scholarly journals Geniposide Ameliorates Liver Fibrosis Through Reducing Oxidative Stress and Inflammatory Respose, Inhibiting Apoptosis and Modulating Overall Metabolism

2021 ◽  
Vol 12 ◽  
Author(s):  
Lu Yang ◽  
Liping Bi ◽  
Lulu Jin ◽  
Yuming Wang ◽  
Yuting Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Inflammatory Response ◽  
Protein Expression ◽  
B Cell Lymphoma ◽  
Untargeted Metabolomics ◽  
Tissue Homogenate ◽  
Therapeutic Effects ◽  
Pathological Changes ◽  
Hepatic Enzymes

Liver fibrosis is a progressive liver damage condition caused by various factors and may progress toward liver cirrhosis, and even hepatocellular carcinoma. Many studies have found that the disfunction in metabolism could contribute to the development of liver fibrosis. Geniposide, derived from Gardenia jasminoides J. Ellis, has been demonstrated with therapeutic effects on liver fibrosis. However, the exact molecular mechanisms of such liver-protection remain largely unknown. The aim of this study was to explored the effect of geniposide on metabolic regulations in liver fibrosis. We used carbon tetrachloride (CCl4) to construct a mouse model of liver fibrosis and subsequently administered geniposide treatment. Therapeutic effects of geniposide on liver fibrosis were accessed through measuring the levels of hepatic enzymes in serum and the pathological changes in liver. We also investigated the effects of geniposide on inflammatory response, oxidative stress and apoptosis in liver. Furthermore, serum untargeted metabolomics were used to explore the metabolic regulatory mechanisms behind geniposide on liver fibrosis. Our results demonstrated that geniposide could reduce the levels of hepatic enzymes in serum and ameliorate the pathological changes in liver fibrosis mice. Geniposide enhanced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased methane dicarboxylic aldehyde (MDA) levels in liver. Geniposide treatment also decreased the levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor-alpha (TNF-a) in liver tissue homogenate. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining demonstrated that geniposide could reduce the apoptosis of hepatocytes. Geniposide increased the protein expression of B-cell lymphoma-2 (Bcl-2) and downregulated the protein expression of Bcl-2 Associated X (Bax), cleaved-Caspase 3, and cleaved-Caspase 9. Serum untargeted metabolomics analysis demonstrated that geniposide treatment improved the metabolic disorders including glycerophospholipid metabolism, arginine and proline metabolism, and arachidonic acid (AA) metabolism. In conclusion, our study demonstrated the protective effects of geniposide on liver fibrosis. We found that geniposide could treat liver fibrosis by inhibiting oxidative stress, reducing inflammatory response and apoptosis in the liver, and modulating glycerophospholipid, and arginine, proline, and AA metabolism processes.

Testicular Injury Attenuated by Rapamycin Through Induction of Autophagy and Inhibition of Endoplasmic Reticulum Stress in Streptozotocin- Induced Diabetic Rats

2019 ◽  
Vol 19 (5) ◽  
pp. 665-675 ◽  
Author(s):  
Wenjiao Shi ◽  
Zhixin Guo ◽  
Ruixia Yuan
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Protective Effect ◽  
Er Stress ◽  
B Cell Lymphoma ◽  
Diabetic Rats ◽  
Pathological Changes ◽  
Rapamycin Treatment ◽  
Related Proteins

