scholarly journals Antioxidant and Anti-Inflammatory Effects of Nano-Selenium against Cypermethrin-Induced Liver Toxicity

CellBio ◽  
2019 ◽  
Vol 08 (04) ◽  
pp. 53-65
Author(s):  
Rania H. Abdou ◽  
Noha Sayed
Keyword(s):  
Liver Toxicity ◽  
Anti Inflammatory

Protective role of protocatechuic acid in carbon tetrachloride-induced oxidative stress via modulation of proinflammatory cytokines levels in brain and liver of Wistar rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Anne A. Adeyanju ◽  
Folake O. Asejeje ◽  
Olorunfemi R. Molehin ◽  
Olatunde Owoeye ◽  
Esther O. Olatoye ◽  
...  
Keyword(s):  
Cholesterol Level ◽  
Protocatechuic Acid ◽  
Liver Toxicity ◽  
Total Cholesterol Level ◽  
Density Lipoprotein ◽  
Albino Rats ◽  
Antioxidant Enzyme Activities ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
The Brain

Abstract Objectives Protocatechuic acid (PCA) possesses numerous pharmacological activities, including antioxidative and anti-inflammatory activities. This study seeks to investigate its underlying mechanism of action in the liver and brain toxicity induced by CCl4 in male albino rats. Methods Rats were given PCA at 10 and 20 mg/kg daily and orally as a pretreatment for seven days. A single injection of CCl4 was given 2 h later to induce brain and liver toxicity. Results CCl4 moderately elevated the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). PCA lowered AST level significantly when compared to control. Total protein and albumin levels presented insignificant changes (p>0.05) in all groups while lipid profile showed increased total cholesterol level and reduced high-density lipoprotein (HDL) by CCl4. PCA (10 mg/kg) significantly reduced the cholesterol level while the 20 mg/kg dose moderately prevented HDL reduction. There was an increased MDA production with a corresponding low GSH level in the group treated with CCl4. Activities of superoxide dismutase, catalase, and glutathione-S-transferase in both organs also declined. PCA, especially at 10 mg/kg attenuated lipid peroxidation by increasing GSH level in the organs. Biochemical assays revealed the improvement of antioxidant enzyme activities by PCA in these organs. Furthermore, PCA lowered the level of proinflammatory cytokine COX 2 in the brain and liver while NF-kB expression was inhibited in the brain. Histopathology reports validated the effects of PCA. Conclusions PCA exhibited protection against toxicity in these tissues through antioxidant and anti-inflammatory activities and the potential mechanism might be through modulation of the NF-κB/COX-2 pathway.

scholarly journals Antiseptic Effect of Ps-K18: Mechanism of Its Antibacterial and Anti-Inflammatory Activities

2019 ◽  
Vol 20 (19) ◽  
pp. 4895 ◽  
Author(s):  
Mihee Jang ◽  
Jieun Kim ◽  
Yujin Choi ◽  
JeongKyu Bang ◽  
Yangmee Kim
Keyword(s):  
Septic Shock ◽  
Antibacterial Activity ◽  
Bioactive Peptides ◽  
Liver Toxicity ◽  
Inflammatory Responses ◽  
Lung Damage ◽  
Peptide Antibiotic ◽  
Gram Negative ◽  
Innate Defense ◽  
Anti Inflammatory

Recently, bioactive peptides have attracted attention for their therapeutic applications in the pharmaceutical industry. Among them, antimicrobial peptides are candidates for new antibiotic drugs. Since pseudin-2 (Ps), isolated from the skin of the paradoxical frog Pseudis paradoxa, shows broad-spectrum antibacterial activity with high cytotoxicity, we previously designed Ps-K18 with a Lys substitution for Leu18 in Ps, which showed high antibacterial activity and low toxicity. Here, we examined the potency of Ps-K18, aiming to develop antibiotics derived from bioactive peptides for the treatment of Gram-negative sepsis. We first investigated the antibacterial mechanism of Ps-K18 based on confocal micrographs and field emission scanning electron microscopy, confirming that Ps-K18 targets the bacterial membrane. Anti-inflammatory mechanism of Ps-K18 was investigated by secreted alkaline phosphatase reporter gene assays and RT-PCR, which revealed that Ps-K18 activates innate defense via Toll-like receptor 4-mediated nuclear factor-kappa B signaling pathways. Moreover, we investigated the antiseptic effect of Ps-K18 using a lipopolysaccharide or Escherichia coli K1-induced septic shock mouse model. Ps-K18 significantly reduced bacterial growth and inflammatory responses in the septic shock model. Ps-K18 showed low renal and liver toxicity and attenuated lung damage effectively. This study suggests that Ps-K18 is a potent peptide antibiotic that could be applied therapeutically to Gram-negative sepsis.

