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.

scholarly journals Puerarin mitigates acute liver injury in septic rats by regulating proinflammatory factors and oxidative stress levels

2021 ◽  
Vol 20 (11) ◽  
pp. 2305-2310
Author(s):  
Jinan Zheng ◽  
Qing Huang ◽  
Jingjing Fang
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Serum Levels ◽  
Expression Level ◽  
Sepsis Group ◽  
Control Group ◽  
Sprague Dawley ◽  
Tnf Α ◽  
Proinflammatory Factors

Purpose: To determine the protective effect of puerarin against acute liver injury in septic rats, and the mechanism involved.Methods: Eighty-seven Sprague-Dawley (SD) rats were assigned to control, sepsis and puerarin groups (each having 29 rats). Serum levels of NF-kB, TNF-α, IL-1 β, IL-6, ALT and AST were assayed. Liver lesions and levels of NO, SOD, iNOS and malondialdehyde (MDA) were measured using standard procedures.Results: Compared with the control group, the levels of NF-kB, TNF-α, IL-1β, IL-6, AST, ALT, NO, MDA and iNOS significantly increased in the sepsis group, while SOD level decreased significantly. In contrast, there were marked decreases in NF-kB, TNF-α, IL-1β, AST, ALT, NO, MDA and iNOS in puerarin group, relative to the sepsis group, while SOD expression level was significantly increased (p <0.05). The level of p-p38 in liver of septic rats was up-regulated, relative to control rats, while Nrf2 significantly decreased (p < 0.05). The expression level of p-p38 in the puerarin group was significantly decreased, relative to the sepsis group, while the expression level of Nrf2 significantly increased (p < 0.05).Conclusion: Puerarin mitigates acute liver injury in septic rats by inhibiting NF-kB and p38 signaling pathway, down-regulating proinflammatory factors, and suppressing oxidative stress. Thus, puerarin may be developed for use in the treatment liver injury.

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.

scholarly journals Comparison of Effects of Different Statins on Contrast-Induced Acute Kidney Injury in Rats: Histopathological and Biochemical Findings

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-lei Wang ◽  
Tuo Zhang ◽  
Liu-hua Hu ◽  
Shi-qun Sun ◽  
Wei-feng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Lipid Lowering ◽  
Control Group ◽  
Sprague Dawley ◽  
Atorvastatin Group ◽  
New Strategy ◽  
Ameliorative Effect ◽  
Markers Of Oxidative Stress

Statins are a promising new strategy to prevent contrast-induced acute kidney injury (CI-AKI). In this study we compared the ameliorative effect of different statins in a rat model of CI-AKI. Sprague-Dawley rats were divided into five groups: control group; CI-AKI group; CI-AKI + rosuvastatin group (10 mg/kg/day); CI-AKI + simvastatin group (80 mg/kg/day); and CI-AKI + atorvastatin group (20 mg/kg/day). CI-AKI was induced by dehydration for 72 hours, followed by furosemide intramuscular injection 20 minutes before low-osmolar contrast media (CM) intravenous injection. Statins were administered by oral gavage once daily for 3 consecutive days before CM injection and once 4 hours after CM injection. Rats were sacrificed 24 hours after CM injection, and renal function, kidney histopathology, nitric oxide (NO) metabolites, and markers of oxidative stress, inflammation, and apoptosis were evaluated. The results showed that atorvastatin and rosuvastatin but not simvastatin ameliorated CM-induced serum creatinine elevation and histopathological alterations. Atorvastatin and rosuvastatin showed similar effectiveness against CM-induced oxidative stress, but simvastatin was less effective. Atorvastatin was most effective against NO system dysfunction and cell apoptosis, whereas rosuvastatin was most effective against inflammation. Our findings indicate that statins exhibit differential effects in preventing CI-AKI when given at equivalent lipid-lowering doses.

