulation Mechanism ◽  
Perivascular Inflammation

Objective: Hypertension (HT) is associated with perivascular inflammation and increased vascular fibrosis. MicroRNAs (miR) are a novel gene expression regulation mechanism and play a pivotal role in a range of pathological processes. The role and mechanism of miR214 in vascular fibrosis is unknown. Methods: 3-month-old C57BL/6, miR214KO and wild-type littermates were treated with angiotensin II (AngII, 490ng/kg/min; n=6-10) or control buffer for 14 days. PVATs from C57BL/6 animals were analysed using TaqMan_Rodent_microRNA_Arrays. Histological studies, wire myography, lucigenin-enhanced luminometry and cytometrical analysis was conducted, followed by statistical analysis with ANOVA or t-test. Data are expressed as a mean±SEM. Results: Out of 381 miRs, 16 were significantly overexpressed in C57BL/6 AngII animals, with only miR214 showing 8-fold induction (p<0.01) after Bonferroni correction. Also, 3-fold elevation of pri-miR-214 was observed. Interestingly, hydralazine treatment prevented both these changes (p<0.01). AngII infusion in miR214 KO animals did not alter blood pressure when compared to WT mice. Mir214 KOs exhibited diminished peri-aortic fibrosis (44779±2491 vs 78805±8696μm, p<0.01), upon AngII hypertension. This was associated with a significantly reduced induction of COL1A1, COL3A1 and TGFβ1 mRNA expression in PVAT and aortas (p<0.05). Vascular studies revealed improved endothelial function (69±10 vs. 22±4%, p<0.01), protection against oxidative stress (66±7 vs 118±19 RLU/sec/mg, p<0.001) and NOX2 mRNA expression (1.9±0.2 vs1.1±0.1, p<0.05) in AngII miR-214-KO aortas, while these parameters were not altered in mesenteric arteries. Recruitment of T cells into aortic PVAT was abolished in KO HT animals in comparison to control group (192±65 vs. 603±164 cell/mg; p<0.05). AngII HT was associated with 4-fold increase of miR-214 expression in the circulating peripheral blood T cells and 2-fold in the spleen. Moreover, AngII infusion increased TNFα mRNA expression in WT T cells (1±0.1 vs 1.6±0, p<0.01) whereas this effect was not seen in miR214 KO T cells (0.9±0.3 vs 0.9±0.1). Conclusions: MiR-214 plays a major role in modulation of aortic fibrosis, vascular function, oxidative stress and perivascular inflammation.

Betaine (Trimethylglycine) as a nutritional agent prevents oxidative stress after chronic ethanol consumption in pancreatic tissue of rats

2009 ◽  
Vol 79 (2) ◽  
pp. 79-86 ◽  
Author(s):  
Gungör Kanbak ◽  
Ali Dokumacioglu ◽  
Aysegul Tektas ◽  
Kazim Kartkaya ◽  
Mine Erden Inal
Keyword(s):  
Oxidative Stress ◽  
Ethanol Consumption ◽  
Pancreatic Tissue ◽  
Chronic Ethanol ◽  
Control Group ◽  
Sod Activity ◽  
Cytotoxic Effects ◽  
Ethanol Group ◽  
Chronic Ethanol Consumption ◽  
Male Wistar Rats

In this study, we investigated the free radical-mediated cytotoxic effects of chronic ethanol consumption on the pancreatic tissue and a possible cytoprotective effect of betaine as a methyl donor and an important participant in the methionine cycle. Twenty-four male Wistar rats were divided into control, ethanol, and ethanol+betaine groups. Prior to sacrifice, all groups were fed 60 mL/diet per day for two months. Rats in the ethanol group were fed with ethanol 8 g/kg/day. The ethanol+betaine groups were fed ethanol plus betaine (0.5 % w/v). Malondialdehyde levels and adenosine deaminase, superoxide dismutase, and xanthine oxidase activities were determined in pancreatic tissues of rats. Compared to control group, MDA levels increased significantly in the ethanol group (p<0.05). MDA levels in the ethanol+betaine group were significantly decreased compared to the ethanol group (p<0.05). ADA activity in the ethanol+betaine group decreased significantly when compared to the ethanol group (p<0.05). XO activities in ethanol-fed rats were decreased significantly compared to the control group (p<0.05). XO activity in the betaine group was increased significantly (p<0.05) compared to the ethanol group. SOD activity in the ethanol group decreased significantly compared to control group (p<0.001). SOD activity in the ethanol+betaine group decreased significantly (p<0.05) compared to the control group. We think that betaine, as a nutritional methylating agent, may be effective against ethanol-mediated oxidative stress in pancreatic tissue.

