scholarly journals Ameliorative Effect of Beta vulgaris Root Extract on Chlorpyrifos-Induced Oxidative Stress, Inflammation and Liver Injury in Rats

Biomolecules ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. 261 ◽  
Author(s):  
Gadah Albasher ◽  
Rafa Almeer ◽  
Fatimah O. Al-Otibi ◽  
Noorah Al-Kubaisi ◽  
Ayman M. Mahmoud
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Liver Injury ◽  
Inflammatory Cytokines ◽  
Elevated Serum ◽  
Serum Levels ◽  
Antioxidant Defenses ◽  
Root Extract ◽  
Histological Alterations ◽  
Pro Inflammatory Cytokines

Exposure to organophosphorus insecticides causes several health problems to animals and humans. Red beetroot (RBR) is rich in antioxidant ingredients and possesses a promising hepatoprotective activity. This study evaluated the potential of RBR extract to prevent chlorpyrifos (CPF)-induced liver injury, with an emphasis on oxidative stress, inflammation and apoptosis. Rats received 10 mg/kg CPF and were treated with 300 mg/kg RBR extract for 28 days. CPF caused liver injury evidenced by elevated serum levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and bilirubin, along with several histological alterations. Hepatic lipid peroxidation (LPO) and nitric oxide (NO) levels, as well as inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines were increased in CPF-intoxicated rats. RBR prevented CPF-induced histological alterations, and ameliorated liver function, LPO, NO, iNOS and pro-inflammatory cytokines. RBR boosted glutathione and antioxidant enzymes, and increased Nrf2 expression. In addition, RBR diminished Bax and caspase-3, and increased Bcl-2 expression. In conclusion, RBR prevented CPF-induced liver injury via attenuation of oxidative stress, inflammation and apoptosis. RBR enhanced antioxidant defenses, suggesting that it could be used as a potential therapeutic intervention to minimize CPF hepatotoxicity.

scholarly journals Arctium lappa Root Extract Prevents Lead-Induced Liver Injury by Attenuating Oxidative Stress and Inflammation, and Activating Akt/GSK-3β Signaling

Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 582
Author(s):  
Ahlam Alhusaini ◽  
Laila Fadda ◽  
Iman H. Hasan ◽  
Hanaa M. Ali ◽  
Naglaa F. El Orabi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Dna Fragmentation ◽  
Caspase 3 ◽  
Glycogen Synthase ◽  
Elevated Serum ◽  
Antioxidant Defenses ◽  
Root Extract ◽  
Arctium Lappa ◽  
Gsk 3Β

Arctium lappa L. (A. lappa) is a popular medicinal plant with promising hepatoprotective activity. This study investigated the protective effect of A. lappa root extract (ALRE) on lead (Pb) hepatotoxicity, pointing to its ability to modulate oxidative stress, inflammation, and protein kinase B/Akt/glycogen synthase kinase (GSK)-3β signaling. Rats received 50 mg/kg lead acetate (Pb(Ac)2) and 200 mg/kg ALRE or vitamin C (Vit. C) for 7 days, and blood and liver samples were collected. Pb(Ac)2 provoked hepatotoxicity manifested by elevated serum transaminases and lactate dehydrogenase, and decreased total protein. Histopathological alterations, including distorted lobular hepatic architecture, microsteatotic changes, congestion, and massive necrosis were observed in Pb(II)-induced rats. ALRE ameliorated liver function and prevented all histological alterations. Pb(II) increased hepatic lipid peroxidation (LPO), nitric oxide (NO), caspase-3, and DNA fragmentation, and serum C-reactive protein, tumor necrosis factor-α, and interleukin-1β. Cellular antioxidants, and Akt and GSK-3β phosphorylation levels were decreased in the liver of Pb(II)-induced rats. ALRE ameliorated LPO, NO, caspase-3, DNA fragmentation and inflammatory mediators, and boosted antioxidant defenses in Pb(II)-induced rats. In addition, ALRE activated Akt and inhibited GSK-3β in the liver of Pb(II)-induced rats. In conclusion, ALRE inhibits liver injury in Pb(II)-intoxicated rats by attenuating oxidative injury and inflammation, and activation of Akt/GSK-3β signaling pathway.

Essential Oils Downregulate Pro-Inflammatory Cytokines and Nitric Oxide-mediated Oxidative Stress in Alloxan-induced Diabetogenic Rats.