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 Hydroethanolic Extract of Defatted Buchholzia coriacea Seeds Alleviates Tamoxifen-Induced Hepatic Triglyceride Accumulation, Inflammation and Oxidative Distress in Rat

Medicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 1
Author(s):  
Ayokanmi Ore ◽  
Abideen Idowu Adeogun ◽  
Oluseyi Adeboye Akinloye
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Liver Injury ◽  
Hepatic Function ◽  
Protein Carbonyls ◽  
Control Group ◽  
Hepatic Triglyceride ◽  
Triglyceride Accumulation ◽  
Group I ◽  
Hydroethanolic Extract

Background: Tamoxifen (TMX) has proven to be effective in the prevention and treatment of breast cancer. However, long-term use of TMX is associated with hepatic steatosis, oxidative liver injury and hepatocarcinoma. Buchholzia coriacea seeds (BCS) have been widely applied in traditional medicine due to their nutritional and therapeutic potentials. This study investigates the protective effect of hydroethanolic extract of (defatted) B. coriacea seeds (HEBCS) against TMX–induced hepatotoxicity in rats. Methods: Thirty-six (36) male albino rats were divided into six groups (n = 6/group). Group I served as control. Group II received 50 mg/kg/day TMX orally (p.o.) (TMX) for 21 days, group III received TMX plus 125 mg/kg/d HEBCS p.o. (HEBCS 125) for 21 days, group IV received TMX plus 250 mg/kg/d HEBCS p.o. (HEBCS 250) for 21 days and rats in group V and VI received HEBCS 125 and HEBCS 250 respectively for 21 days. Results: Compared with the control, TMX caused a significant increase (p < 0.05) in serum hepatic function biomarkers: alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase by 57%, 60% and 68% respectively. TMX also caused a significant increase in hepatic triglycerides level by 166% when compared with control and a significant decrease in serum HDL-cholesterol level by 37%. Compared with control, hepatic marker of inflammation, tumour necrosis factor alpha (TNF-α) increased significantly by 220%, coupled with significant increase in expression of interleukin 6 and cyclooxygenase 2. There was also significant increase in levels of Biomarkers of oxidative stress, nitric oxide, malondialdehyde and protein carbonyls in the TMX group by 89%, 175% and 114% respectively when compared with the control. Hepatic antioxidants, reduced glutathione (GSH) level and activities of superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) and glutathione peroxidase (GSH-Px) decreased significantly in the TMX group by 35%, 67%, 41%, 59% and 53% respectively when compared with the control. However, HEBCS at 250 mg/kg significantly protected against TMX–induced hepatotoxicity by decreasing hepatic triglyceride content, serum hepatic function biomarkers, hepatic inflammation and oxidative stress with significant improvement in hepatic antioxidant system. Histopathological findings show that HEBCS alleviate TMX–induced hepatocyte ballooning. Conclusions: Current data suggest that HEBCS protected against TMX–induced hepatotoxicity in rats. HEBCS may be useful in managing TMX–induced toxicities in breast cancer patients. It may also be helpful against other forms of liver injury involving steatosis, inflammation, free radicals, and oxidative damage.

scholarly journals To Evaluate the Effect of Vitamin E Therapy on the Oxidative Stress Markers (Nitric Oxide, SOD, Glutathione Peroxidase) & Vitamin E Levels in Pulmonary Tuberculosis Patients

2020 ◽  
Vol 9 (40) ◽  
pp. 2970-2975
Author(s):  
Rohit John Chaudhary ◽  
Bharti Kwatra Uppal
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Glutathione Peroxidase ◽  
Pulmonary Tuberculosis ◽  
Older Age ◽  
Control Group ◽  
Ros Production ◽  
Age Group ◽  
Sod Activity

BACKGROUND Severe oxidative stress has been reported in TB patients because of infection associated with malnutrition and poor immunity. Mycobacteria can induce reactive oxygen species (ROS) production by activating phagocytes, and enhanced ROS production may promote tissue injury and inflammation. We wanted to compare the effect of antioxidant administration in the outcome of ATT treatment between the test and the control group. METHODS This perspective study was conducted in the Departments of Biochemistry and Chest Medicine, CMC & Hospital. Hundred patients (fifty controls and fifty tests) who were diagnosed as pulmonary tuberculosis and started on DOT therapy under RNTCP during this period were included in the study. Each participant in the study was subjected to the following test at the first visit, 2nd month and 6th month follow up (biochemical markers Nitric oxide, SOD, Glutathione Peroxidase and Vitamin E levels). Statistical analysis was done using SPSS version. RESULTS The results were based on four categories (male / female, alcoholic / non-alcoholic, smoker / non-smoker, and younger / older age group). Females had responded better with greater fall in percentage of nitric oxide values (69 %) than males (64.1 %). The mean of SOD activity (277.5 + / - 31.5) was more in smokers than non-smokers (261.3 + / - 36.0) & percentage fall of nitric oxide in smokers (65 %) & non-smokers (67 %). In alcoholics the percentage fall of nitric oxide (68.3 %) was higher with more SOD activity (Mean 278.7 + / - 27.6) than non-alcoholics (Mean 256 + / - 38.0) indicating a positive correlation of smoking & alcoholism with tuberculosis. Younger age group responded better with more fall in the percentage of nitric oxide (67 %) & mean SOD activity (265.8 + / - 30.1) than older age group. CONCLUSIONS Antioxidant supplementation reduces oxidative stress, improves the effectiveness of ATT therapy, and thus helps in improving the outcome in pulmonary tuberculosis. KEY WORDS Pulmonary TB, ATT (Anti-Tubercular Treatment), Antioxidants & Free Radicals