Mechanism Involved in Fortification by Berberine in CDDP-Induced Nephrotoxicity

2020 ◽  
Vol 13 (4) ◽  
pp. 342-352 ◽  
Author(s):  
Vipin K. Verma ◽  
Salma Malik ◽  
Ekta Mutneja ◽  
Anil K. Sahu ◽  
Kumari Rupashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Tissue ◽  
Isoquinoline Alkaloid ◽  
Experimental Models ◽  
Beclin 1 ◽  
Control Treatment ◽  
Control Group ◽  
Treatment Groups ◽  
Single Intraperitoneal Injection ◽  
Male Wistar Rats

Background: The activation of Nrf2/HO-1 pathway has been shown to protect against cisplatin- induced nephrotoxicity by reducing oxidative stress. Berberine (Ber), an isoquinoline alkaloid, has demonstrated antioxidant, anti-inflammatory and anti-apoptotic activities in various experimental models. Aim: To check the effect of Ber on cisplatin-induced nephrotoxicity and to explore the involved mechanism. Methods: Adult male Wistar rats were divided into 6 groups: Normal, cisplatin-control, treatment groups and per se group. Normal saline and Ber (20, 40 and 80 mg/kg; p.o.) was administered to rats for 10 days. A single intraperitoneal injection of cisplatin (8 mg/kg) was injected on 7th day to induced nephrotoxicity. On 10th day, rats were sacrificed, the kidney was removed and stored for the estimation of various parameters. Results: As compared to cisplatin-control group, Ber pretreatment improved renal function system and preserved renal architecture. It also diminished oxidative stress by upregulating the expression of Nrf2/HO-1 proteins. In addition, Ber attenuated the cisplatin mediated inflammation and apoptosis. Furthermore, it also reduced the phosphorylation of p38/JNK and PARP/Beclin-1 expression in the kidney. Conclusion: Ber attenuated renal injury by activating Nrf2/HO-1 and inhibiting JNK/p38MAPKs/ PARP/Beclin-1 expression which prevented oxidative stress, inflammation, apoptosis and autophagy in renal tissue.

scholarly journals Curcumin Decreased Oxidative Stress, Inhibited NF-κB Activation, and Improved Liver Pathology in Ethanol-Induced Liver Injury in Rats

2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Suchittra Samuhasaneeto ◽  
Duangporn Thong-Ngam ◽  
Onanong Kulaputana ◽  
Doungsamon Suyasunanont ◽  
Naruemon Klaikeaw
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Early Stage ◽  
Control Group ◽  
Liver Pathology ◽  
Sprague Dawley ◽  
Hepatocyte Apoptosis ◽  
Sod Activity ◽  
Ethanol Group ◽  
Liver Histopathology

To study the mechanism of curcumin-attenuated inflammation and liver pathology in early stage of alcoholic liver disease, female Sprague-Dawley rats were divided into four groups and treated with ethanol or curcumin via an intragastric tube for 4 weeks. A control group treated with distilled water, and an ethanol group was treated with ethanol (7.5 g/kg bw). Treatment groups were fed with ethanol supplemented with curcumin (400 or 1 200 mg/kg bw). The liver histopathology in ethanol group revealed mild-to-moderate steatosis and mild necroinflammation. Hepatic MDA, hepatocyte apoptosis, and NF-κB activation increased significantly in ethanol-treated group when compared with control. Curcumin treatments resulted in improving of liver pathology, decreasing the elevation of hepatic MDA, and inhibition of NF-κB activation. The 400 mg/kg bw of curcumin treatment revealed only a trend of decreased hepatocyte apoptosis. However, the results of SOD activity, PPARγprotein expression showed no difference among the groups. In conclusion, curcumin improved liver histopathology in early stage of ethanol-induced liver injury by reduction of oxidative stress and inhibition of NF-κB activation.

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