scholarly journals Amelioration of Hepatic Encephalopathy Using Dunaliella salina Microalgae in Rats: Modulation of Hyperammonemia/TLR4

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Farouk K. El-Baz ◽  
Rania Elgohary ◽  
Abeer Salama
Keyword(s):  
Oxidative Stress ◽  
Hepatic Encephalopathy ◽  
Dunaliella Salina ◽  
Inflammatory Mediator ◽  
Therapeutic Potential ◽  
Behavioral Changes ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Chronic Liver Failure ◽  
Nuclear Pyknosis

Hepatic encephalopathy (HE) is a neuropsychiatric disease that is developed as a complication of both acute and chronic liver failure affecting psychomotor dysfunction, memory, and concentration. This study is aimed at evaluating the therapeutic effects of Dunaliella salina (D. salina) microalgae in thioacetamide- (TAA-) induced HE in rats. HE was induced by TAA (200 mg/kg; i.p.) for three successive days. Forty male Wister albino rats were divided into 4 groups; the first group was served as a normal, and the second group was injected with TAA and served as TAA control. The third and fourth groups were administered D. salina (100 and 200 mg/kg; p.o.), respectively, after TAA injection for 7 days. The behavioral and biochemical markers as well as histological aspects of HE were estimated. This study revealed that TAA caused behavioral changes, oxidative stress, neuroinflammation, nuclear pyknosis, and neurons degeneration. D. salina improved liver function and decreased oxidative stress and inflammatory mediator as TLR4 protein expression. Also, D. salina elevated HSP-25 and IGF-1 as well as improved brain histopathological alterations. In conclusion, D. salina exerted a therapeutic potential against HE via its antioxidant, antiinflammatory and cytoprotective effects.

scholarly journals N-Acetyl Cysteine Targets Hepatic Lipid Accumulation to Curb Oxidative Stress and Inflammation in NAFLD: A Comprehensive Analysis of the Literature

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1283
Author(s):  
Phiwayinkosi V. Dludla ◽  
Bongani B. Nkambule ◽  
Sithandiwe E. Mazibuko-Mbeje ◽  
Tawanda M. Nyambuya ◽  
Fabio Marcheggiani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Accumulation ◽  
Randomized Clinical Trials ◽  
Therapeutic Potential ◽  
Therapeutic Effects ◽  
Metabolic Complications ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Acetyl Cysteine

Impaired adipose tissue function and insulin resistance remain instrumental in promoting hepatic lipid accumulation in conditions of metabolic syndrome. In fact, enhanced lipid accumulation together with oxidative stress and an abnormal inflammatory response underpin the development and severity of non-alcoholic fatty liver disease (NAFLD). There are currently no specific protective drugs against NAFLD, and effective interventions involving regular exercise and healthy diets have proved difficult to achieve and maintain. Alternatively, due to its antioxidant and anti-inflammatory properties, there has been growing interest in understanding the therapeutic effects of N-acetyl cysteine (NAC) against metabolic complications, including NAFLD. Here, reviewed evidence suggests that NAC blocks hepatic lipid accumulation in preclinical models of NAFLD. This is in part through the effective regulation of a fatty acid scavenger molecule (CD36) and transcriptional factors such as sterol regulatory element-binding protein (SREBP)-1c/-2 and peroxisome proliferator-activated receptor gamma (PPARγ). Importantly, NAC appears effective in improving liver function by reducing pro-inflammatory markers such as interleukin (IL)-6 IL-1β, tumour necrosis factor alpha (TNF-α) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). This was primarily through the attenuation of lipid peroxidation and enhancements in intracellular response antioxidants, particularly glutathione. Very few clinical studies support the beneficial effects of NAC against NAFLD-related complications, thus well-organized randomized clinical trials are still necessary to confirm its therapeutic potential.

scholarly journals What is a Therapeutic Potential of N-Acetylcysteine in Lung Silicosis?

