Protective effects of matrine against progression of high-fructose diet-induced steatohepatitis by enhancing antioxidant and anti-inflammatory defences involving Nrf2 translocation

Zhang, He-Fang; Shi, Liyun; Song, Guangyao; Cai, Zhi‐Gang; Wang, Chao; An, Rui-Jin

doi:10.1016/j.fct.2012.12.043

Cited by 78 publications

(45 citation statements)

References 55 publications

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“…Compelling evidences have demonstrated the antioxidant function of matrine via enhancing antioxidant enzymes activities and reducing free radical species [5, 17–20]. In the diabetic cardiomyopathy in rats, the cardiac tissues showed a marked excessive free radical species production, while pretreatment with matrine significantly improved oxidative balance and reduced free radical species [21].…”

Section: Discussionmentioning

confidence: 99%

Matrine alleviates lipopolysaccharide-induced intestinal inflammation and oxidative stress via CCR7 signal

Zhou

Zhao³

et al. 2017

Oncotarget

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The aim of this study was to investigate the protective effects of matrine on lipopolysaccharide (LPS)-induced inflammation and oxidative stress in vivo and in vitro. The results showed that matrine improved intestinal inflammatory status and oxidative balance and enhanced chemokine receptor 7 (CCR7) expression. In LPS-challenged mice and Caco-2 cells, matrine alleviated LPS-induced inflammation and oxidative stress via downregulating pro-inflammatory cytokines (IL-1β and IL-17) and malondialdehyde (MDA) production. CCR7-siRNA transfection blocked the protective effects of matrine on LPS-induced inflammation and oxidative stress and exacerbated LPS caused injury. In conclusion, matrine alleviates LPS-induced intestinal inflammation and oxidative stress in mice and Caco-2 cells, which may be associated with CCR7 signal.

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Section: Discussionmentioning

confidence: 99%

Matrine alleviates lipopolysaccharide-induced intestinal inflammation and oxidative stress via CCR7 signal

Zhou

Zhao³

et al. 2017

Oncotarget

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“…Additionally, matrine exhibited antinociceptive effects on neuropathic pain induced by chronic constriction injury in mice (9). Matrine was also effective in preventing the conversion of high-fructose diet-induced hepatic steatosis into non-alcoholic steatohepatitis in rats via regulating Nrf2 (5).…”

Section: Introductionmentioning

confidence: 98%

“…The active compounds of Sophora flavescens AIT consist of alkaloids, flavones and aralosides (2). As a major quinolizindine alkaloid isolated from Sophora flavescens AIT, matrine possesses antitumor, antivirus, antioxidant and anti-inflammatory actions (1,(3)(4)(5). The anticancer effects of matrine were reported in murine hepatocellular carcinoma cells via regulating Bcl-2 and Bax expression (1).…”

Section: Introductionmentioning

confidence: 99%

Matrine improved the function of heart failure in rats via inhibiting apoptosis and blocking β3-adrenoreceptor/endothelial nitric oxide synthase pathway

Yang

Wang

et al. 2014

Molecular Medicine Reports

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Abstract. Matrine, an alkaloid isolated from the traditional Chinese medicine Sophora flavescens AIT has exhibited a number of therapeutic effects on cardiovascular and liver diseases. The purpose of the present study was to investigate whether matrine has a protective effect on heart failure in rats. Coronary artery ligation was used to induce a heart failure (CHF) model in rats. Four weeks following the procedure, the rats were treated with different doses of matrine for one month. Histopathological examination demonstrated that matrine treatment alleviated myocardial hypertrophy and cardiac fibrosis in failing hearts. Furthermore, matrine administration also inhibited the increase of plasma aspartate amino transferase, creatine phosphokinase and lactate dehydrogenase levels in CHF rats. The rats with heart failure exhibited a significant reduction in ejection fraction and fractional shortening, as well as an increase in the left ventricular end systolic dimension, and matrine attenuated this decline in heart function. Further investigation demonstrated that matrine treatment also inhibited the upregulation of Bax and increase in the Bcl-2 expression in the failing hearts. Furthermore, the upregulation of β3-adrenoreceptor (AR) and endothelial nitric oxide synthase proteins following heart failure were also attenuated by matrine. In conclusion, matrine had a preventive role in heart failure in rats at least in part by inhibiting myocardial apoptosis and the β3-AR pathway.