scholarly journals IL-23 Promotes Myocardial I/R Injury by Increasing the Inflammatory Responses and Oxidative Stress Reactions

2016 ◽  
Vol 38 (6) ◽  
pp. 2163-2172 ◽  
Author(s):  
Xiaorong Hu ◽  
Ruisong Ma ◽  
Jiajia Lu ◽  
Kai Zhang ◽  
Weipan Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Tunel Staining ◽  
Ischemia And Reperfusion ◽  
Stress Reactions ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Myocardial Ischemia And Reperfusion ◽  
Tnf Α ◽  
And Oxidative Stress

Background/Aims: Inflammation and oxidative stress play an important role in myocardial ischemia and reperfusion (I/R) injury. We hypothesized that IL-23, a pro-inflammatory cytokine, could promote myocardial I/R injury by increasing the inflammatory response and oxidative stress. Methods: Male Sprague-Dawley rats were randomly assigned into sham operated control (SO) group, ischemia and reperfusion (I/R) group, (IL-23 + I/R) group and (anti-IL-23 + I/R) group. At 4 h after reperfusion, the serum concentration of lactate dehydrogenase (LDH), creatine kinase (CK) and the tissue MDA concentration and SOD activity were measured. The infarcte size was measured by TTC staining. Apoptosis in heart sections were measured by TUNEL staining. The expression of HMGB1 and IL-17A were detected by Western Blotting and the expression of TNF-α and IL-6 were detected by Elisa. Results: After 4 h reperfusion, compared with the I/R group, IL-23 significantly increased the infarct size, the apoptosis of cardiomyocytes and the levels of LDH and CK (all P < 0.05). Meanwhile, IL-23 significantly increased the expression of eIL-17A, TNF-α and IL-6 and enhanced both the increase of the MDA level and the decrease of the SOD level induced by I/R (all P<0.05). IL-23 had no effect on the expression of HMGB1 (p > 0.05). All these effects were abolished by anti-IL-23 administration. Conclusion: The present study suggested that IL-23 may promote myocardial I/R injury by increasing the inflammatory responses and oxidative stress reaction.

Zataria multiflora extract and carvacrol affect cardiotoxicity induced by Adriamycin in rat

2018 ◽  
Vol 30 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Abolfazl Khajavi Rad ◽  
Reza Mohebbati
Keyword(s):  
Oxidative Stress ◽  
Cardiac Tissue ◽  
Male Rats ◽  
Control Group ◽  
Sod Activity ◽  
Serum Glutamic Oxaloacetic Transaminase ◽  
Zataria Multiflora ◽  
Total Thiol ◽  
Group 2 ◽  
Stress Damage