2021 ◽  
Vol 21 (3) ◽  
pp. 80-89
Author(s):  
Adamcakova Jana ◽  
Mokra Daniela
Keyword(s):  
Oxidative Stress ◽  
Lung Injury ◽  
Silicon Dioxide ◽  
Pulmonary Disease ◽  
Therapeutic Potential ◽  
Therapeutic Effects ◽  
Clinical Use ◽  
Fundamental Factor ◽  
Long Term Experience

Abstract Lung silicosis is a serious pulmonary disease caused by an exposure of lung to inhaled silicon dioxide (SiO2) or silica. Although pathomechanisms of the disease have not been fully elucidated, oxidative stress has been recognized as a fundamental factor triggering a fibrotizing inflammation leading to irreversible changes in lung tissue. Based on this knowledge, therapeutic potential of various antioxidants has been intensively discussed. Among them, N-acetylcysteine with its multiple anti-inflammatory and antioxidant actions and a long-term experience with its clinical use in various diseases appears as a very promising choice. The purpose of this article is to review the therapeutic effects of N-acetylcysteine particularly in relation to a lung injury and to point out a potential of N-acetylcysteine in the treatment of lung silicosis.

Beneficial effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin in rats

2015 ◽  
Vol 35 (3) ◽  
pp. 276-281 ◽  
Author(s):  
H Elbe ◽  
Z Dogan ◽  
E Taslidere ◽  
A Cetin ◽  
Y Turkoz
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Histopathological Changes ◽  
Tubular Atrophy ◽  
Beneficial Effects ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

Ciprofloxacin is a broad-spectrum quinolone antibiotic commonly used in clinical practice. Quercetin is an antioxidant belongs to flavonoid group. It inhibits the production of superoxide anion. In this study, we aimed to evaluate the effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin. Twenty-eight female Wistar albino rats were divided into four groups: control, quercetin (20 mg kg−1 day−1 gavage for 21 days), ciprofloxacin (20 mg kg−1 twice a day intraperitoneally for 10 days), and ciprofloxacin + quercetin. Samples were processed for histological and biochemical evaluations. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), and catalase (CAT) activities were measured in kidney tissue. The ciprofloxacin group showed histopathological changes such as infiltration, dilatation in tubules, tubular atrophy, reduction of Bowman’s space, congestion, hemorrhage, and necrosis. In the ciprofloxacin + quercetin group, these histopathological changes markedly reduced. MDA levels increased in the ciprofloxacin group and decreased in the ciptofloxacin + quercetin group. SOD and CAT activities and GSH levels significantly decreased in the ciprofloxacin group. On the other hand, in the ciprofloxacin + quercetin group, SOD and CAT activities and GSH levels significantly increased with regard to the ciprofloxacin group. We concluded that quercetin has antioxidative and therapeutic effects on renal injury and oxidative stress caused by ciprofloxacin in rats.

scholarly journals Neuroprotective Effects of dl-3-n-Butylphthalide against Doxorubicin-Induced Neuroinflammation, Oxidative Stress, Endoplasmic Reticulum Stress, and Behavioral Changes

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Dehua Liao ◽  
Daxiong Xiang ◽  
Ruili Dang ◽  
Pengfei Xu ◽  
Jiemin Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Therapeutic Potential ◽  
Interleukin 1 ◽  
Behavioral Changes ◽  
Anxiety And Depression ◽  
Stress Markers ◽  
Neural Apoptosis