scholarly journals The use of liver slices from the Cape vulture ( Gyps coprotheres ) to better understand the role of liver toxicity of non-steroidal anti-inflammatory drugs (NSAIDs) in vultures

2018 ◽  
Vol 62 ◽  
pp. 147-155 ◽  
Author(s):  
Emmanuel Oluwasegun Adawaren ◽  
Lilian Mukandiwa ◽  
Emmanuel Mfotie Njoya ◽  
Lizette Bekker ◽  
Neil Duncan ◽  
...  
Keyword(s):  
Liver Toxicity ◽  
Liver Slices ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Galectin-1 exhibits a protective effect against hepatotoxicity induced by dextran sulfate sodium in mice

2019 ◽  
Vol 39 (4) ◽  
pp. 423-432
Author(s):  
P Arda-Pirincci ◽  
O Sacan ◽  
C Ozal-Coskun ◽  
G Aykol-Celik ◽  
O Karabulut-Bulan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Antioxidant System ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Liver Toxicity ◽  
Interleukin 10 ◽  
Control Group ◽  
Protective Agent ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Galectin-1 is an important mediator that regulates the T-cell-mediated immune response. It has many other biological functions such as cell growth, immunomodulation, and wound healing. The aim of this study was to reveal the role of galectin-1 on liver morphology, cell proliferation, apoptosis, inflammatory and anti-inflammatory mediators, oxidative stress, and antioxidant system in colitis-mediated hepatotoxicity induced by dextran sulfate sodium (DSS). In the present study, adult mice were divided into four groups: The control group intraperitoneally injected with phosphate buffer saline (I), the group which was orally administered with DSS (II), the control group which was injected with galectin-1 (III), and the group which was given DSS and galectin-1 (IV). DSS administration caused degenerative changes and diffuse necrotic damage, an increase in caspase-3 and cyclooxygenase-2 expression, the levels of lipid peroxidation and tumor necrosis factor-alpha, lactate dehydrogenase, and myeloperoxidase activities, and a decrease in cell proliferation, interleukin-10 levels, and antioxidant system parameters in liver tissues. Treatment of DSS group with galectin-1 reversed these effects and prevented liver damage. This study showed that galectin-1 has proliferative, antiapoptotic, anti-inflammatory, and antioxidant effects against DSS-induced liver injury in mice. It is expected considering all results of this study that galectin-1 may be useful as a protective agent against liver toxicity.

scholarly journals Myristica fragrans Kernels Prevent Paracetamol-Induced Hepatotoxicity by Inducing Anti-Apoptotic Genes and Nrf2/HO-1 Pathway

2019 ◽  
Vol 20 (4) ◽  
pp. 993 ◽  
Author(s):  
Mohamed Dkhil ◽  
Ahmed Abdel Moneim ◽  
Taghreed Hafez ◽  
Murad Mubaraki ◽  
Walid Mohamed ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cytochrome P450 ◽  
Oral Administration ◽  
Liver Toxicity ◽  
B Cell Lymphoma ◽  
Hepatoprotective Effect ◽  
Nuclear Factor ◽  
Myristica Fragrans ◽  
Apoptotic Genes ◽  
Anti Inflammatory

Paracetamol is responsible for acute liver failure in humans and experimental animals when taken at high doses and transformed into a reactive metabolite by the liver cytochrome P450. On the other hand, nutmeg is rich with many phytochemical ingredients that are known for their ability to inhibit cytochrome P450. Hence, the present experiment was aimed at studying the hepatoprotective effect of Myristica fragrans (nutmeg), kernel extract (MFKE) in respect to paracetamol (acetaminophen; N-acetyl-p-amino-phenol (APAP))-induced hepatotoxicity in rats, focusing on its antioxidant, anti-inflammatory, and anti-apoptotic activities. Liver toxicity was induced in rats by a single oral administration of APAP (2 g/kg). To evaluate the hepatoprotective effect of MFKE against this APAP-induced hepatotoxicity, rats were pre-treated with either oral administration of MFKE at 300 mg/kg daily for seven days or silymarin at 50 mg/kg as a standard hepatoprotective agent. APAP intoxication caused a drastic elevation in liver function markers (transaminases, alkaline phosphatase, and total bilirubin), oxidative stress indicators (lipid peroxidation and nitric oxide), inflammatory biomarkers (tumour necrosis factor-α, interleukin-1β, inducible nitric oxide synthase, and nuclear factor ĸB) and the pro-apoptotic BCL2 Associated X (Bax) and caspases-3 genes. Furthermore, analyses of rat liver tissue revealed that APAP significantly depleted glutathione and inhibited the activities of antioxidant enzymes in addition to downregulating two key anti-apoptotic genes: Cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein (c-FLIP) and B-cell lymphoma 2 (Bcl-2). Pre-treatment with MFKE, however, attenuated APAP-induced liver toxicity by reversing all of these toxicity biomarkers. This hepatoprotective effect of MFKE was further confirmed by improvement in histopathological findings. Interestingly, the hepatoprotective effect of MFKE was comparable to that offered by the reference hepatoprotector, silymarin. In conclusion, our results revealed that MFKE had antioxidant, anti-inflammatory, and anti-apoptotic properties, and it is suggested that this hepatoprotective effect could be linked to its ability to promote the nuclear factor erythroid 2–related factor 2 (Nrf2)/antioxidant responsive element (ARE) pathway.

