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.

scholarly journals Protective effect of erdosteine against methotrexateinduced hepatotoxicity in rats

2020 ◽  
Vol 19 (7) ◽  
pp. 1465-1471
Author(s):  
Osama Abdelaziz Hassan ◽  
Entesar Farghally Amin ◽  
Rabab Ahmed Moussa
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Reduced Glutathione ◽  
Histopathological Examination ◽  
Immunohistochemical Analysis ◽  
Serum Levels ◽  
Hepatic Tissue ◽  
Control Group ◽  
Sprague Dawley ◽  
Tnf Α

Purpose: To study the possible mitigating effect of erdosteine (ERD) against methotrexate (MTX)-induced liver toxicity.Methods: Male albino Sprague-Dawley rats were randomly assigned to four groups of 8 rats each, viz, vehicle control, MTX (20 mg/kg i.p.), MTX (20 mg/kg i.p.) + ERD (300 mg/kg) and ERD (300 mg/kg) groups. Serum levels of alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were determined by enzymatic colorimetric commercial kits while Hepatic tissue content of malondialdehyde (MDA), reduced glutathione (GSH), SOD and catalase (CAT) were also evaluated. In addition, measurement of the inflammatory cytokine, TNF-α, as well as histopathological  examination and histochemical assessment were carried out.Results: The results indicate that, compared to the control group, MTX group showed a remarkable elevation in oxidative stress as indicated by significantly lower levels of SOD, CAT and reduced glutathione, and increased tissue malondialdehyde (p < 0.05). MTX group exhibited significantly higher blood activities of ALT, AST and TNF-α, reflective of hepatocyte damage and inflammation (p < 0.05). In MTX group, significant hepatic degenerative changes were detected on histological examination, while marked apoptotic alternations were observed following  immunohistochemical analysis of caspase-3 expression, when compared to control group. However, administration of ERD to rats ameliorated thechanges in these parameters (p < 0.05).Conclusion: Treatment with ERD in rats produced alleviation in hepatic oxidative stress, apoptosis, inflammation, and histological damage, when compared to MTX group. This study is the first to demonstrate the potentially protective effect of ERD-pretreatment against hepatotoxicity associated with MTX. Keywords: Erdosteine, Methotrexate, Hepatotoxicity, Oxidant, Anti-oxidant                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                            

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 The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

2019 ◽  
Author(s):  
Jie Guo ◽  
Xiaolu Cao ◽  
Xianmin Hu ◽  
Shulan Li ◽  
Jun Wang
Keyword(s):  
Oxidative Stress ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Tunel Staining ◽  
High Dose ◽  
Sprague Dawley ◽  
Curcumin Treatment ◽  
Concurrent Administration ◽  
Tnf Α ◽  
Anti Inflammatory

Abstract Background: As a chemical extensively used in industrial areas as well as formed during heating of carbohydrate-rich food and tobacco, acrylamide (ACR) has been known as well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats. Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in cerebral homogenates were detected using ELISA assay. Results: Concurrent administration of curcumin at the oral doses of 50 and 100 mg/kg with ACR significantly protected the rats from ACR-induced weigh loss and motor function deficits, and improved the pathological alterations in the ACR-intoxicated brains. Curcumin treatment especially at a high dose enhanced the TERT mRNA expression level and increased the number of TERT-positive nerve cells in cortex tissues of ACR intoxicated rats. The levels of MDA, TNF-α and IL-1β in the cerebral homogenates were reduced, the contents of GSH as well as the activities of SOD and GSH-Px were increased by curcumin treatment, compared to ACR control group. Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. And maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

scholarly journals TNF-alpha but not IL-1alpha are Correlated with PGE1-Dependent Protection Against Acute D-Galactosamine-Induced Liver Injury

2000 ◽  
Vol 14 (3) ◽  
pp. 175-180 ◽  
Author(s):  
J Muntané ◽  
JL Montero ◽  
JM Lozano ◽  
A Miranda-Vizuete ◽  
M de la Mata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Experimental Studies ◽  
Acute Hepatic Failure ◽  
Inflammatory Cells ◽  
Control Group ◽  
Prostaglandin E ◽  
Necrosis Factor Alpha ◽  
Tnf Α