Doxorubicin (DOX) is a broad-spectrum antitumor drug while its use is limited due to its neurobiological side effects associated with depression. We investigated the neuroprotective efficacy of dl-3-n-butylphthalide (dl-NBP) against DOX-induced anxiety- and depression-like behaviors in rats. dl-NBP was given (30 mg/kg) daily by gavage over three weeks starting seven days before DOX administration. Elevated plus maze (EPM) test, forced swimming test (FST), and sucrose preference test (SPT) were performed to assess anxiety- and depression-like behaviors. Our study showed that the supplementation of dl-NBP significantly mitigated the behavioral changes induced by DOX. To further explore the mechanism of neuroprotection induced by dl-NBP, several biomarkers including oxidative stress markers, endoplasmic reticulum (ER) stress markers, and neuroinflammatory cytokines in the hippocampus were quantified. The results showed that dl-NBP treatment alleviated DOX-induced neural apoptosis. Meanwhile, DOX-induced oxidative stress and ER stress in the hippocampus were significantly ameliorated in dl-NBP pretreatment group. Our study found that dl-NBP alleviated the upregulation of malondialdehyde (MDA), nitric oxide (NO), CHOP, glucose-regulated protein 78 kD (GRP-78), and caspase-12 and increased the levels of reduced glutathione (GSH) and activities of catalase (CAT), glutathione reductase (GR), and glutathione peroxidase (GPx) in the hippocampus of rats exposed to DOX. Additionally, the gene expression of interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-alpha (TNF-α) and protein levels of inducible nitric oxide synthase (iNOS) were significantly increased in DOX-treated group, whereas DOX-induced neuroinflammation was significantly attenuated in dl-NBP supplementation group. In conclusion, dl-NBP could alleviate DOX-induced anxiety- and depression-like behaviors via attenuating oxidative stress, ER stress, inflammatory reaction, and neural apoptosis, providing a basis as a therapeutic potential against DOX-induced neurotoxicity.

Cadmium acts as a silent killer of liver by inducing oxidative stress and hepatocellular injury and a possible amelioration by vitamin B12 and folic acid in rat model

2019 ◽  
Vol 1 ◽  
pp. 105-117
Author(s):  
A. Banerjee ◽  
P. Nandi ◽  
C. Bhattacharya ◽  
Z. Kabir ◽  
S. Mukherjee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Rat Model ◽  
Male Rats ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Hepatocellular Injury ◽  
Male Adult ◽  
Wistar Albino Rats

<br/><b>Purpose:</b> To investigate the involvement of oxidative stress in Cadmium (Cd) induced alteration in the functional status of the liver. And to assess the efficacy of folic acid and vitamin B12 in preventing Cd-induced damage in the same. <br/><b>Materials and methods:</b> The experiment was carried out for four weeks. For the experiment, 25 healthy male adult Wistar albino rats were randomly selected and were divided into five equal groups and treated as control, treated with Cd, supplemented with vitamin B12 and folic acid and in the combination of these two. After 28 days the liver function enzymes and oxidative stress parameters were measured. <br/><b>Results:</b> Cd is the silent killer of the hepatic system through the induction of oxidative stress in male rats. From this investigation, it is evident that the folic acid+vitamin B12 possess significant hepatoprotective and antioxidant activity against Cd-induced hepatotoxicity in the rat model. In addition, results revealed that the folic acid alone and or in combination with vitamin B12 blunted the hepatotoxic effect significantly. <br/><b>Conclusions:</b> Based on results obtained, it can be concluded that folic acid and vitamin B12 offer a protective effect in Cd-induced oxidative stress associated with hepatocellular injury. Folic acid and vitamin B12 can be considered as a potent natural antioxidant which has the capacity to provide protection against Cd-induced oxidative stress in the liver in rats. However, to elucidate the exact mechanism of this modulatory effect and to examine its potential therapeutic effects further studies are essential.

scholarly journals Role of SIRT1 in Hepatic Encephalopathy: In Vivo and In Vitro Studies Focusing on the NLRP3 Inflammasome

2021 ◽  
Vol 2021 ◽  
pp. 1-23
Author(s):  
Fangzhou Jiao ◽  
Yao Wang ◽  
Qian Chen ◽  
Pan Cao ◽  
Chunxia Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Encephalopathy ◽  
Nlrp3 Inflammasome ◽  
Microglial Activation ◽  
Male Rats ◽  
Therapeutic Effects ◽  
Ht22 Cells ◽  
Brain Oxidative Stress