Synthesis, Molecular Docking, biological potentials, and Structure-Activity Relationship of new quinazoline & quinazoline-4-one derivatives

2021 ◽  
Vol 22 ◽  
Author(s):  
Rita M. Borik ◽  
Mohammed Abdalla Abdalla
Keyword(s):  
Molecular Docking ◽  
Active Sites ◽  
Liver Toxicity ◽  
Hepatoprotective Activity ◽  
Albino Rats ◽  
Oxidative Stress Biomarkers ◽  
Radical Method ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Peritoneal Macrophage Cells

Context: Quinazolines are a common class of nitrogen-containing heterocyclic scaffolds exhibiting a broad spectrum of pharmacological activities. Objective: In the present study, quinazoline and quinazolin-4-one derivatives were prepared, characterized to evaluate their biological which may pave the way for possible therapeutic applications. Materials amp; Methods: A new derivative of quinazoline and quinazolin-4-one derivatives was prepared and tested for antiulcerogenic, anti-inflammatory and hepatoprotective activity. Results: The synthesized compounds were characterized by elemental analysis and spectral data. Also, the median lethal doses (LD50s) of compounds 1-3 in rats were 1125, 835 and 1785 mg/kg b.w., respectively. IC50 values of compounds (1-3) as measured by ABTS+ radical method was 0.8, 0.92 and 0.08 mg/mL, respectively. Antiulcerogenic activities at dose 1/20 LD50 in albino rats were 47.94, 24.60 and 56.45%, respectively. Anti-inflammatory effect at dose 1/20 LD50 of compounds (1-3) induced edema model after 120 min. The prepared compounds possess hepato gastric mucosa protective activity against ibuprofen-induced ulceration and LPS-induced liver toxicity, respectively in rats via normalization of oxidative stress biomarkers and inflammatory mediators were inhibited in peritoneal macrophage cells at concentration of 100 µg/L. Molecular docking suggested that the most active compounds 1 and 2 can be positioned within the active sites of COX-2 at Arg121 & Tyr356 similar to ibuprofen (Arg-120, Glu-524, and Tyr-355). The compound 3–COX-2 complex generated by docking revealed intricate interactions with a COX-2 channel. Conclusion: These findings suggest that compounds 1-3 exhibited good antioxidant, antiulcer, anti-inflammatory activity and safe on liver enzymes in rats.

Anti‐inflammatory and antioxidant effects of Apium graveolens L. extracts mitigate against fatal acetaminophen‐induced acute liver toxicity

2020 ◽  
Vol 44 (10) ◽  
Author(s):  
Ayat M. Emad ◽  
Sherifa F. Ali ◽  
Engy A. Abdel‐Rahman ◽  
Meselhy R. Meselhy ◽  
Mohamed A. Farag ◽  
...  
Keyword(s):  
Liver Toxicity ◽  
Apium Graveolens ◽  
Anti Inflammatory ◽  
Antioxidant Effects

scholarly journals Dipeptide YA is Responsible for the Positive Effect of Oyster Hydrolysates on Alcohol Metabolism in Single Ethanol Binge Rodent Models

Marine Drugs ◽  
2020 ◽  
Vol 18 (10) ◽  
pp. 512
Author(s):  
Adrian S. Siregar ◽  
Marie Merci Nyiramana ◽  
Eun-Jin Kim ◽  
Eui-Jung Shin ◽  
Min Seok Woo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Inflammatory Mediators ◽  
Liver Toxicity ◽  
High Dose ◽  
Alcohol Metabolism ◽  
Single High Dose ◽  
Anti Inflammatory