Background and Objective: This study investigated whether rapamycin has a protective effect on the testis of diabetic rats by regulating autophagy, endoplasmic reticulum stress, and oxidative stress. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups: control, diabetic, and diabetic treated with rapamycin, which received gavage of rapamycin (2mg.kg-1.d-1) after induction of diabetes. Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ, 65mg.Kg-1). All rats were sacrificed at the termination after 8 weeks of rapamycin treatment. The testicular pathological changes were determined by hematoxylin and eosin staining. The protein or mRNA expression of autophagy-related proteins (Beclin1, microtubule-associated protein light chain 3 (LC3), p62), ER stress marked proteins (CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), caspase-12), oxidative stress-related proteins (p22phox, nuclear factor erythroid2-related factor 2 (Nrf2)) and apoptosis-related proteins (Bax, B cell lymphoma-2 (Bcl-2)) were assayed by western blot or real-time fluorescence quantitative PCR. Results: There were significant pathological changes in the testes of diabetic rats. The expression of Beclin1, LC3, Nrf2, Bcl-2 were significantly decreased and p62, CHOP, caspase12, p22phox, and Bax were notably increased in the testis of diabetic rats (P <0.05). However, rapamycin treatment for 8 weeks significantly reversed the above changes in the testis of diabetic rats (P <0.05). Conclusion: Rapamycin appears to produce a protective effect on the testes of diabetic rats by inducing the expression of autophagy and inhibiting the expression of ER-stress, oxidative stress, and apoptosis.

scholarly journals Dandelion prevents liver fibrosis, inflammatory response, and oxidative stress in rats

2020 ◽  
Vol 81 (1) ◽  
Author(s):  
Alaaeldin Ahmed Hamza ◽  
Mona Gamel Mohamed ◽  
Fawzy Mohamed Lashin ◽  
Amr Amin
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Inflammatory Response ◽  
And Oxidative Stress

Preventive and therapeutic effects of quercetin on lipopolysaccharide-induced oxidative stress and vascular dysfunction in mice

2012 ◽  
Vol 90 (10) ◽  
pp. 1345-1353 ◽  
Author(s):  
Upa Kukongviriyapan ◽  
Kwanjit Sompamit ◽  
Patchareewan Pannangpetch ◽  
Veerapol Kukongviriyapan ◽  
Wanida Donpunha
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Redox Status ◽  
Protein Carbonyl ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Vascular Responsiveness

Quercetin, a dietary antioxidant flavonoid, possesses strong anti-inflammatory and cytoprotective activities. The effects were investigated in an animal model of lipopolysaccharide (LPS)-induced endotoxaemia and vascular dysfunction in vivo. Male ICR mice were injected with LPS (10 mg/kg; i.p.). Quercetin (50 or 100 mg/kg) was intragastrically administered either before or after LPS administration. Fifteen hours after LPS injection, mice were found in endotoxaemic condition, as manifested by hypotension, tachycardia, and blunted vascular responses to vasodilators and vasoconstrictor. The symptoms were accompanied by increased aortic iNOS protein expression, decreased aortic eNOS protein expression, marked suppression of cellular glutathione (GSH) redox status, enhanced aortic superoxide production, increased plasma malodialdehyde and protein carbonyl, and elevated urinary nitrate/nitrite. Treatment with quercetin either before or after LPS preserved the vascular function, as blood pressure, heart rate, vascular responsiveness were restored to near normal values, particularly when quercetin was given as a preventive regimen. The vascular protective effects were associated with upregulation of eNOS expression, reduction of oxidative stress, and maintained blood GSH redox ratio. Overall findings suggest the beneficial effect of quercetin on the prevention and restoration of a failing eNOS system and alleviation of oxidative stress and vascular dysfunction against endotoxin-induced shock in mice.

scholarly journals Cannabidiol Attenuates Methamphetamine-Induced Cardiac Inflammatory Response and Necrosis through The PKA/CREB Signaling Pathway

2021 ◽  
Author(s):  
Qianyun Nie ◽  
Wenjuan Dong ◽  
Baoyu Shen ◽  
Genmeng Yang ◽  
Hao Yu ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Troponin I ◽  
Weight Ratio ◽  
Public Health Problem ◽  
Enzyme Linked Immunosorbent Assay ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Expression Levels

