scholarly journals Protective Effects of Açai in Combination with Vitamin C against Aluminum-Induced Toxicity in Rat Liver

2017 ◽  
Vol 9 (1) ◽  
pp. 1 ◽  
Author(s):  
Nevien Mahmoud Ahmed ◽  
Fatma A. M. Hamaad
Keyword(s):  
Vitamin C ◽  
Protective Effect ◽  
Control Group ◽  
Protective Effects ◽  
Super Oxide Dismutase ◽  
Biochemical Alterations ◽  
Inflammatory Parameters ◽  
Antioxidant Parameters ◽  
Factor Α ◽  
Necrosis Factor

Aluminum is associated with the pathogenesis of several diseases. Açai has recently emerged as a natural source of antioxidants. The present study was conducted to evaluate the protective effect of Açai in combination with vitamin C against the aluminum chloride induced toxicity. Seventy rats were divided into 7 groups:- Group (GP) 1: control group, GP 2: treated with AlCl3, GP 3: treated with Açai, GP 4: treated with vitamin C, GP 5: treated with AlCl3 and Açai , GP 6: treated with AlCl3 and vitamin C, GP 7: treated with AlCl3, Açai and vitamin C. After 4 weeks, blood and liver specimens were collected to evaluate biochemical alterations and hepatic antioxidant and inflammatory parameters. AlCl3 treatment decreased liver enzymes (alanine aminotransferase, aspartate amino transferase, alkaline phosphatase), tumor necrosis factor-α and IL-6 while hepatic malondialdehyde was elevated. In contrast, hepatic glutathione, super oxide dismutase, catalase were decreased. Açai and vitamin C treatment improved the adverse effects induced by AlCl3, while co-administration with vitamin C promoted the action of açai on hepatic damage and antioxidant parameters. Açai showed a protective effect against AlCl3 induced toxicity, particularly in combination with vitamin C.

Protective effect of irbesartan against doxorubicin-induced nephrotoxicity in rats: implication of AMPK, PI3K/Akt, and mTOR signaling pathways

2018 ◽  
Vol 96 (12) ◽  
pp. 1209-1217 ◽  
Author(s):  
Eman A. Mohamed ◽  
Hebatalla I. Ahmed ◽  
Heba S. Zaky
Keyword(s):  
Protein Kinase ◽  
Protective Effect ◽  
Critical Role ◽  
Mammalian Target Of Rapamycin ◽  
Protective Effects ◽  
Phosphatidylinositol 3 Kinase ◽  
Factor Α ◽  
Amp Activated Protein Kinase ◽  
Renal Expression ◽  
Necrosis Factor

Nephrotoxicity is one of the serious undesirable effects related to doxorubicin (DOX). Herein, we have investigated the potential protective effect of irbesartan (IRB) against chronic nephrotoxicity induced by DOX, and the implication of different mechanistic pathways underlying these effects. Rats were treated with either DOX (2.5 mg/kg i.p., 3 times/week) for 2 weeks, and (or) IRB (40 mg/kg, daily) for 3 weeks. IRB prohibited nephrotoxicity induced by DOX, which was evident by the increase in blood urea nitrogen and creatinine levels and histopathological changes. IRB improved DOX-induced alterations in oxidative status by diminishing lipid peroxidation and upregulating the antioxidant enzymes. Also, upon DOX treatment, the renal expression of tumor necrosis factor-α, interleukin-6, and caspase-3 were significantly increased; IRB diminished DOX-induced alterations in these parameters. Moreover, DOX significantly decreased the expression level of AMP-activated protein kinase (AMPK). Meanwhile, DOX induced activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt/PKB) and mammalian target of rapamycin (mTOR) pathways that cross talked with AMPK. On the contrary, IRB successfully counterbalanced all these effects. Collectively, these outcomes suggest that the modulation of AMPK, PI3K, Akt, and mTOR pathways plays a critical role in conferring the protective effects of IRB against DOX nephrotoxicity.

scholarly journals Neurological Alterations and Testicular Damages in Aging Induced by D-Galactose and Neuro and Testicular Protective Effects of Combinations of Chitosan Nanoparticles, Resveratrol and Quercetin in Male Mice

Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa
Keyword(s):  
Oxidative Stress ◽  
Chitosan Nanoparticles ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Wide Range ◽  
Neurological Alterations

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.