Accumulative alcohol hangovers cause liver damage through oxidative and inflammatory stress. Numerous antioxidant and anti-inflammatory reagents have been developed to reduce alcohol hangovers, but these reagents are still insignificant and have limitations in that they can cause liver toxicity. Oyster hydrolysate (OH), another reagent that has antioxidant and anti-inflammatory activity, is a product extracted through an enzymatic hydrolysis process from oysters (Crassostrea gigas), which can be easily eaten in meals. This study was aimed at determining the effects of OH on alcohol metabolism, using a single high dose of ethanol (EtOH) administered to rodents, by monitoring alcohol metabolic enzymes, oxidative stress signals, and inflammatory mediators. The effect of tyrosine-alanine (YA) peptide, a main component of OH, on EtOH metabolism was also identified. In vitro experiments showed that OH pretreatment inhibited EtOH-induced cell death, oxidative stress, and inflammation in liver cells and macrophages. In vivo experiments showed that OH and YA pre-administration increased alcohol dehydrogenase, aldehyde dehydrogenase, and catalase activity in EtOH binge treatment. In addition, OH pre-administration alleviated CYP2E1 activity, ROS production, apoptotic signals, and inflammatory mediators in liver tissues. These results showed that OH and YA enhanced EtOH metabolism and had a protective effect against acute alcohol liver damage. Our findings offer new insights into a single high dose of EtOH drinking and suggest that OH and YA could be used as potential marine functional foods to prevent acute alcohol-induced liver damage.

scholarly journals Hepatoprotective influence of quercetin and ellagic acid on thioacetamide-induced hepatotoxicity in rats

2018 ◽  
Vol 96 (6) ◽  
pp. 624-629 ◽  
Author(s):  
Nehal A. Afifi ◽  
Marwa A. Ibrahim ◽  
Mona K. Galal
Keyword(s):  
Ellagic Acid ◽  
Liver Toxicity ◽  
Underlying Mechanism ◽  
Redox Status ◽  
Expression Level ◽  
Male Rats ◽  
Reference Drug ◽  
Liver Injuries ◽  
Anti Inflammatory ◽  
New Treatment

Despite all the studies performed to date, therapy choices for liver injuries are very few. Therefore, the search for a new treatment that could safely and effectively block or reverse liver injuries remains a challenge. Quercetin (QR) and ellagic acid (EA) had potent antioxidant and anti-inflammatory activities. The current study aimed at evaluating the potential hepatoprotective influence of QR and EA against thioacetamide (TAA)-induced liver toxicity in rats and the underlying mechanism using silymarin as a reference drug. Fifty mature male rats were orally treated daily with EA and QR in separate groups for 45 consecutive days, and then were injected with TAA twice with 24 h intervals in the last 2 days of the experiment. Administration of TAA resulted in marked elevation of liver indices, alteration in oxidative stress parameters, and significant elevation in expression level of fibrosis-related genes (MMP9 and MMP2). Administration of QR and EA significantly attenuated the hepatic toxicity through reduction of liver biomarkers, improving the redox status of the tissue, as well as hampering the expression level of fibrosis-related genes. In this study, QR and EA were proved to attenuate the hepatotoxicity through their antioxidant, metal-chelating capacity, and anti-inflammatory effects.

Antioxidant and anti-inflammatory properties of alpha lipoic acid protect against valproic acid induced liver injury

2020 ◽  
Author(s):  
Marwa Abdeltawab Mohammed ◽  
Doaa Mostafa Gharib ◽  
Hoda Ramadan Reyad ◽  
Alaa Aboud Mohamed ◽  
Fadwa A Elroby ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Adverse Effects ◽  
Lipoic Acid ◽  
Liver Toxicity ◽  
Male Rats ◽  
Control Group ◽  
Alpha Lipoic Acid ◽  
Group 4 ◽  
Anti Inflammatory ◽  
Group 2

Valproic acid (VPA) is one of the most used anti-epileptic drugs inspite of its many adverse effects as anemia, leucopenia, thrombocytopenia, and liver toxicity. The hepatoprotective effect of alpha-lipoic acid (ALA) was confirmed. Aim of the study: The aim of this study was to detect the protective effect of ALA against the adverse effects of VPA. Materials& Methods: Thirty white albino Wistar male rats were divided into 4 groups. Group (1) was the control group; Group (2) included rats that received ALA (100mg/kg/day) orally for 14 days; Group (3) and Group (4) included rats that received VPA (500 mg/kg/day) for 15 days intraperitoneal, but group 4 rats received ALA (100mg/kg/day) orally for 14 days prior to VPA. Blood samples were collected and livers were excised from rats for colorimetric analysis and rt-PCR. Results: Rats that received VPA showed leucopenia, thrombocytopenia, a significant decrease of SOD, glutathione, Nrf2, and Sirt1, besides a significant increase of MDA and TNF alpha. Prior treatment with ALA prevented all these results. Conclusion: ALA protected against VPA-induced liver damage and hematological disturbance via anti-oxidant and anti-inflammatory properties.

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