Hepatic encephalopathy (HE) is a neuropsychiatric disorder resulting from acute or chronic liver failure. This study is aimed at investigating the therapeutic effects and mechanisms of SIRT1 in thioacetamide- (TAA-) induced rat HE models. A selective activator (CAY10602) and inhibitor (EX527) of SIRT1 were used in this study. All male rats were separated into control, TAA, CAY10602+TAA, and EX527+TAA groups. Histological damage, liver function, serum ammonia, behavioral changes, and brain oxidative stress were measured in each group. Western blotting was used to measure SIRT1, NLRP3, ASC, and IL-1β protein expression. The results showed that CAY10602 alleviated liver injury, improved neurological decline, reduced microglial activation and brain oxidative stress, and improved the survival rates of HE rats. Moreover, CAY10602 inhibited activation of the NLRP3 inflammasome in microglia of the brain cortex in HE rats. Next, cell experiments confirmed that CAY10602 inhibited activation of the NLRP3 inflammasome in BV2 microglial cells. However, inhibition of SIRT1 by EX527 or lentivirus could enhance activation of the NLRP3 inflammasome in this process. Finally, CAY10602 reduced the neurotoxicity induced by high levels of ammonia in HT22 cells. Taken together, CAY10602 alleviates TAA-induced HE by suppressing microglial activation and the NLRP3 inflammasome and reducing the neurotoxicity of NH4Cl in HT22 cells. A pharmacologic activator of SIRT1 may be a promising approach for the treatment of HE.

scholarly journals Nrf2 activation as a future target of therapy for chronic diseases

2014 ◽  
Vol 4 (12) ◽  
pp. 510 ◽  
Author(s):  
Rame Taha ◽  
Gilbert Blaise
Keyword(s):  
Oxidative Stress ◽  
Chronic Diseases ◽  
Therapeutic Potential ◽  
Antioxidant Response ◽  
Premature Aging ◽  
Therapeutic Effects ◽  
Related Factor ◽  
Nrf2 Activation ◽  
Inflammatory Drugs ◽  
Therapeutic Alternatives

Background: Chronic inflammation integrally related to oxidative stress has been increasingly recognized as a contributing factor in various chronic diseases such as neurodegenerative diseases, pulmonary diseases, metabolic syndrome, and cardiovascular diseases as well as premature aging. Thus, inhibiting this vicious circle has the potential to delay, prevent progression, and treat those diseases. However, adverse effects of current anti-inflammatory drugs and the failure of exogenous antioxidant encourage scientists to develop new therapeutic alternatives. The nuclear factor E2-related factor 2 (Nrf2) is the transcription factor that is responsible for the expression of antioxidant response element (ARE)-regulated genes and have been described as having many therapeutic effects. In this review, we have discussed the role of oxidative stress in various chronic diseases. Furthermore, we have also explored various novel ways to activate Nrf2 either directly or indirectly, which may have therapeutic potential in attenuating oxidative stress, inflammation and mitochondrial dysfunction that contributes to chronic diseases.Keywords: Oxidative stress, Mitochondria, Inflammation, Nrf2, Nutrition, Chronic diseases

scholarly journals Behavioral and electroencephalographic manifestations of thioacetamide-induced encephalopathy: Possible mechanisms of neurotoxic effects

2012 ◽  
Vol 64 (3) ◽  
pp. 829-841 ◽  
Author(s):  
D. Mladenovic ◽  
D. Hrncic ◽  
A. Rasic-Markovic ◽  
Olivera Stanojlovic
Keyword(s):  
Oxidative Stress ◽  
Hepatic Encephalopathy ◽  
Liver Failure ◽  
Experimental Model ◽  
Alpha Power ◽  
Dependent Manner ◽  
Chronic Liver Failure ◽  
Toxic Metabolites ◽  
Neurotoxic Effects ◽  
Dose Dependent

Although there is still no ideal experimental model of hepatic encephalopathy, thioacetamide is widely used for the induction of acute and chronic liver failure. Thioacetamide exerts hepatotoxic effects through the formation of toxic metabolites in hepatocytes, oxidative stress and calcium mobilization. An ideal experimental model of hepatic encephalopathy should have similar behavioral and electroencephalographic manifestations as human encephalopathy. Thioacetamide induces motor manifestations in a dose-dependent manner. Milder forms of thioacetamide-induced encephalopathy are associated with an increase in relative alpha power, while more severe forms are followed by a flattening of the electroencephalogram. liver failure-induced hyperammonemia has a pivotal role in the neurotoxic effects of thioacetamide. Hyperammonemia induces brain edema, alterations in neurotransmission, oxidative stress, mitochondrial dysfunction and neuronal death. The aim of this article is to review the behavioral and electroencephalographic manifestations of thioacetamide-induced encephalopathy, as well as to summarize potential mechanisms involved in thioacetamide neurotoxicity.