Abstract Background Because of the antioxidant effects of Zataria multiflora (ZM) and carvacrol (CAR) and also the role of oxidative stress in the induction of cardiotoxicity induced by Adriamycin (ADR), the aim of this study was to investigate the improvement effects of ZM extract and CAR on cardiotoxicity induced by ADR in rats. Methods Twenty-eight male rats were randomly assigned to four groups including (1) the control group; (2) the ADR group, which received ADR intravenously at the beginning of the study and the (3) ZM+ADR and (4) CAR+ADR groups, which received ZM and CAR by gavage for 28 consecutive days and ADR as single dose. Blood samples were collected on days 0 and 28 to determine serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT) and lactate dehydrogenase (LDH). Also, cardiac tissue was removed for redox marker evaluation. Results In the ADR group, malondialdehyde (MDA) significantly increased and superoxide dismutase (SOD) activity and total thiol contents significantly reduced, as compared with the control group, while CAR administration significantly improved this condition. Treatment with ZM significantly increased the SOD activity and total thiol content, as compared with the ADR group. The level of LDH significantly increased on day 28 in the ADR group compared to the control group, and administration of ZM and CAR significantly decreased it. The SGPT and SGOT levels in the ADR group significantly increased, and CAR administration significantly reduced them. Conclusion The results indicate that the administration of ZM hydroalcoholic extracts and its active ingredient, CAR, could reduce the oxidative stress damage through promotion of the cardiac and systemic antioxidant system. Also, CAR administration demonstrated better improvement in cardiotoxicity with ADR in rats.

OXIDATIVE STRESS AND MORPHOLOGICAL ASSESSMENT OF BONE MARROW IN MONOSODIUM GLUTAMATE-TREATED RAT

2018 ◽  
Vol 80 (2) ◽  
Author(s):  
Nor Janna Yahya ◽  
Zariyantey Abd Hamid ◽  
Erni Norfardila Abu Hanipah ◽  
Esther Mathias Ajik ◽  
Nur Afizah Yusoff ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Monosodium Glutamate ◽  
Protein Carbonyl ◽  
Morphological Alteration ◽  
Control Group ◽  
Bone Marrow Smear ◽  
Sprague Dawley ◽  
Oxidative Stress Status

Excess consumption of monosodium glutamate (MSG) was reported to cause oxidative stress on brain, liver and renal and altered haematological parameters. Therefore, this study was aimed to investigate the effect of MSG on oxidative stress status on bone marrow of rats. Male Sprague-Dawley rats (n=24) weighing between 160-200 g were divided randomly into three groups: Control which was given distilled water (1 mg/kg), MSG 60 and MSG 120 which were given 60 mg/kg MSG and 120 mg/kg MSG, respectively. All substances were oral force fed for 28 days consecutively. At the end of the study, bone marrow cells were isolated by flushing technique for measurement of the oxidative stress status and bone marrow smear observation. Results showed that the superoxide dismutase activity and protein carbonyl level were significantly increased in MSG 120 group than to control and MSG 60 groups (p<0.05). Conversely, glutathione level had declined significantly in both MSG groups as compared to control group (p<0.05). The malondialdehyde level was not significantly affected in MSG groups than to control group. Bone marrow smear indicated no evidence of morphological alteration in all groups. In conclusion, MSG at both doses caused oxidative stress on bone marrow after 28 days of exposure.

Liver asialoglycoprotein receptor levels correlate with severity of alcoholic liver damage in rats

2004 ◽  
Vol 96 (1) ◽  
pp. 76-80 ◽  
Author(s):  
Carol A. Casey ◽  
Benita L. McVicker ◽  
Terrence M. Donohue ◽  
Melinda A. McFarland ◽  
Robert L. Wiegert ◽  
...  
Keyword(s):  
Liver Injury ◽  
Oral Administration ◽  
Liver Damage ◽  
Medium Chain Triglyceride ◽  
Asialoglycoprotein Receptor ◽  
Mrna Levels ◽  
Liver Pathology ◽  
Medium Chain ◽  
Ethanol Group ◽  
Liver Changes

It has been demonstrated that the oral administration of ethanol (Lieber-DeCarli liquid diet) to rats results in a decreased expression and content of the asialoglycoprotein receptor (ASGP-R) in the resultant fatty liver. In the present study, we wanted to determine whether the extent of impaired receptor content was correlated with the severity of liver pathology by using the intragastric feeding model. When ASGP-R protein and mRNA levels were measured in animals infused with ethanol or dextrose in the presence of fish oil (FO) or medium-chain triglyceride as the source of fat, more significant impairments to the ASGP-R were observed in the FO-ethanol group compared with the medium-chain triglyceride-ethanol group. Furthermore, only the FO-ethanol group showed pathological liver changes. These results demonstrate that a correlation exists between the progression of alcohol-associated liver injury, as defined by the severity of liver pathology, and an ethanol-induced decline in ASGP-R content.

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