2020 ◽  
Vol 20 ◽  
Author(s):  
Muhammad Ejaz ul Haq ◽  
Muhammad Sajid Hamid Akash ◽  
Kanwal Rehman ◽  
Malik Hassan Mahmood
Keyword(s):  
Nitric Oxide ◽  
Essential Oils ◽  
Inflammatory Cytokines ◽  
Diabetic Complications ◽  
Nitrosative Stress ◽  
Serum Levels ◽  
Control Group ◽  
Therapeutic Effects ◽  
Peripheral Tissues ◽  
Pro Inflammatory Cytokines

Introduction: Hyperglycemia is associated with elevated level of reactive nitrogen species (RNS) that leads to nitrosative stress and exacerbates progression of diabetic complications. Method: Present study was aimed to evaluate therapeutic effects of essential oils (EOs) on increased serum level of nitric oxide (NO) in diabetogenic rats. Diabetogenic rats were treated with EOs separately and/or in combination at the dose of 100 mg/kg, orally for one month. Blood sampling was done at 1st, 15th and 30th day of treatment period to investigate the effect of treatment on biomarkers of diabetic complications. Results: In diabetogenic rats, serum levels of NO, malondialdehyde (MDA) and pro-inflammatory cytokines were significantly increased when compared with that of control group. Whereas, diabetogenic rats treated with EOs decreased serum levels of NO, MDA and pro-inflammatory cytokines up to significant extent when compared with that diabetogenic rats treated with standard antidiabetic drug. Moreover, EOs also increased insulin sensitivity in peripheral tissues and insulin secretion from β-cells of pancreatic islets more efficiently when compared with that of diabetogenic rats. Additionally, it was also found that EOs improved lipid profile and normal functions of kidney and liver as compared to that of diabetogenic rats. Conclusion: Findings of this study indicate that EOs may reduce pro-inflammatory cytokine level by modulating the expression of NO. EOs may also ameliorate the nitrosative stress and maintain glucose homeostasis that are major culprits of diabetic complications.

Inducible nitric oxide synthase (iNOS) mediates ethanol-induced redox imbalance and up-regulation of inflammatory cytokines in the kidney

2021 ◽  
Author(s):  
Carla Brigagão Pacheco da Silva ◽  
Carla Speroni Ceron ◽  
Atlante Mendes ◽  
Bruno De Martinis ◽  
Michele Mazzaron de Castro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inflammatory Cytokines ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Ethanol Consumption ◽  
Tnf Α ◽  
Oxide Synthase ◽  
Deficient Mice

Overexpression of the inducible isoform of the enzyme nitric oxide synthase (iNOS) has been associated to pathological processes in the kidney. Ethanol consumption induces the renal expression of iNOS. However, the contribution of this enzyme to the deleterious effects of ethanol in the kidney remains elusive. We examined whether iNOS plays a role in the renal dysfunction and oxidative stress induced by ethanol consumption. With this purpose, male C57BL/6 wild-type (WT) or iNOS-deficient (iNOS-/-) mice were treated with ethanol (20% v/v) for 10 weeks. Treatment with ethanol increased the expression of Nox4 as well as the concentration of thiobarbituric acid reactive substances (TBARS) and the levels of tumor necrosis factor (TNF)-α in the renal cortex of WT, but not iNOS-deficient mice. Augmented serum levels of creatinine and increased systolic blood pressure were found in WT and iNOS-deficient mice treated with ethanol. WT mice treated with ethanol showed increased production of reactive oxygen species (ROS) and myeloperoxidase (MPO) activity, but these responses were attenuated in iNOS-deficient mice. We concluded that iNOS played a role in ethanol-induced oxidative stress and pro-inflammatory cytokines production in the kidney. These are mechanisms that may contribute to the renal toxicity induced by ethanol.

scholarly journals The Antioxidant and Anti-Inflammatory Properties of Rice Bran Phenolic Extracts

Foods ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 829 ◽  
Author(s):  
Nancy Saji ◽  
Nidhish Francis ◽  
Lachlan J. Schwarz ◽  
Christopher L. Blanchard ◽  
Abishek B. Santhakumar
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Inflammatory Cytokines ◽  
Rice Bran ◽  
Intracellular Reactive Oxygen Species ◽  
Oxygen Species ◽  
Ifn Γ ◽  
Pro Inflammatory Cytokines ◽  
Phenolic Extracts