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“…The antioxidant transcription factor nuclear factor (erythroidderived-2)-like 2 (Nrf2) represses TXNIP expression in response to oxidative stress (11). However, Nrf2, which is activated by oxidative stress in livers of NASH patients (52), and upregulated in livers of male Wistar rats with fructoseinduced steatohepatitis (60), can also activate NLRP3 inflammasome (61). It is currently unknown whether the ROS-TXNIP pathway or the ROS-Nrf2 pathway is responsible for NLRP3 inflammasome activation in hepatocytes in the context of fructose-induced NAFLD.…”

Section: Introductionmentioning

confidence: 99%

Reactive Oxygen Species-Induced TXNIP Drives Fructose-Mediated Hepatic Inflammation and Lipid Accumulation Through NLRP3 Inflammasome Activation

Zhang

Chen

et al. 2015

Antioxidants & Redox Signaling

207

144

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Aims: Increased fructose consumption predisposes the liver to nonalcoholic fatty liver disease (NAFLD), but the mechanisms are elusive. Thioredoxin-interacting protein (TXNIP) links oxidative stress to NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation and this signaling axis may be involved in fructose-induced NAFLD. Here, we explore the role of reactive oxygen species (ROS)-induced TXNIP overexpression in fructose-mediated hepatic NLRP3 inflammasome activation, inflammation, and lipid accumulation. Results: Rats were fed a 10% fructose diet for 8 weeks and treated with allopurinol and quercetin during the last 4 weeks. Five millimolars of fructose-exposed hepatocytes (primary rat hepatocytes, rat hepatic parenchymal cells [RHPCs], HLO2, HepG2) were co-incubated with antioxidants or caspase-1 inhibitor or subjected to TXNIP or NLRP3 siRNA interference. Fructose induced NLRP3 inflammasome activation and proinflammatory cytokine secretion, janus-activated kinase 2/signal transducers and activators of transcription 3-mediated inflammatory signaling, and expression alteration of lipid metabolism-related genes in cultured hepatocytes and rat livers. NLRP3 silencing and caspase-1 suppression blocked these effects in primary rat hepatocytes and RHPCs, confirming that inflammasome activation alters hepatocyte lipid metabolism. Hepatocellular ROS and TXNIP were increased in animal and cell models. TXNIP silencing blocked NLRP3 inflammasome activation, inflammation, and lipid metabolism perturbations but not ROS induction in fructoseexposed hepatocytes, whereas antioxidants addition abrogated TXNIP induction and diminished the detrimental effects in fructose-exposed hepatocytes and rat livers. Innovation and Conclusions: This study provides a novel mechanism for fructose-induced NAFLD pathogenesis by which the ROS-TXNIP pathway mediates hepatocellular NLRP3 inflammasome activation, inflammation and lipid accumulation. Antioxidant-based interventions can inhibit the ROS-TXNIP pathway. Antioxid. Redox Signal. 22, 848-870.

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Protective effects of matrine against progression of high-fructose diet-induced steatohepatitis by enhancing antioxidant and anti-inflammatory defences involving Nrf2 translocation

Cited by 78 publications

References 55 publications

Matrine alleviates lipopolysaccharide-induced intestinal inflammation and oxidative stress via CCR7 signal

Matrine alleviates lipopolysaccharide-induced intestinal inflammation and oxidative stress via CCR7 signal

Matrine improved the function of heart failure in rats via inhibiting apoptosis and blocking β3-adrenoreceptor/endothelial nitric oxide synthase pathway

Reactive Oxygen Species-Induced TXNIP Drives Fructose-Mediated Hepatic Inflammation and Lipid Accumulation Through NLRP3 Inflammasome Activation

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