BACKGROUND: Prostaglandin E1(PGE1) treatment of humans and rodents during acute hepatic failure ameliorates different parameters of hepatic dysfunction.PURPOSE: To investigate whether prevention of acute liver injury induced by D-galactosamine (D-GalN) with preadministration of PGE1is correlated with a change in the concentration of two proinflammatory cytokines, as tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-1α, and/or nitrite+nitrate (NOx), as nitric oxide-related end products in serum.RESULTS: D-GalN significantly increased alanine aminotransferase (ALT) and TNF- αconcentration in serum 5 and 10 mins, respectively, after treatment compared with the control group (P&#8804;0.05). D-GalN did not change the IL-1α concentration at any time during the study. Preadministration of PGE1to D-GalN-treated rats significantly reduced the ALT content and increased significantly the TNF-α concentration in serum 1, 2.5, 5 and 10 mins after D-GalN treatment compared with the D-GalN group (P&#8804;0.05). Nitric oxide was not involved in either the toxic effect due to D-GalN or the protection observed with PGE1against D-GalN toxicity.CONCLUSIONS: Acute liver injury induced by D-GalN is correlated with an increased TNF-α release. Preadministration of PGE1to D-GalN-treated rats exerted a priming effect on inflammatory cells to release enhanced levels of TNF-α but not IL-1α. These findings indicate that stimulation of TNF-α release may be involved in the acute D-GalN-induced liver injury and also in PGE1protection from hepatotoxicity in clinical and experimental studies.

scholarly journals Aloperine attenuates carbon tetrachloride-induced mouse hepatic injury via Nrf2/HO-1 pathway

2020 ◽  
Vol 19 (5) ◽  
pp. 983-988
Author(s):  
Rui Xiong ◽  
Shuzhong Shan ◽  
Xiaoming Wang ◽  
Xiaowen Zhang ◽  
Haixia Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Control Group ◽  
Histopathological Analysis ◽  
Dependent Manner ◽  
Oxidative Stress Biomarkers ◽  
Cox 2

Purpose: To investigate whether aloperine pretreatment ameliorates acute liver injury in carbon tetrachloride (CCl4)-treated mice.Methods: Mice were injected with CCl4 and orally administered aloperine. Blood samples and liver tissues were used for histopathological and biochemical analyses, respectively. Protein expression levels were determined by western blotting.Results: Histopathological analysis indicate that aloperine pretreatment significantly alleviated CCl4- induced mouse hepatic injury. CCl4 treatment induced the upregulation of aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine amino transferase (ALT), and total bilirubin (p < 0.05). However, these alterations were significantly inhibited by aloperine treatment. Moreover, aloperine pretreatment markedly decreased (p < 0.05) the CCl4-induced expression of oxidative stress biomarkers, including malondrialdeline (MDA), glutathione (GSH), catalase (CAT), and  superoxide dismutase (SOD). Compared to the control group, the protein levels of Nrf2, HO-1, iNOS, and COX-2 were significantly increased in the CCl4 group, while Nrf2 and HO-1 were upregulated. Furthermore, iNOS and COX-2 were downregulated in mouse liver in CCl4 + aloperine group compared to CCl4 group in a concentration-dependent manner (p < 0.05).Conclusion: Aloperine pretreatment appears to markedly upregulate Nrf2 and HO-1 and downregulate iNOS and COX-2 to suppress hepatic injury in mice. Thus, aloperine is a promising treatment for acute liver injury. Keywords: Hepatic injury, Aloperine, Oxidative stress, Nrf2/HO-1 pathway

scholarly journals Antioxidant Herbs Supplementation Inhibits Endometriosis Extension in Mice

2019 ◽  
Vol 5 (2) ◽  
pp. 53-61
Author(s):  
Yuli Trisetiyono ◽  
Widjiati Widjiati ◽  
Syarief Thaufik Hidayat ◽  
Noor Pramono
Keyword(s):  
Oxidative Stress ◽  
Green Tea ◽  
Cucumis Melo ◽  
Serum Levels ◽  
Green Tea Extract ◽  
Control Group ◽  
Vegf Expression ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Tea Extract