Oxidative stress and inflammation are known to be linked to the development of chronic inflammatory conditions, such as type 2 diabetes and cardiovascular disease. Dietary polyphenols have been demonstrated to contain potent bioactivity against specific inflammatory pathways. Rice bran (RB), a by-product generated during the rice milling process, is normally used in animal feed or discarded due to its rancidity. However, RB is known to be abundant in bioactive polyphenols including phenolic acids. This study investigates the antioxidant and anti-inflammatory effects of RB phenolic extracts (25, 50, 100, and 250 µg/mL) on RAW264.7 mouse macrophage cells stimulated with hydrogen peroxide and lipopolysaccharide. Biomarkers of oxidative stress and inflammation such as malondialdehyde (MDA), intracellular reactive oxygen species, nitric oxide and pro-inflammatory cytokines such as interleukin-6 (IL-6), monocyte chemoattractant protein 1 (MCP-1), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), interleukin-12, p70 (IL-12p70), and interferon-γ (IFN-γ) were measured in vitro. Treatment with RB extracts significantly decreased the production of MDA, intracellular reactive oxygen species, nitric oxide and pro-inflammatory cytokines (IL-6, IL-12p70, and IFN-γ) when compared to the control. It is proposed that RB phenolic extracts, via their metal chelating properties and free radical scavenging activity, target pathways of oxidative stress and inflammation resulting in the alleviation of vascular inflammatory mediators.

scholarly journals Allopurinol ameliorates liver injury in type 1 diabetic rats through activating Nrf2

2021 ◽  
Vol 35 ◽  
pp. 205873842110314
Author(s):  
Fei Zeng ◽  
Jierong Luo ◽  
Hong Han ◽  
Wenjie Xie ◽  
Lingzhi Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Caspase 3 ◽  
Serum Levels ◽  
Diabetic Rats ◽  
Heme Oxygenase 1 ◽  
Liver Protein ◽  
Lipid Peroxidation Product ◽  
Protein Expressions

Hyperglycemia-induced oxidative stress plays important roles in the development of non-alcoholic fatty liver disease (NAFLD), which is a common complication in diabetic patients. The Nrf2-Keap1 pathway is important for cell antioxidant protection, while its role in exogenous antioxidant mediated protection against NAFLD is unclear. We thus, postulated that antioxidant treatment with allopurinol (ALP) may attenuate diabetic liver injury and explored the underlying mechanisms. Control (C) and streptozotocin (STZ)-induced diabetes rats (D) were untreated or treated with ALP for 4 weeks starting at 1 week after diabetes induction. Serum levels of alanine aminotransferase (ALT) and aspartate transaminase (AST), production of lipid peroxidation product malondialdehyde (MDA), and serum superoxide dismutase (SOD) were detected. Liver protein expressions of cleaved-caspase 3, IL-1β, nuclear factor-erythroid-2-related factor-2 (Nrf2), heme oxygenase-1 (HO-1), P62, Kelch-like ECH-associated protein 1 (Keap1), and LC3 were analyzed. In vitro, cultured rat normal hepatocytes BRL-3A were grouped to normal glucose (5.5 mM, NG) or high glucose (25 mM, HG) and treated with or without allopurinol (100 µM) for 48 h. Rats in the D group demonstrated liver injury evidenced as increased serum levels of ALT and AST. Diabetes increased apoptotic cell death, enhanced liver protein expressions of cleaved-caspase 3 and IL-1β with concomitantly increased production of MDA while serum SOD content was significantly reduced (all P < 0.05 vs C). In the meantime, protein levels of Nrf2, HO-1, and P62 were reduced while Keap1 and LC3 were increased in the untreated D group as compared to control ( P < 0.05 vs C). And all the above alterations were significantly attenuated by ALP. Similar to our findings obtained from in vivo study, we got the same results in in vitro experiments. It is concluded that ALP activates the Nrf2/p62 pathway to ameliorate oxidative stress and liver injury in diabetic rats.

Acute Ischemic Stroke is Associated with Increased Serum Levels of Pro-inflammatory Cytokines

2020 ◽  
Author(s):  
Bhagirath Ramawat ◽  
Alvee Saluja ◽  
Jayashree Bhatacharjee ◽  
Anshuman Srivastava ◽  
Rajinder K. Dhamija
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Inflammatory Cytokines ◽  
Serum Levels ◽  
Pro Inflammatory Cytokines
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