scholarly journals Antihepatocarcinoma Effect of Portulaca oleracea L. in Mice by PI3K/Akt/mTOR and Nrf2/HO-1/NF-κB Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Zheng Guoyin ◽  
Peng Hao ◽  
Li Min ◽  
Gu Wei ◽  
Chen Zhe ◽  
...  
Keyword(s):  
Nuclear Factor Kappa B ◽  
Mammalian Target Of Rapamycin ◽  
Portulaca Oleracea ◽  
Control Group ◽  
Related Factor ◽  
Protective Effects ◽  
Phosphatidylinositol 3 Kinase ◽  
Pathological Alteration ◽  
Hepatocellular Carcinomas ◽  
Necrosis Factor

The purpose of the present study was to evaluate the pharmacological effects of Portulaca oleracea L. (Purslane) (PL) on N-nitrosodiethylamine- (NDEA-) induced hepatocellular carcinomas (HCC) and explore its potential mechanism. Mice were randomly assigned to four groups: control group, NDEA group, NDEA + Purslane (100 mg/kg) group, and NDEA + Purslane (200 mg/kg) group. The animal of each group was given NDEA (100 ppm) in drinking water. 1 h later, Purslane dissolved in PBS was intragastrically administered for continuous seven days. The results showed that Purslane reduced the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in liver and serum. Purslane also reduced the contents of interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), and methane dicarboxylic aldehyde (MDA) and restored the activity of superoxygen dehydrogenises (SOD) in serum. Purslane could obviously attenuate the hepatic pathological alteration. Furthermore, treatment with Purslane effectively inhibited the phosphorylations of phosphatidylinositol 3 kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR), nuclear factor-kappa B (NF-κB), and inhibitor of NF-κBα (IκBα) and upregulated the expressions of NF-E2-related factor 2 (Nrf2) and heme oxygenase- (HO-) 1. In conclusion, our research suggested that Purslane exhibited protective effects on NDEA-induced hepatocellular carcinomas by anti-inflammatory and antioxidative properties via the PI3K/Akt/mTOR and Nrf2/HO-1/NF-κB pathway.

The effects of desferrioxamine on cisplatininduced lipid peroxidation and the activities of antioxidant enzymes in rat kidneys

2004 ◽  
Vol 23 (1) ◽  
pp. 29-34 ◽  
Author(s):  
G Kadikoylu ◽  
Z Bolaman ◽  
S Demir ◽  
M Balkaya ◽  
N Akalin ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Vitamin C ◽  
Isotonic Saline ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Group V ◽  
Super Oxide Dismutase ◽  
Cervical Dislocation ◽  
Rat Kidneys

Cisplatin-induced nephrotoxicity is associated with an increase in lipid peroxidation and oxygen free radicals in rat kidneys. In this study, the effects of desferrioxamine were compared to vitamin C and E on cisplatin-induced lipid peroxidation and antioxidant enzyme activities in rat kidneys. Rats were divided into five groups, with 15 Wistar rats in each group. In the control group, rats received 1 mL/100 g isotonic saline solution intraperitoneally (i.p.). In Group II, 10 mg/kg cisplatin i.p. was injected to rats. Thirty minutes before the same dosage of cisplatin administration, 100 mg/kg i.p. vitamin C or E was given to rats in groups III and IV, respectively. Rats in Group V received 250 mg/kg desferrioxamine i.p., before the same dose of cisplatin administration. All rats were killed by cervical dislocation after 72 hours. The kidneys were immediately removed and washed in cold saline. Spectrophotometric method was used for all analyses. While catalase, glutathione reductase (GR), and super oxide dismutase (SOD) levels were found to be significantly decreased (P B < 0.001), malondialdehyde (MDA) (P < 0.05) and hydrogen peroxide (H2O2) (P < 0.001) levels were significantly increased in the cisplatin group when compared to the controls. MDA levels were decreased by desferrioxamine (P < 0.005) as well as vitamin C and E (P < 0.05 and P < 0.001, respectively). These three compounds induced a significant increase in SOD levels (P B < 0.05), but only in the vitamin C group, were SOD levels not significantly different than the levels of the controls (P > 0.05). In the desferrioxamine (P < 0.05), vitamin C and E groups (P < 0.001 for both), the cisplatin elevated H2O2 levels were decreased. None of these drugs had any effect on GR and catalase levels (P > 0.05). Desferrioxamine is useful to prevent cisplatin-induced lipid peroxidation, however, vitamin C and E are more effective on antioxidant enzymes than desferrioxamine.