scholarly journals The potential therapeutic effects of the gut microbiome manipulation by synbiotic containing-Lactobacillus plantarum on neuropsychological performance of diabetic rats

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Mohammad Morshedi ◽  
Maryam Saghafi-Asl ◽  
Elaheh-Sadat Hosseinifard
Keyword(s):  
Oxidative Stress ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Therapeutic Potential ◽  
Diabetic Rats ◽  
Therapeutic Effects ◽  
Microbial Composition ◽  
Stress Markers ◽  
Oxidative Stress Status ◽  
The Impact

Abstract Background The manipulation of gut microbiota as a target has been suggested to reduce the risks for a number of diseases such as type 2 diabetes mellitus (T2DM). Conversely, T2DM is associated with complications such as gut and brain disorders. Furthermore, the impact of probiotics and prebiotics to improve T2DM complications are reported. Thus, the present study seeks to investigate the therapeutic and neuropsychological effects of L. plantarum and inulin in diabetic rats. Methods Throughout the investigation, L. plantarum, inulin or their combination (synbiotic) was administered to diabetic rats. in the end, fecal samples were collected to evaluate the gut microbial composition. Then behavioral tests were conducted. Subsequently, the obtainment of the prefrontal cortex (PFC) and hippocampal samples. Results Our data demonstrated that administration of L. plantarum and inulin could improve gut dysbiosis and oxidative stress status. In addition, it could ameliorate serotonin and BDNF/TrkB signaling pathway. Notably, a strong correlation between the gut microbiota changes and cognition responses was observed. Interestingly, synbiotics intake exploited a rather powerful effect on oxidative stress markers. Conclusion The findings confirm that there is a beneficial therapeutic potential of supplements, especially symbiotic. Moreover, neuropsychological improvement associated with balanced gut microbiome.

scholarly journals Preliminary Investigation of the Antioxidant, Anti-Diabetic, and Anti-Inflammatory Activity of Enteromorpha intestinalis Extracts

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 1171
Author(s):  
Biswajita Pradhan ◽  
Srimanta Patra ◽  
Chhandashree Behera ◽  
Rabindra Nayak ◽  
Bimal Prasad Jit ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Denaturation ◽  
Therapeutic Potential ◽  
Preliminary Investigation ◽  
Total Phenolic ◽  
Therapeutic Effects ◽  
Enteromorpha Intestinalis ◽  
Ic50 Values ◽  
Anti Inflammatory ◽  
Promising Source

Marine algae are a promising source of potent bioactive agents against oxidative stress, diabetes, and inflammation. However, the possible therapeutic effects of many algal metabolites have not been exploited yet. In this regard, we explored the therapeutic potential of Enteromorpha intestinalis extracts obtained from methanol, ethanol, and hexane, in contrasting oxidative stress. The total phenolic (TPC) and flavonoids (TFC) content were quantified in all extracts, with ethanol yielding the best values (about 60 and 625 mg of gallic acid and rutin equivalents per gram of extract, respectively). Their antioxidant potential was also assessed through DPPH•, hydroxyl radical, hydrogen peroxide, and superoxide anion scavenging assays, showing a concentration-dependent activity which was greater in the extracts from protic and more polar solvents. The α-amylase and α-glucosidase activities were estimated for checking the antidiabetic capacity, with IC50 values of about 3.8 µg/mL for the methanolic extract, almost as low as those obtained with acarbose (about 2.8 and 3.3 µg/mL, respectively). The same extract also showed remarkable anti-inflammatory effect, as determined by hemolysis, protein denaturation, proteinase and lipoxygenase activity assays, with respectable IC50 values (about 11, 4, 6, and 5 µg/mL, respectively), also in comparison to commercially used drugs, such as acetylsalicylic acid.

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