Abstract Methamphetamine (MA) abuse is a major global public health problem, with cardiovascular issues becoming an increasingly recognized complication. Cannabidiol (CBD) has gained recent attention, due to its various pharmacological properties. However, whether CBD has therapeutic effects on MA-induced cardiotoxicity remains unknown. In the present study, we investigated whether CBD has a protective or therapeutic effect on MA-induced cardiac damage in rats via the protein kinase A (PKA)/cyclic adenosine monophosphate response element-binding (CREB) signaling pathway. Thirty rats were randomly divided into five groups. The rats were administered MA by intraperitoneal injection (IP) once a day for 4 weeks, with CBD (40 or 80 mg/kg, IP) treatment 1 h prior to the MA injections. Body and heart weights were measured, and morphological changes were determined using hematoxylin & eosin and Masson’s trichrome staining. The serum levels of interleukin-6 (IL-6) and IL-10 were detected using enzyme linked immunosorbent assay (ELISA) kits. The protein expression levels of PKA, phospho-PKA (p-PKA), CREB, phospho-CREB (p-CREB) and cardiac troponin I (cTnI) in the myocardium were detected by western blot analysis. Results showed that the heart-to-body weight ratio increased significantly following MA administration but decreased with CBD treatment. Chronic administration of MA resulted in a cardiac inflammatory response and progressive development of fibrosis, while CBD treatment attenuated these lesions in a dose-dependent manner. MA administration increased IL-6 but decreased IL-10 levels, which were reversed by CBD pretreatment. Moreover, MA significantly increased the cTnI level, but this was decreased by CBD treatment at 80 mg/kg. The protein expression levels of PKA, p-PKA, CREB, and p-CREB increased following MA administration, but significantly decreased with CBD treatment. Overall, these results indicate that chronic MA administration leads to cardiotoxicity, including cardiac inflammatory response, fibrosis, and myocardial necrosis, but these effects can be attenuated by CBD pretreatment. Our research suggests a potential application of CBD for MA-induced cardiotoxicity, which may attenuate inflammatory response and necrosis through the PKA/CREB signaling pathway.

scholarly journals Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Huan Liu ◽  
Hongrui Guo ◽  
Zhijie Jian ◽  
Hengmin Cui ◽  
Jing Fang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Mouse Liver ◽  
B Cell Lymphoma ◽  
Death Domain ◽  
Expression Levels ◽  
Mrna And Protein Expression ◽  
High Doses ◽  
Induced Apoptosis

Copper (Cu) is an essential trace element involved in the normal physiological processes of animals. However, excessive exposure to Cu can produce numerous detrimental impacts. The aim of this study was to investigate the effects of Cu on oxidative stress and apoptosis as well as their relationship in the mouse liver. Four-week-old ICR mice (n=240) were randomly assigned to different Cu (Cu2+-CuSO4) treatment groups (0, 4, 8, and 16 mg/kg) for periods of 21 and 42 days. The high doses of Cu exposure could induce oxidative stress, by increasing the levels of reactive oxygen species (ROS) and protein carbonyls (PC) and decreasing the activities of antisuperoxide anion (ASA) and antihydroxyl radical (AHR) and content of glutathione (GSH), as well as activities and mRNA expression levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Moreover, high doses of Cu exposure induced hepatic apoptosis via the mitochondrial apoptotic pathway, as characterized by the depolarization of mitochondrial membrane potential (MMP); significantly increased mRNA and protein expression levels of cytosolic cytochrome (Cyt c), apoptosis-inducing factor (AIF), endonuclease G (Endo G), apoptosis protease-activating factor-1 (Apaf-1), cleaved caspase-9, cleaved caspase-3, cleaved PARP, Bcl-2 antagonist killer (Bak), Bcl-2-associated X protein (Bax), and Bcl-2-interacting mediator of cell death (Bim); and decreased mRNA and protein expression levels of B-cell lymphoma-2 (Bcl-2) and Bcl-extra-large (Bcl-xL). Furthermore, the activation of the tumor necrosis factor receptor-1 (TNF-R1) signaling pathway was involved in Cu-induced apoptosis, as characterized by the significantly increased mRNA and protein expression levels of TNF-R1, Fas-associated death domain (FADD), TNFR-associated death domain (TRADD), and cleaved caspase-8. These results indicated that exposure to excess Cu could cause oxidative stress triggered by ROS overproduction and diminished antioxidant function, which in turn promoted hepatic apoptosis via mitochondrial apoptosis and that the TNF-R1 signaling pathway was also involved in the Cu-induced apoptosis.