Abstract 309: Role of Hemeoxygenase in the Reno-Protective Effects of Soluble Epoxide Hydrolase Inhibition In Diabetic Spontaneously Hypertensive Rats

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Ahmed A Elmarakby ◽  
Jessica Faulkner ◽  
Chelsey Pye ◽  
Babak Baban ◽  
Katelyn Rouch ◽  
...  
Keyword(s):  
Protective Effect ◽  
Renal Injury ◽  
Renal Fibrosis ◽  
Spontaneously Hypertensive Rats ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase ◽  
Control Group ◽  
Protective Effects ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

We previously showed that inhibition of soluble epoxide hydrolase (sEH) increased epoxyeicosatrienoic acids (EETs) levels and reduced renal injury in diabetic mice and these changes were associated with induction of hemeoxygenase-1 (HO-1). The present study determines whether the inhibition of HO negates the reno-protective effect of sEH inhibition in diabetic spontaneously hypertensive rats as a model of diabetic nephropathy in which hypertension coexists with diabetes. After six weeks of induction of diabetes with streptozotocin, SHR were divided into the following groups: untreated, treated with the sEH inhibitor, trans -4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (AUCB), treated with the HO inhibitor, stannous mesoporphyrin (SnMP), and treated with both inhibitors for four more weeks; non diabetic SHR served as a control group. Although inhibition of sEH increased renal EETs/DHETEs ratio and HO-1 activity in diabetic SHR, it did not significantly alter blood pressure (plasma EETs/DHETEs ratio was 0.5± 0.1 in AUCB-treated vs. 0.1± 0.01 in untreated diabetic SHR, P<0.05). Treatment of diabetic SHR with AUCB reduced the elevation in urinary albumin and nephrin excretion (albuminuria was 6.5± 0.5 in AUCB-treated diabetic SHR vs. 9± 1.7 mg/day in untreated diabetic SHR and nephrinuria was 70±11 in AUCB-treated diabetic SHR vs. 111± 9 μg/day in untreated diabetic SHR, P<0.05) whereas co-administration of SnMP with AUCB prevented these changes (albuminuria was 10.6± 0.6 mg/day and nephrinuria was 91±11 μg/day). Immunohistochemical analysis revealed elevations in renal fibrosis and apoptosis as evidenced by increased renal TGF-β, fibronectin and annexin V expression in diabetic SHR and these changes were reduced with sEH inhibition. Co-administration of SnMP with AUCB prevented its ability to reduce renal fibrosis and apoptosis in diabetic SHR. In addition, SnMP treatment also prevented AUCB-induced decreases in renal macrophage infiltration and renal TGF-β, NFκB and MCP-1 levels in diabetic SHR. These data suggest that HO-1 induction is involved in the protective effect of sEH inhibition against diabetic renal injury.

Protective effect of vanillin against carbon tetrachloride (CCl4)-induced oxidative brain injury in rats

2011 ◽  
Vol 28 (7) ◽  
pp. 655-662 ◽  
Author(s):  
Mohamed Makni ◽  
Yassine Chtourou ◽  
Mohamed Barkallah ◽  
Hamadi Fetoui
Keyword(s):  
Carbon Tetrachloride ◽  
Protective Effect ◽  
Brain Damage ◽  
Glutathione Transferase ◽  
Single Injection ◽  
Male Rats ◽  
Control Group ◽  
Protective Effects ◽  
Degree Of Protection ◽  
Oxidative Brain Injury

This study investigated the protective effects of vanillin against acute brain damage induced by carbon tetrachloride (CCl4) in rats. The study was performed on 32 male rats divided into four groups: a control group, vanillin group ([Va] 150 mg/kg/day, intraperitoneally [i.p.]) and CCl4 toxication groups received a single injection of CCl4 (1 ml/kg, i.p.; CCl4 and Va + CCl4 groups). The degree of protection in brain tissue was evaluated by the levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase, glutathione transferase, glutathione peroxidase and nitric oxide (NO). Vanillin showed a significant brain-protective effect by decreasing the level of lipid peroxidation and NO2 and elevated the activities of antioxidative enzymes and level of GSH. Consequently vanillin blocked oxidative brain damage induced by CCl4 in rats.

