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Sulforaphane protects liver injury induced by intestinal ischemia reperfusion through Nrf2-ARE pathway

World Journal of Gastroenterology 2010年第24期16卷 3002-3010页

作者： Zhao, Hai-Dong Zhang, Feng Shen, Gang Li, Yu-Bing Li, Ying-Hua Jing, Hui-Rong Ma, Ling-Fei Yao, Ji-Hong Tian, Xiao-Feng Dalian Med Univ Affiliated Hosp 2 Dept Gen Surg Dalian 116023 Liaoning Prov Peoples R China Dalian Med Univ Dept Pharmacol Dalian 116044 Liaoning Prov Peoples R China

AIM: To investigate the effect of sulforaphane (SFN) on regulation of NF-E2-related factor-2 (Nrf2)-antiox-idant response element (ARE) pathway in liver injury induced by intestinal ischemia/reperfusion (I/R). METHODS: Rats were divided randomly into four ex-perimental groups: control, SFN control, intestinal I/R and SFN pretreatment groups (n = 8 in each group). The intestinal I/R model was established by clamping the superior mesenteric artery for 1 h and 2 h reperfu-sion. In the SFN pretreatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg SFN 1 h before the op-eration. Intestine and liver histology was investigated. Serum levels of aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured. Liver tissue superoxide dismutase (SOD), myeloperoxidase (MPO), glutathione (GSH) and glutathione peroxidase (GSH-Px) activity were assayed. The liver transcription factor Nrf2 and heme oxygenase-1 (HO-1) were determined by immunohistochemical analysis and Western blotting ***: Intestinal I/R induced intestinal and liver injury, characterized by histological changes as well as a signif icant increase in serum AST and ALT levels (AST: 260.13 ± 40.17 U/L vs 186.00 ± 24.21 U/L, P < 0.01; ALT: 139.63 ± 11.35 U/L vs 48.38 ± 10.73 U/L, P < 0.01), all of which were reduced by pretreatment with SFN, respectively (AST: 260.13 ± 40.17 U/L vs 216.63 ± 22.65 U/L, P < 0.05; ALT: 139.63 ± 11.35 U/L vs 97.63 ± 15.56 U/L, P < 0.01). The activity of SOD in the liver tissue decreased after intestinal I/R (P < 0.01), which was enhanced by SFN pretreatment (P < 0.05). In ad-dition, compared with the control group, SFN markedly reduced liver tissue MPO activity (P < 0.05) and elevat-ed liver tissue GSH and GSH-Px activity (P < 0.05, P < 0.05), which was in parallel with the increased level of liver Nrf2 and HO-1 ***: SFN pretreatment attenuates liver injury induced by intestinal I

关键词： Sulforaphane Liver injury Intestinal isch-emia reperfusion NF-E2-related factor-2 antioxidant response element

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Pachymic Acid Ameliorates Pulmonary Hypertension by Regulating Nrf2-Keap1-ARE Pathway

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Current Medical Science 2022年第1期42卷 56-67页

作者： Yuan HE Jian-hua ZHONG Xiao-dong WEI Chu-ying HUANG Pai-lan PENG Jun YAO Xiu-sheng SONG Wan-li FAN Guang-cai LI Department of Ultrasound the Central Hospital ofEnshi Tujia and Miao Autonomous PrefectureEnshi 445000China Department of Neurology the Central Hospital of Enshi Tujia and Miao Autonomous PrefectureEnshi 445000China Department of Thoracic and Cardiovascular Surgery Minda Hospital of Hubei Minzu UniversityEnshi 445000China Department of Pulmonary and Critical Care Medicine the Central Hospital of Enshi Tujia and Miao Autonomous PrefectureEnshi 445000China

Objective:Pulmonary hypertension(PH)is a severe pulmonary vascular disease that eventually leads to right ventricular failure and *** purpose of this study was to investigate the mechanism by which pachymic acid(PA)pretreatment affects PH and pulmonary vascular remodeling in ***:PH was induced via hypoxia exposure and administration of PA(5 mg/kg per day)in male Sprague-Dawley *** parameters were measured using a right ventricular floating catheter and pulmonary vascular morphometry was measured by hematoxylin-eosin(HE),a-SMA and Masson *** assays and EdU staining were used to detect cell proliferation,and apoptosis was analyzed by TUNEL *** blotting and immunohistochemistry were used to detect the expression of proteins related to the Nrf2-Keapl-ARE pathway.

关键词： pulmonary hypertension pachymic acid nuclear factor erythroid 2-related factor 2 Kelch-like epichlorohydrin-related protein 1 antioxidant response element

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Total saponins of Aralia taibaiensis protects myocardial cells against oxidative stress through the Nrf2-dependent antioxidant pathway

Total saponins of Aralia taibaiensis protects myocardial cel...

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2013年中国药学大会暨第十三届中国药师周

作者： DUAN Jialin CUI Jia GUAN Yue YIN Ying WEI Guo WENG Yan ZHU Yanrong GUO Chao WANG Yanhua YAN Jiajia WU Xiaoxiao XI Miaomiao WEN Aidong Department of pharmacy Xijing hospital The Fourth Military Medical University

Background: Patients with type 2 diabetes have increased cardiovascular disease risk compared with those without diabetes. Hyperglycemia can induce reactive oxygen species （ROS） generation, which contributes to development of diabetic cardiomyopathy. Our previous study has demonstrated that total saponins of Aralia taibaiensis （sAT）, a frequently-used antidiabetic in traditional Chinese medicine （TCM）, can scavenge free radicals in vivo and have good antioxidant ability on lipid peroxidation of rat liver microsomes. To investigate whether sAT could protect the heart, while it was in the treatment of diabetes, we designed this study to elucidate cardioprotective effects of sAT. Methods and results: Oxidative stress was induced in H9c2 cells by high glucose （33 mM） and glucose oxidase （15mU） and the protective effects of sAT were evaluated. Treatment of H9c2 cells with G/GO resulted in an increase in cell death, intracellular ROS level and cell oxidative injury, which were markedly reduced by sAT treatment. Further study revealed that sAT induced the nuclear translocation of Nrf2, enhanced the expression of Nrf2-related antioxidant proteins heme oxygenase （HO-1） and NAD （P） H quinone oxidoreductase-1 （NQO-1）. Inhibition of Nrf2 by siRNA reduced sAT-induced upregulation of these antioxidant genes. Western blotting and luciferase assay revealed sAT activated Nrf2 via the PI3K/Akt pathway. Moreover, Nrf2 siRNA markedly reduced the cytoprotective effects of sAT. Conclusions: sAT exerts cytoprotective effects against oxidative stress induced by hyperglycemia. This cardioprotection is mediated, at least in part, through PI3K/Akt/Nrf2 pathways, which further activates Nrf2-regulated antioxidant enzymes. sAT might be a promising candidate for the treatment of diabetic cardiomyopathy.

关键词： Type 2 diabetes Reactive oxygen species antioxidant response element Total saponins of Aralia taibaiensis Nfr2 AKT

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