Se deficiency induces renal pathological changes by regulating selenoprotein expression, disrupting redox balance, and activating inflammation

Metallomics ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1576-1584 ◽  
Author(s):  
Shuang Li ◽  
Qingyu Zhao ◽  
Kai Zhang ◽  
Wenjuan Sun ◽  
Xueting Jia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Selenium Deficiency ◽  
Redox Balance ◽  
Pathological Changes ◽  
Se Deficiency ◽  
Subsequent Activation

This work demonstrates that selenium deficiency causes oxidative stress through a decrease in selenoproteins and subsequent activation of the inflammatory response through the NF-κB and HIF-1α pathways.

scholarly journals Metformin Activates the Protective Effects of the AMPK Pathway in Acute Lung Injury Caused by Paraquat Poisoning

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Liaozhang Wu ◽  
Yifang Cen ◽  
Menglong Feng ◽  
Yanna Zhou ◽  
Hui Tang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protein Expression ◽  
Lung Tissue ◽  
Tissue Homogenate ◽  
Rat Lung ◽  
Pathological Changes ◽  
Expression Levels ◽  
Oxidation Index ◽  
Paraquat Poisoning

Objective. To observe whether metformin (MET) plays a protective role in acute lung injury (ALI) induced by paraquat (PQ) poisoning in rats by activating the AMPK/NF-κB signaling pathway. Methods. PQ exposure was used to construct a rat model of ALI and a model of acute type II alveolar epithelial cell (RLE-6TN) injury, and MET intervention was performed. Rat lung tissue samples were collected to evaluate pathological changes in rat lung tissue, the oxidation index, and inflammatory factors; cell viability was detected by CCK-8 assays, and the protein expression levels of phospho-AMPK and phospho-NF-κBp65 in rat lung tissue and RLE-6TN cells were observed by Western blotting. Results. Compared with the PQ group, the MET treatment group showed significantly (1) reduced lung wet/dry ratio (W/D: 4.67±0.31 vs. 5.45±0.40, P<0.001), (2) reduced pathological changes in lung tissue, (3) decreased MDA levels (nmol/mg prot: 2.70±0.19 vs. 3.08±0.15, P<0.001) and increased SOD and GSH-Px activities (U/mg prot: 76.17±5.22 vs. 45.23±6.58, 30.40±2.84 vs. 21.00±3.20; all P<0.001) in lung tissue homogenate, (4) reduced levels of IL-1β, IL-6, and TNF-α in lung tissue homogenates (pg/mL: 47.87±5.06 vs. 66.77±6.55; 93.03±7.41 vs. 107.39±9.81; 75.73±6.08 vs. 89.12±8.94; all P<0.001), (5) increased activity of RLE-6TN cells (%: 0.69±0.09, 0.76±0.06, and 0.58±0.03 vs. 0.50±0.05; all P<0.05), (6) decreased protein levels of phospho-NF-κBp65 in lung homogenates and RLE-6TN cells (p-NF-κB/NF-κB: 0.47±0.09 vs. 0.81±0.13; 0.26±0.07 vs. 0.79±0.13; all P<0.01), and (7) upregulated protein expression of phospho-AMPK in lung homogenates and RLE-6TN cells (p-AMPK/AMPK: 0.88±0.05 vs. 0.36±0.12; 0.93±0.03 vs. 0.56±0.15; all P<0.01). After the addition of the AMPK inhibitor Compound C (Com C), the protein expression levels of phospho-AMPK and phospho-NF-κBp65 returned to baseline. Conclusion. MET can effectively alleviate ALI induced by paraquat poisoning and increase the viability of cells exposed to paraquat. The mechanism may be related to the activation of the AMPK/NF-κB pathway, downregulation of inflammatory mediators such as IL-6 and TNF-α, and upregulation of the SOD and GSH-Px oxidation index, and these effects can be inhibited by the AMPK inhibitor Com C.