Background: Increased oxidative stress causes inflammation and increases angiogenesis. It presumed to promote the proliferation of endometriosis tissue. Kebar grass (Biophytum petersianum) and other herbs such as green tea and Cucumis melo, which contain high antioxidants, are expected to decrease oxidative stress, inflammation, angiogenesis, and reduced endometriosis implants.Objective: To investigate the effects of Kebar grass, green tea, and Cucumis melo to malondialdehyde serum, tumor necrosis factor alpha, and vascular endothelial growth factor expression, and the area of the endometriotic implants.Methods: Twenty-eight mice were divided into four groups, i.e., the first group of endometriosis mice was given Kebar grass extract; the second group was assigned green tea extract, the third group was given the combination of Cucumis melo extract–gliadin, and the last containing the untreated endometriosis mice as the control. Each treatment was given for 14 days. The data of MDA serum level, the area of the endometriotic implants, TNF-α, and VEGF expression were collected and analyzed.Results: The MDA serum levels of the groups treated with Kebar grass extract, green tea extract, and Cucumis melo extract – gliadin were significantly lower (p=0.001) than the control group. TNF-α expression of the groups provided with each treatment also lower than the control groups (p=0.002). However, only the administration of the Cucumis melo extract–gliadin resulted in lower VEGF expression compare with the control (p=0.017). Finally, the area of the endometriotic implants of the mice models administered with each treatment was smaller than the control group (p=0.003).Conclusion: Kebar grass as well as green tea and Cucumis melo–gliadin inhibits endometriotic implants extension by decreasing MDA serum and TNF-α expression.

scholarly journals Chilean Strawberry Consumption Protects against LPS-Induced Liver Injury by Anti-Inflammatory and Antioxidant Capability in Sprague-Dawley Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Sebastian Molinett ◽  
Francisca Nuñez ◽  
María Alejandra Moya-León ◽  
Jessica Zúñiga-Hernández
Keyword(s):  
Liver Injury ◽  
Aqueous Extract ◽  
Inflammatory Responses ◽  
Animal Health ◽  
Antioxidant Properties ◽  
Serum Levels ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

The Chilean strawberry fruit has high content of antioxidants and polyphenols. Previous studies evidenced antioxidant properties byin vitromethods. However, the antioxidant effect and its impact as functional food on animal health have not been evaluated. In this study, rats were fed with a Chilean strawberry aqueous extract (4 g/kg of animal per day) and then subjected to LPS-induced liver injury (5 mg/kg). Transaminases and histological studies revealed a reduction in liver injury in rats fed with strawberry aqueous extract compared with the control group. Additionally, white strawberry supplementation significantly reduced the serum levels and gene expression of TNF-α, IL-6, and IL-1βcytokines compared with nonsupplemented rats. The level of F2-isoprostanes and GSH/GSSG indicated a reduction in liver oxidative stress by the consumption of strawberry aqueous extract. Altogether, the evidence suggests that dietary supplementation of rats with a Chilean white strawberry aqueous extract favours the normalization of oxidative and inflammatory responses after a liver injury induced by LPS.

scholarly journals Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
C. S. Bruells ◽  
P. Duschner ◽  
G. Marx ◽  
G. Gayan-Ramirez ◽  
N. Frank ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Liver Injury ◽  
Liver Damage ◽  
Acute Liver Injury ◽  
Serum Levels ◽  
Acute Liver Damage ◽  
Markers Of Inflammation ◽  
Amino Phenol ◽  
And Oxidative Stress

AbstractN-acetyl-para-amino phenol (APAP, usually named paracetamol), which is commonly used for its analgesic and antipyretic properties may lead to hepatotoxicity and acute liver damage in case of overdoses. Released cytokines and oxidative stress following acute liver damage may affect other organs’ function notably the diaphragm, which is particularly sensitive to oxidative stress and circulating cytokines. We addressed this issue in a mouse model of acute liver injury induced by administration of APAP. C57BL/6J mice (each n = 8) were treated with N-acetyl-para-amino phenol (APAP) to induce acute drug caused liver injury and sacrificed 12 or 24 h afterwards. An untreated group served as controls. Key markers of inflammation, proteolysis, autophagy and oxidative stress were measured in diaphragm samples. In APAP treated animals, liver damage was proven by the enhanced serum levels of alanine aminotransferase and aspartate aminotransferase. In the diaphragm, besides a significant increase in IL 6 and lipid peroxidation, no changes were observed in key markers of the proteolytic, and autophagy signaling pathways, other inflammatory markers and fiber dimensions. The first 24 h of acute liver damage did not impair diaphragm atrophic pathways although it slightly enhanced IL-6 and lipid peroxidation. Whether longer exposure might affect the diaphragm needs to be addressed in future experiments.