Evaluation of the toxic effect of silver nanoparticles and the possible protective effect of ascorbic acid on the parotid glands of albino rats: An in vivo study

2020 ◽  
Vol 36 (6) ◽  
pp. 446-453
Author(s):  
Salma Awad Taghyan ◽  
Hend El Messiry ◽  
Medhat Ahmed El Zainy
Keyword(s):  
Silver Nanoparticles ◽  
Ascorbic Acid ◽  
Vitamin C ◽  
Protective Effect ◽  
Toxic Effect ◽  
Toxic Effects ◽  
Control Group ◽  
Albino Rats ◽  
Parotid Glands ◽  
Ductal Cells

This study aimed to evaluate the toxic effect of silver nanoparticles (AgNPs) on the parotid glands (PGs) of albino rats histologically and ultrastructurally and assess the possible protective effect of ascorbic acid as an antioxidant. Thirty male albino rats weighing between 150 mg and 200 mg were divided into three groups: the control group (C1) contained 10 rats that received 2 mg/kg (body weight (bw)) of aqueous nitrate buffer by intraperitoneal (IP) injection daily for 28 days; the AgNPs group contained 10 rats that received 2 mg/kg (bw) IP AgNPs daily for 28 days; and the AgNPs-vitamin C group contained 10 albino rats that received 2 mg/kg (bw) AgNPs IP daily for 28 days with oral administration of 100 mg/kg (bw) vitamin C in drinking water daily for 28 days. The PG acinar and ductal cells of the AgNPs group showed signs of toxicity and degeneration characterized as pleomorphic nuclei, binucleation, cytoplasmic vacuolations, and stagnated secretion in the ductal lumen. In addition to degenerated mitochondria, dilated rough endoplasmic reticulum and lysosomes were filled with AgNPs ( p < 0.001). The AgNPs-vitamin C group showed significantly less degenerative changes histologically and ultrastructurally compared to the AgNPs group ( p = 0.002). AgNPs produced significant toxic effects on the PG of albino rats, presumably through the generation of reactive oxygen species and toxic ion release, and administration of vitamin C was shown effective in decreasing these toxic effects.

scholarly journals Inflammatory Cytokines and Comorbidity Development in Breast Cancer Survivors Versus Noncancer Controls: Evidence for Accelerated Aging?

2017 ◽  
Vol 35 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Catherine M. Alfano ◽  
Juan Peng ◽  
Rebecca R. Andridge ◽  
Monica E. Lindgren ◽  
Stephen P. Povoski ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Survivors ◽  
Cancer Treatment ◽  
Breast Cancer Survivors ◽  
Accelerated Aging ◽  
Premature Mortality ◽  
Control Group ◽  
Factor Α ◽  
Necrosis Factor ◽  
Over Time

Purpose The sequelae of cancer treatment may increase systemic inflammation and create a phenotype at increased risk of functional decline and comorbidities, leading to premature mortality. Little is known about how this trajectory compares with natural aging among peers of the same age without cancer. This longitudinal study investigated proinflammatory cytokines and comorbidity development over time among breast cancer survivors and a noncancer control group. Methods Women (N = 315; 209 with breast cancer and 106 in the control group) were recruited at the time of their work-up for breast cancer; they completed the baseline questionnaire, interview, and blood draw (lipopolysaccharide-stimulated production of interleukin [IL] -6, tumor necrosis factor-α, and IL-1β). Measures were repeated 6 and 18 months after primary cancer treatment (cancer survivors) or within a comparable time frame (control group). Results There were no baseline differences in comorbidities or cytokines between survivors and the control group. Over time, breast cancer survivors had significantly higher tumor necrosis factor-α and IL-6 compared with the control group. Survivors treated with surgery, radiation, and chemotherapy accumulated a significantly greater burden of comorbid conditions and suffered greater pain associated with inflammation over time after cancer treatment than did the control group. Conclusion Survivors who had multimodal treatment had higher cytokines and comorbidities, suggestive of accelerated aging. Comorbidities were related to inflammation in this sample, which could increase the likelihood of premature mortality. Given that many comorbidities take years to develop, future research with extended follow-up beyond 18 months is necessary to examine the evidence of accelerated aging in cancer survivors and to determine the responsible mechanisms.

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