Astragalus Polysaccharide Nano-Liposomes Modulate the Inflammatory Response and Oxidative Stress in Stroke-Associated Pneumonia by Increasing OIP5-AS1 to Regulate the miR-128-3p/SIRT1 Pathway

2020 ◽  
Vol 12 (12) ◽  
pp. 1422-1430
Author(s):  
Weidong Zhu ◽  
Lifeng Yu ◽  
Ze Zhu ◽  
Dongmei Zhang ◽  
Yuyan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Lung Epithelial Cells ◽  
Herbal Extract ◽  
Therapeutic Effects ◽  
Serum Samples ◽  
Sirt1 Expression ◽  
Astragalus Polysaccharide ◽  
And Oxidative Stress

Stroke-associated pneumonia (SAP) is major reason for the poor prognosis of stroke patients. Astragalus polysaccharide (APS) is a commonly used Chinese herbal extract that regulates the inflammatory response, however, its therapeutic effects on APS as well as its underlying mechanism of action are unclear. In this study, we evaluated the effects of APS nano-liposomes on SAP, including regulation of the inflammatory response and oxidative stress, as well as the underlying molecular mechanism. Serum samples of SPA were collected from patients and healthy controls and the expression of OIP5-AS1 and miR-128-3p was measured. Lipopolysaccharide (LPS) was used to construct an in vitro lung injury model using RLE-6TN lung epithelial cells and APS nanoliposomes were used for treatment. Several cellular processes were evaluated including OIP5-AS1, miR-128-3p, and SIRT1 expression by RT-PCR, SIRT1 protein expression by western blot analysis, IL-1β, TNF-α, and IL-6 expression by ELISA, a bioinformatics analysis for downstream molecular targets of OIP5-AS1, and dual luciferase and RNA immunoprecipitation (RIP) assays to identify interactions between miR-128-3p, OIP5-AS1, and SIRT1. Our results revealed low expression of OIP5-AS1 and high expression of miR-128-3p in SAP. Treatment with APS nano-liposomes reduced LPS-induced apoptosis of RLE-6TN cells, inhibited the inflammatory response and oxidative stress, and increased OIP5-AS1 and SIRT1 expression. Furthermore, the overexpression of miR-128-3p reversed the protective effect of APS nano-liposomes on LPS-induced RLE-6TN cells. In summary, OIP5-AS1 is an endogenous competitor that inhibits miR-128-3p targeting of SIRT1. APS nanoliposomes significantly reduced miR-128-3p expression resulting in increased OIP5-AS1 expression.

scholarly journals SIRT5-Related Desuccinylation Modification Contributes to Quercetin-Induced Protection against Heart Failure and High-Glucose-Prompted Cardiomyocytes Injured through Regulation of Mitochondrial Quality Surveillance

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Xing Chang ◽  
Tian Zhang ◽  
Junyan Wang ◽  
Yan Liu ◽  
Peizheng Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Inflammatory Response ◽  
Cardiac Function ◽  
Myocardial Fibrosis ◽  
High Glucose ◽  
Enzyme Linked Immunosorbent Assay ◽  
Therapeutic Effects ◽  
Stress Injury ◽  
Mitochondrial Energy Metabolism