scholarly journals Puerarin Prevents Acute Liver Injury via Inhibiting Inflammatory Responses and ZEB2 Expression

2021 ◽  
Vol 12 ◽  
Author(s):  
Junfa Yang ◽  
Maomao Wu ◽  
Hui Fang ◽  
Yue Su ◽  
Lingling Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Acute Liver Injury ◽  
Expression Level ◽  
Inflammatory Factors ◽  
Tnf Α ◽  
Zeb2 Expression ◽  
Pro Inflammatory Cytokines

Puerarin, an isoflavone component extracted from herb radix puerariae, is widely used in China in the treatment of immune diseases and inflammation. Previous studies have demonstrated that puerarin prevented acute lung injury by regulating inflammatory responses. However, the effect of puerarin on acute liver injury (ALI) was unclear. The purpose of this study was to explore the beneficial effects of puerarin when applied to ALI. We found that puerarin inhibited liver injury and inflammatory cell infiltration in lipopolysaccharide (LPS)/D-galactose (D-Gal)-induced acute liver failure and the liver pro-inflammatory cytokines interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) in liver tissues with ALI and LPS-induced L-02 cells but upregulated the expression level of zinc finger E-box-binding homeobox 2 (ZEB2). Significantly, the results of this study showed that the inhibition of liver pro-inflammatory cytokine (IL-1β, IL-6, and TNF-α) production in LPS-induced L-02 cells was caused by ZEB2 overexpression. However, knocking down ZEB2 promoted LPS-mediated secretion of liver pro-inflammatory cytokines in L-02 cells. Additional experiments showed that puerarin inhibited the activation of the NF-κB signaling pathway by elevating ZEB2 expression in L-02 cells. In summary, puerarin most likely prevented activation of the pro-inflammatory factors and reduced LPS/D-Gal-induced liver injury by enhancing the ZEB2 expression level and, consequently, blocking activation of the NF-κB signaling pathway in the liver.

Modulatory effects of artichoke (Cynara scolymus L.) leaf extract against oxidative stress and hepatic TNF-α gene expression in acute diazinon-induced liver injury in rats

2019 ◽  
Vol 30 (5) ◽  
Author(s):  
Arezoo Ahmadi ◽  
Esfandiar Heidarian ◽  
Keihan Ghatreh-Samani
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Liver Injury ◽  
Leaf Extract ◽  
Protein Carbonyl ◽  
Male Rats ◽  
Control Group ◽  
Cynara Scolymus ◽  
Tnf Α ◽  
Vit C

Abstract Background Diazinon (DZN) causes serious liver damage in both humans and animals. In the present study, the hepatoprotective effects of Cynara scolymus L. leaf extract against DZN-induced liver injury were examined. Methods Forty male rats were divided into five groups. The control group received a normal diet. The DZN group received DZN only (25 mg/kg, po). The DZN + Syl group received DZN (25 mg/kg, po) and silymarin (Syl) (50 mg/kg, po). The DZN + Art group received DZN (25 mg/kg, po) and artichoke (Art) leaf extract (1500 mg/kg, po). The Art group received Art leaf extract only (1500 mg/kg, po). After 15 days, serum tumor necrosis factor α (TNF-α), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lipid profile, protein carbonyl content, serum and hepatic malondialdehyde (MDA), hepatic TNF-α gene expression, hepatic catalase (CAT), superoxide dismutase (SOD), and vitamin C (Vit C) were measured and histopathological examination was performed. Results DZN caused a significant elevation in serum ALP, AST, ALT, MDA, TNF-α, protein carbonyl, hepatic MDA, and TNF-α gene expression in the DZN group as opposed to the control group. Also, DZN led to the reduction of hepatic CAT, SOD, and Vit C in the DZN group relative to the control group. The administration of Art extract resulted in not only a significant reduction in serum ALP, AST, ALT, MDA, TNF-α, and protein carbonyl but also an improvement of liver histopathological changes and hepatic CAT and SOD activities as opposed to the DZN group. Conclusions This study confirmed that Art leaf extract has liver protective effects and causes downregulation of oxidative stress in acute DZN-induced liver injury in rats.

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