Myocardial fibrosis represents the primary pathological change associated with diabetic cardiomyopathy and heart failure, and it leads to decreased myocardial compliance with impaired cardiac diastolic and systolic function. Quercetin, an active ingredient in various medicinal plants, exerts therapeutic effects against cardiovascular diseases. Here, we investigate whether SIRT5- and IDH2-related desuccinylation is involved in the underlying mechanism of myocardial fibrosis in heart failure while exploring related therapeutic drugs for mitochondrial quality surveillance. Mouse models of myocardial fibrosis and heart failure, established by transverse aortic constriction (TAC), were administered with quercetin (50 mg/kg) daily for 4 weeks. HL-1 cells were pretreated with quercetin and treated with high glucose (30 mM) in vitro. Cardiac function, western blotting, quantitative PCR, enzyme-linked immunosorbent assay, and immunofluorescence analysis were employed to analyze mitochondrial quality surveillance, oxidative stress, and inflammatory response in myocardial cells, whereas IDH2 succinylation levels were detected using immunoprecipitation. Myocardial fibrosis and heart failure incidence increased after TAC, with abnormal cardiac ejection function. Following high-glucose treatment, HL-1 cell activity was inhibited, causing excess production of reactive oxygen species and inhibition of mitochondrial respiratory complex I/III activity and mitochondrial antioxidant enzyme activity, as well as increased oxidative stress and inflammatory response, imbalanced mitochondrial quality surveillance and homeostasis, and increased apoptosis. Quercetin inhibited myocardial fibrosis and improved cardiac function by increasing mitochondrial energy metabolism and regulating mitochondrial fusion/fission and mitochondrial biosynthesis while inhibiting the inflammatory response and oxidative stress injury. Additionally, TAC inhibited SIRT5 expression at the mitochondrial level and increased IDH2 succinylation. However, quercetin promoted the desuccinylation of IDH2 by increasing SIRT5 expression. Moreover, treatment with si-SIRT5 abolished the protective effect of quercetin on cell viability. Hence, quercetin may promote the desuccinylation of IDH2 through SIRT5, maintain mitochondrial homeostasis, protect mouse cardiomyocytes under inflammatory conditions, and improve myocardial fibrosis, thereby reducing the incidence of heart failure.

scholarly journals Therapeutic Effects and Molecular Mechanisms of Ginkgo Biloba Extract on Liver Fibrosis in Rats

2006 ◽  
Vol 34 (01) ◽  
pp. 99-114 ◽  
Author(s):  
Shi-Quan Liu ◽  
Jie-Ping Yu ◽  
Hong-Lei Chen ◽  
He-Sheng Luo ◽  
Shi-Ming Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Ginkgo Biloba ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Ginkgo Biloba Extract ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Mobility Shift

Oxidative stress can be implicated as a cause of liver fibrosis. In this sense, Ginkgo Biloba Extract (EGB), an antioxidant, may be beneficial in restraining liver fibrosis. The aim of this study was to evaluate the effects of EGB on experimental liver fibrosis. Rat liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride ( CCl 4) twice a week for 8 weeks. Three groups of rats received EGB (0.25, 0.5 and 1.0 g/kg, respectively) by stomach everyday. CCl 4 administration induced liver fibrosis, which was inhibited by EGB in a dose-dependent manner. The histopathologic score of fibrosis, liver function and the levels of plasma hyaluronic acid (HA) and laminin (LN) were significantly improved in rats treated with CCl 4 + EGB , compared with those treated with CCl 4 only ( p < 0.01 or p < 0.05). The activities of superoxide dismutase (SOD) and glutathione pero xidase (GSH-Px) were notably elevated, while malondialdehyde (MDA) content was significantly decreased in the rats treated with CCl 4 + EGB ( p < 0.01 or p < 0.05). Inhibition of hepatic stellate cell (HSC) activation and nuclear factor kappaBP65 (NF-κBP65) expression was demonstrated in the livers of EGB-treated rats. The activation of NF-κB was significantly suppressed in EGB-treated rats determined by electrophoretic mobility shift assay (EMSA). Furthermore, EGB reduced expressions of transforming growth factor-β1 (TGF-β1) and collagen I mRNA. In conclusion, EGB is able to ameliorate liver injury and prevent rats from CCl 4-induced liver fibrosis by suppressing oxidative stress. This process may be related to inhibiting the induction of NF-κB on HSC activation and the expression of TGF-β1.

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